WorldWideScience

Sample records for bp deletion induced

  1. Association between the CCR5 32-bp deletion allele and late onset of schizophrenia

    DEFF Research Database (Denmark)

    Rasmussen, H.B.; Timm, S.; Wang, A.G.;

    2006-01-01

    OBJECTIVE: The 32-bp deletion allele in chemokine receptor CCR5 has been associated with several immune-mediated diseases and might be implicated in schizophrenia as well. METHOD: The authors genotyped DNA samples from 268 schizophrenia patients and 323 healthy subjects. Age at first admission...... of the deletion allele in the latter subgroup of patients. CONCLUSIONS: These findings suggest that the CCR5 32-bp deletion allele is a susceptibility factor for schizophrenia with late onset. Alternatively, the CCR5 32-bp deletion allele may act as a modifier by delaying the onset of schizophrenia without...

  2. Frequency of the mtDNA 9-bp deletion in Chinese ethnic groups

    Institute of Scientific and Technical Information of China (English)

    姚永刚; 袁志刚; 周曾娣; 耿排力; 李庆伟; 张亚平

    2001-01-01

    The 9-bp deletion in the COIl/tRNALys intergenic region (region V) of human mitochondrial DNA was screened in 1521 Chinese from 16 ethnic groups and 9 Han geographic groups. The highest frequency was found in populations of Miao (32.4%) and Bouyei (30.8%) from Guizhou Province, whereas no deletion was found in Kazak population in Xinjiang. In the populations of Wa and Lahu from Yunnan Province, Uygur and Mongolian from Xinjiang,the deletion frequency was relatively low ( ≤ 4 % ), while in the remaining 18 groups, the frequency was moderate (6 % ~ 24% ). Except those Hans in Xinjiang, Guizhou and that reported in Taiwan, the deletion frequency in the Han geo graphic groups did not show a substantial difference. However, the deletion frequency in some ethnic groups from the same geographic region or with similar ethnohistory did not show similarity. A general decrease tendency in the deletion frequency was found from south to north and from coastal to inland. The frequency of the 9-bp deletion was approximate ly 17.20% in all Chinese we studied and reported elsewhere. Additionally, 4 individuals were found to carry the tripli cation of 9-bp segment in region V; one individual had X. II type of 9-bp deletion; and no other length polymorphisms were detected in this region in 27 randomly selected individuals with or without the deletion.

  3. Study on 4977-bp deletion mutation of mitochondrial DNA in lung cancer

    Institute of Scientific and Technical Information of China (English)

    DAI Ji-gang; XIAO Ying-bin; MIN Jia-xin; ZHANG Guo-qiang; YAO Ke; ZHOU Ren-jie

    2005-01-01

    Objective: To study the 4977-bp deletion of mitochondiral DNA in lung cancer, adjacent normal tissue and health lung and its significance in the development of cancer. Methods: Thirty-seven matched lung cancer/adjacent histologically normal and 20 "true" normal lung tissue samples from patients without lung cancer were analyzed by long PCR technique. Results: Mitochondrial DNA 4977-bp deletion was detected in 54. 1% (20/37) of lung cancers, 59.5% (22/37) of adjacent normal and 30.0% (6/30) of"true" normal lung tissues. The correlation of 4977-bp deletion with age and smoking factors was present in our data. Conclusion: Mitochondrial DNA 4977-bp deletion is not specific to lung cancer and unlikely to play an important role in carcinogenesis, and may only reflect the environmental and genetic influences during tumor progression.

  4. Association between the CCR5 32-bp deletion allele and late onset of schizophrenia

    DEFF Research Database (Denmark)

    Rasmussen, Henrik Berg; Timm, Sally; Wang, August G;

    2006-01-01

    OBJECTIVE: The 32-bp deletion allele in chemokine receptor CCR5 has been associated with several immune-mediated diseases and might be implicated in schizophrenia as well. METHOD: The authors genotyped DNA samples from 268 schizophrenia patients and 323 healthy subjects. Age at first admission......-onset schizophrenia) and healthy subjects differed significantly. This was reflected in an increased frequency of the deletion allele in the patient subgroup. Patients with ages at first admission below and above 40 years significantly differed in distribution of genotypes and alleles, with an overrepresentation...... of the deletion allele in the latter subgroup of patients. CONCLUSIONS: These findings suggest that the CCR5 32-bp deletion allele is a susceptibility factor for schizophrenia with late onset. Alternatively, the CCR5 32-bp deletion allele may act as a modifier by delaying the onset of schizophrenia without...

  5. Large Scale 7436-bp Deletions in Human Sperm Mitochondrial DNA with Spermatozoa Dysfunction and Male Infertility

    Science.gov (United States)

    Ambulkar, Prafulla S.; Waghmare, Jwalant E.; Chaudhari, Ajay R.; Wankhede, Vandana R.; Tarnekar, Aaditya M.; Shende, Moreshwar R.

    2016-01-01

    Introduction Mitochondria and mitochondrial DNA are essential to sperm motility and fertility. It controls growth, development and differentiation through oxidation energy supply. Mitochondrial (mtDNA) deletions or mutation are frequently attributed to defects of sperm motility and finally these deletions lead to sperm dysfunction and causes infertility in male. Aim To investigate the correlation between large scale 7436-bp deletions in sperm mtDNA and non-motility of sperm in asthenozoospermia and Oligoasthenoteratozoospermia (OAT) infertile men. Materials and Methods The present prospective study was carried out in Human Genetic Division, Department of Anatomy, Mahatma Gandhi Institute of Medical Sciences, Sevagram from June 2014 to July 2016. We have studied 110 asthenozoospermia and OAT infertile men whose semen profile indicated abnormal motility and 50 normal fertile controls. Of 110 infertile men, 70 had asthenozoospermia and 40 had OAT. Fractionations of spermatozoa were done in each semen sample on the basis of their motility by percoll gradients discontinuous technique. Long-range PCR was used for detection of 7436-bp deletions in sperm mtDNA and was confirmed by primer shift technique. Results Overall eight subjects (8/110; 7.2%) of which six (6/70; 8.57%) asthenozoospermia and two (2/40; 5%) OAT had shown deletions of 7436-bp. In 40% percoll fraction had more non-motile spermatozoa than 80% percoll fraction. The non-motile spermatozoa in 40% percoll fractions showed more mtDNA deletions (7.2%) than the motile spermatozoa in 80% percoll fraction (2.7%). The sequencing of flanking regions of deleted mtDNA confirmed 7436-bp deletions. Interestingly, no deletions were found in control subjects. Conclusion Though, the frequency of 7436-bp deletions in sperm mtDNA was low in infertile cases but meaningful indications were there when results were compared with controls. It is indicated that large scale deletions 7436-bp of mtDNA is associated with abnormal

  6. Association of large scale 4977-bp "common" deletions in sperm mitochondrial DNA with asthenozoospermia and oligoasthenoteratozoospermia

    Directory of Open Access Journals (Sweden)

    Prafulla S Ambulkar

    2016-01-01

    Full Text Available OBJECTIVE: To determine the association of large-scale mitochondrial DNA (mtDNA deletions with abnormal sperm or abnormal flagellar movement of human spermatozoa in asthenozoospermia and oligoasthenoteratozoospermia (OAT subjects using percoll gradients fractionation and long-range polymerase chain reaction (PCR. DESIGN: We investigated sixty infertile men and thirty normal healthy fertile controls. Of sixty infertile men, 39 were asthenozoospermia and 21 were OAT. MATERIALS AND METHODS: Percoll gradients discontinuous technique was used for separation of spermatozoa on the basis of their motility. Long-range PCR was used for detection of “common ” 4977-bp deletions, and primer shift technique was used for confirmation of deletions. RESULTS: Overall fourteen subjects (14/60; 23.3% of which eight (8/39; 20.5% asthenozoospermia and six (6/21; 28.6% OAT had shown deletions of 4977-bp. Deletions were more common (23.3% in 40% fraction than 60% (11.6% and 80% (5% fractions. Sequencing results had shown deleted region of mtDNA. CONCLUSION: Abnormal spermatozoa had more number of mtDNA deletions than normal sperm, and abnormal spermatozoa had lost genes for the oxidative phosphorylation. Our findings suggest that large-scale 4977-bp mtDNA deletions in the spermatozoa from the infertile subjects cause the asthenozoospermic and OAT pathophysiological conditions in infertile males.

  7. Role of CCR5 Delta 32 bp deletion in RA and SLE

    NARCIS (Netherlands)

    Martens, H. A.; Kallenberg, C. G. M.; Bijl, M.

    2009-01-01

    CCR5 and its ligands play important roles in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). A deletion of 32 bp in its gene leads to the production of a non-functional receptor. Although a protective effect of CCR5 Delta 32 for the development of RA has been suggested, future stud

  8. Phylogenetic analysis of mitochondrial DNA in a patient with Kearns-Sayre syndrome containing a novel 7629-bp deletion.

    Science.gov (United States)

    Montiel-Sosa, Jose Francisco; Herrero, María Dolores; Munoz, Maria de Lourdes; Aguirre-Campa, Luis Enrique; Pérez-Ramírez, Gerardo; García-Ramírez, Rubén; Ruiz-Pesini, Eduardo; Montoya, Julio

    2013-08-01

    Mitochondrial DNA mutations have been associated with different illnesses in humans, such as Kearns-Sayre syndrome (KSS), which is related to deletions of different sizes and positions among patients. Here, we report a Mexican patient with typical features of KSS containing a novel deletion of 7629 bp in size with 85% heteroplasmy, which has not been previously reported. Sequence analysis revealed 3-bp perfect short direct repeats flanking the deletion region, in addition to 7-bp imperfect direct repeats within 9-10 bp. Furthermore, sequencing, alignment and phylogenetic analysis of the hypervariable region revealed that the patient may belong to a founder Native American haplogroup C4c.

  9. MYBPC3's alternate ending: consequences and therapeutic implications of a highly prevalent 25 bp deletion mutation

    Science.gov (United States)

    Kuster, Diederik W. D.

    2014-01-01

    Hypertrophic cardiomyopathy (HCM) is the most common form of inherited cardiac disease and the leading cause of sudden cardiac death in young people. HCM is caused by mutations in genes encoding contractile proteins. Cardiac myosin binding protein-C (cMyBP-C) is a thick filament contractile protein that regulates sarcomere organization and cardiac contractility. About 200 different mutations in the cMyBP-C gene (MYBPC3) have thus far been reported as causing HCM. Among them, a 25 base pair deletion in the branch point of intron 32 of MYBPC3 is widespread, particularly in South Asia, where it affects ≈4% of South Asian descendants worldwide. This polymorphic mutation results in skipping of exon 33 and a reading frame shift, which, in turn, replaces the last 65 amino acids of the C-terminal C10 domain of cMyBP-C (cMyBP-CC10mut) with a novel sequence of 58 residues. Carriers of the 25 base pair deletion mutation are at increased risk of developing cardiomyopathy and heart failure. Because of the high prevalence of this mutation in certain populations, genetic screening of at-risk groups might be beneficial. Scientifically, the functional consequences of C-terminal mutations and the precise mechanisms leading to HCM should be defined using induced pluripotent stem cells and engineered heart tissue in vitro, or mouse models in vivo. Most importantly, therapeutic strategies that include pharmacology, gene repair and gene therapy should be developed to prevent the adverse clinical effects of cMyBP-CC10mut. This review article aims to examine the effects of cMyBP-CC10mut on cardiac function, emphasizing the need for the development of genetic testing and expanded therapeutic strategies. PMID:24327208

  10. Treacher Collins syndrome with a de Novo 5-bp deletion in the TCOF1 gene.

    Science.gov (United States)

    Su, Pen-Hua; Chen, Jia-Yu; Chen, Suh-Jen; Yu, Ju-Shan

    2006-06-01

    Treacher Collins syndrome (TCS) is an autosomal dominant disorder of craniofacial development with features including malar hypoplasia, micrognathia, microtia, downward slanting palpebral fissures, lower eyelid coloboma, conductive hearing loss, and cleft palate. TCS is caused by mutations in the TCOF1 gene, which encodes the nuclear phosphoprotein treacle. Here, we describe a 1-day-old male infant with classical TCS presentation. A 5-bp deletion in exon 22 of the TCOF1 gene (3469del ACTCT) was found to cause a premature stop codon. This is the first report of TCOF1 gene mutation in the Taiwanese population.

  11. A 57-bp deletion in the ovine KAP6-1 gene affects wool fibre diameter.

    Science.gov (United States)

    Zhou, H; Gong, H; Li, S; Luo, Y; Hickford, J G H

    2015-08-01

    High glycine-tyrosine keratin-associated proteins (HGT-KAPs) are predominantly present in the orthocortex of wool fibres. They vary in abundance in different wools and have been implicated in regulating wool fibre properties, but little is known about the functional roles of these proteins in the fibre matrix. In this study, we used polymerase chain reaction--single-strand conformational polymorphism (PCR-SSCP) analysis to screen for variation in a gene encoding the ovine HGT-KAP6-1 protein. We identified three gene variants (A, B and C). Variants A and B were similar to each other, with only three nucleotide differences occurring downstream of the coding sequence. However, variant C had a 57-bp deletion that would notionally result in a loss of 19 amino acids in the protein. The presence of C was found to be associated with an increase in mean fibre diameter (MFD), fibre diameter standard deviation (FDSD), coefficient of variation of fibre diameter (CVFD) and prickle factor (percentage of fibres over 30 microns; PF). Sheep of genotype BC produced wool of greater MFD, FDSD and PF than sheep of genotypes AA, AB and BB. The CVFD was greater in the BC sheep than the AB sheep. The results suggest that variation in ovine KRTAP6-1 affects wool fibre diameter-associated traits and that the 57-bp deletion in this gene would lead to coarser wool with greater FDSD, CVFD and PF.

  12. A heterozygous 21-bp deletion in CAPN3 causes dominantly inherited limb girdle muscular dystrophy.

    Science.gov (United States)

    Vissing, John; Barresi, Rita; Witting, Nanna; Van Ghelue, Marijke; Gammelgaard, Lise; Bindoff, Laurence A; Straub, Volker; Lochmüller, Hanns; Hudson, Judith; Wahl, Christoph M; Arnardottir, Snjolaug; Dahlbom, Kathe; Jonsrud, Christoffer; Duno, Morten

    2016-08-01

    Limb girdle muscular dystrophy type 2A is the most common limb girdle muscular dystrophy form worldwide. Although strict recessive inheritance is assumed, patients carrying a single mutation in the calpain 3 gene (CAPN3) are reported. Such findings are commonly attributed to incomplete mutation screening. In this investigation, we report 37 individuals (age range: 21-85 years, 21 females and 16 males) from 10 families in whom only one mutation in CAPN3 could be identified; a 21-bp, in-frame deletion (c.643_663del21). This mutation co-segregated with evidence of muscle disease and autosomal dominant transmission in several generations. Evidence of muscle disease was indicated by muscle pain, muscle weakness and wasting, significant fat replacement of muscles on imaging, myopathic changes on muscle biopsy and loss of calpain 3 protein on western blotting. Thirty-one of 34 patients had elevated creatine kinase or myoglobin. Muscle weakness was generally milder than observed in limb girdle muscular dystrophy type 2A, but affected the same muscle groups (proximal leg, lumbar paraspinal and medial gastrocnemius muscles). In some cases, the weakness was severely disabling. The 21-bp deletion did not affect mRNA maturation. Calpain 3 expression in muscle, assessed by western blot, was below 15% of normal levels in the nine mutation carriers in whom this could be tested. Haplotype analysis in four families from three different countries suggests that the 21-bp deletion is a founder mutation. This study provides strong evidence that heterozygosity for the c.643_663del21 deletion in CAPN3 results in a dominantly inherited muscle disease. The normal expression of mutated mRNA and the severe loss of calpain 3 on western blotting, suggest a dominant negative effect with a loss-of-function mechanism affecting the calpain 3 homodimer. This renders patients deficient in calpain 3 as in limb girdle muscular dystrophy type 2A, albeit in a milder form in most cases. Based on findings

  13. Association of large scale 4977-bp “common” deletions in sperm mitochondrial DNA with asthenozoospermia and oligoasthenoteratozoospermia

    Science.gov (United States)

    Ambulkar, Prafulla S.; Chuadhari, Ajay R.; Pal, Asoke K.

    2016-01-01

    OBJECTIVE: To determine the association of large-scale mitochondrial DNA (mtDNA) deletions with abnormal sperm or abnormal flagellar movement of human spermatozoa in asthenozoospermia and oligoasthenoteratozoospermia (OAT) subjects using percoll gradients fractionation and long-range polymerase chain reaction (PCR). DESIGN: We investigated sixty infertile men and thirty normal healthy fertile controls. Of sixty infertile men, 39 were asthenozoospermia and 21 were OAT. MATERIALS AND METHODS: Percoll gradients discontinuous technique was used for separation of spermatozoa on the basis of their motility. Long-range PCR was used for detection of “common” 4977-bp deletions, and primer shift technique was used for confirmation of deletions. RESULTS: Overall fourteen subjects (14/60; 23.3%) of which eight (8/39; 20.5%) asthenozoospermia and six (6/21; 28.6%) OAT had shown deletions of 4977-bp. Deletions were more common (23.3%) in 40% fraction than 60% (11.6%) and 80% (5%) fractions. Sequencing results had shown deleted region of mtDNA. CONCLUSION: Abnormal spermatozoa had more number of mtDNA deletions than normal sperm, and abnormal spermatozoa had lost genes for the oxidative phosphorylation. Our findings suggest that large-scale 4977-bp mtDNA deletions in the spermatozoa from the infertile subjects cause the asthenozoospermic and OAT pathophysiological conditions in infertile males. PMID:27110076

  14. Detection of a 640-bp deletion in the Aggregatibacter actinomycetemcomitans leukotoxin promoter region in isolates from an adolescent of Ethiopian origin

    Directory of Open Access Journals (Sweden)

    Rolf Claesson

    2015-04-01

    Full Text Available The expression of the leukotoxin of Aggregatibacter actinomycetemcomitans is regulated by the leukotoxin promoter. A 530-bp deletion or an 886-bp insertion sequence (IS element in this region has earlier been described in highly leukotoxic isolates. Here, we report on highly leukotoxic isolate with a 640-bp deletion, which was detected in an adolescent of Ethiopian origin.

  15. 30-bp DELETION IN LATENT MEMBRANE PROTEIN 1 (LMP-1) ONCOGENE IN LYMPHOEPITHELIAL CARCINOMA OF SALIVARY GLANDS

    Institute of Scientific and Technical Information of China (English)

    陈彤箴; 杨文涛; 朱雄增

    2004-01-01

    Objective: To investigate the 30 bp deletion in LMP-1 in lymphoepithelial carcinoma of salivary glands, and to clarify the deletion rate. Methods: 46 cases of LEC were subjected to PCR examination for the 3' terminal region of LMP-1 gene, in order to observe the 30 bp deletion. To reduce the influence of unsuccessful DNA extraction from paraffin-embedded tissue sections, a (-actin PCR was performed at the same time. Additionally, DNA sequencing was performed on 1 case without deletion and 1 case with deletion. Results: 4 of 46 specimens were proved to contain no suitable DNA sample by (-actin gene amplification. In the remaining 42 cases, LMP-1 DNA was detected in 35/42 (83.3%) LEC cases. Two kinds of PCR products were found in these 35 cases after further DNA sequencing. 31 cases (88.6%) carried 316 bp product and 4 cases (11.4%) carried 286 bp product. Conclusion: Some LECs of salivary glands carry del-LMP-1. In our study, the deletion rate was 11.4% (4/35).

  16. A heterozygous 21-bp deletion in CAPN3 causes dominantly inherited limb girdle muscular dystrophy

    DEFF Research Database (Denmark)

    Vissing, John; Barresi, Rita; Witting, Nanna;

    2016-01-01

    Limb girdle muscular dystrophy type 2A is the most common limb girdle muscular dystrophy form worldwide. Although strict recessive inheritance is assumed, patients carrying a single mutation in the calpain 3 gene (CAPN3) are reported. Such findings are commonly attributed to incomplete mutation...... creatine kinase or myoglobin. Muscle weakness was generally milder than observed in limb girdle muscular dystrophy type 2A, but affected the same muscle groups (proximal leg, lumbar paraspinal and medial gastrocnemius muscles). In some cases, the weakness was severely disabling. The 21-bp deletion did...... affecting the calpain 3 homodimer. This renders patients deficient in calpain 3 as in limb girdle muscular dystrophy type 2A, albeit in a milder form in most cases. Based on findings in 10 families, our study indicates that a dominantly inherited pattern of calpainopathy exists, and should be considered...

  17. Wasted (wst) mice have 3-bp deletion in the PCNA promoter

    Energy Technology Data Exchange (ETDEWEB)

    Paunesku, T.; Woloschak, G.E. [Argonne National Lab., IL (United States). Center for Mechanistic Biology and Biotechnology

    1997-08-01

    Mice homozygous for the autosomal recessive wasted mutation (wst/wst) have abnormalities in T-lymphocytes and in the anterior motor neuron cells of the spinal cord, leading to sensitivity to ionizing radiation, hind limb paralysis, and immunodeficiency. This defect results in a failure to gain weight by 20 days and death at 28 days of age. Previous results from the authors` group have shown that (1) wasted mice have little if any detectable PCNA protein or mRNA in thymus, but levels in liver, brain, and other tissues are similar to those in controls; and (2) the coding region for PCNA is the same in wasted mice and in control littermates. These observations gave rise to the present study, in which the PCNA promoter was sequenced for wst/wst mice, control littermates ({center_dot}wst/+) and BCF{sub 1} (or BALB/c x C57BL/6) F{sub 1} controls. Sequence analysis revealed only one difference between wst/wst and BALB/c x C57BL/6 F{sub 1} littermates: a 3-bp deletion in the 5 foot upstream region of the PCNA gene of wasted mice that was observed on only one allele or no alleles of normal littermates. The mutated sites in PCNA promoter from two litters plus two additional wst/wst and two known wst/+ animals were screened with 8G and 11G probes, and each confirmed this pattern. The short term DNA segment encompassing the deletion was shown in gel shift experiments to bind a nuclear protein(s) present in a broad variety of cells including thymus and spleen nuclear extract from wst/wst and control mice. The mutated oligomer that was homozygous only in wst/wst mice was not able to bind the same nuclear protein(s).

  18. A novel 30 bp deletion in the FOXL2 gene in a phenotypically normal woman with primary amenorrhoea: case report.

    Science.gov (United States)

    Gersak, Ksenija; Harris, Sarah E; Smale, Wendy J; Shelling, Andrew N

    2004-12-01

    In a Slovene patient with primary amenorrhoea without an association with blepharophimosis/ptosis/epicanthus inversus syndrome (BPES), a novel 30 bp deletion was identified in the FOXL2 gene. We report the clinical features of this woman who has spontaneously conceived and delivered two live healthy babies. The novel deletion was predicted to remove 10 out of 14 alanines (A221_A230del), from the polyalanine tract downstream of the winged helix/forkhead domain of the FOXL2 protein. The patient's parents and sister were shown not to carry this deletion. Despite seeing an anovulatory secretory pattern of FSH, follicles developed spontaneously. Persistent and consistent monitoring have practical implications for genetic and fertility counselling in the era when women with premature ovarian failure usually seek ovum donation. The role of FOXL2 in the development of infertility is still unclear, but several lines of evidence suggest that it plays a central role in follicle development.

  19. Association of an HLA-G 14-bp Insertion/Deletion polymorphism with high HBV replication in chronic hepatitis.

    Science.gov (United States)

    Laaribi, A B; Zidi, I; Hannachi, N; Ben Yahia, H; Chaouch, H; Bortolotti, D; Zidi, N; Letaief, A; Yacoub, S; Boudabous, A; Rizzo, R; Boukadida, J

    2015-10-01

    Identification of an HLA-G 14-bp Insertion/Deletion (Ins/Del) polymorphism at the 3' untranslated region of HLA-G revealed its importance in HLA-G mRNA stability and HLA-G protein level variation. We evaluated the association between the HLA-G 14-bp Ins/Del polymorphism in patients with chronic Hepatitis B virus (HBV) infection in a case-control study. Genomic DNA was extracted from 263 patients with chronic HBV hepatitis and 246 control subjects and was examined for the HLA-G 14-bp Ins/Del polymorphism by PCR. The polymorphic variants were genotyped in chronic HBV seropositive cases stratified according to HBV DNA levels, fibrosis stages and in a control population. There was no statistical significant association between the 14-bp Ins/Del polymorphism and increased susceptibility to HBV infection neither for alleles (P = 0.09) nor for genotypes (P = 0.18). The stratification of HBV patients based on HBV DNA levels revealed an association between the 14-bp Ins/Del polymorphism and an enhanced HBV activity with high HBV DNA levels. In particular, the Ins allele was significantly associated with high HBV DNA levels (P = 0.0024, OR = 1.71, 95% CI 1.2-2.4). The genotype Ins/Ins was associated with a 2.5-fold (95% CI, 1.29-4.88) increased risk of susceptibility to high HBV replication compared with the Del/Del and Ins/Del genotypes. This susceptibility is linked to the presence of two Ins alleles. No association was observed between the 14-bp Ins/Del polymorphism and fibrosis stage of HBV infection. We observed an association between the 14-bp Ins/Del polymorphism and high HBV replication characterized by high HBV DNA levels in chronic HBV patients. These results suggest a potential prognostic value for disease outcome evaluation.

  20. Protective Roles of α-lipoic Acid in Rat Model of Mitochondrial DNA4834bp Deletion in Inner Ear

    Institute of Scientific and Technical Information of China (English)

    彭炜; 胡钰娟; 钟毅; 陈蓓; 孙宇; 杨阳; 孔维佳

    2010-01-01

    The protective roles of α-lipoic acid in the rat model of mitochondrial DNA (mtDNA) 4834bp deletion in inner ear were investigated. Forty female Wistar rats at 4 weeks of age were divided into four groups: group A (D-galactose group, n=10), group B (D-galactose+α-lipoic acid group, n=10), group C (α-lipoic acid group, n=10), and group D (control group, n=10). Auditory brainstem response (ABR) was used to detect the hearing threshold. Colorimetry was used to analyze activity of superoxide dismutase (SOD) and...

  1. The First Report of a 290-bp Deletion in β-Globin Gene in the South of Iran

    Science.gov (United States)

    Hamid, Mohammad; Nejad, Ladan Dawoody; Shariati, Gholamreza; Galehdari, Hamid; Saberi, Alihossein; Mohammadi-Anaei, Marziye

    2017-01-01

    Background: β-thalassemia is one of the most widespread diseases in the world, including Iran. In this study, we reported, for the first time, a 290-bp β-globin gene deletion in the south of Iran. Methods: Four individuals from three unrelated families with Arabic ethnic background were studied in Khuzestan Province. Red blood cell indices and hemoglobin analysis were carried out according to the standard methods. Genomic DNA was obtained from peripheral blood cells by salting out procedures. β-globin gene amplification, multiplex ligation-dependent probe amplification (MLPA), and DNA sequencing were performed. Results: The PCR followed by sequencing and MLPA test of the β-globin gene confirmed the presence of a 290-bp deletion in the heterozygous form, along with -88C>A mutation. All the individuals had elevated hemoglobin A2 and normal fetal hemoglobin levels. Conclusions: This mutation causes β0-thalassemia and can be highly useful for prenatal diagnosis in compound heterozygous condition with different β-globin gene mutations. PMID:26948378

  2. Association between DBH 19 bp insertion/deletion polymorphism and cognition in first-episode schizophrenic patients.

    Science.gov (United States)

    Hui, Li; Zhang, Xuan; Yu, Ya Qin; Han, Mei; Huang, Xu Feng; Chen, Da Chun; Wang, Zhi Ren; Du, Wei Li; Kou, Chang Gui; Yu, Qiong; Kosten, Thomas R; Zhang, Xiang Yang

    2013-07-01

    Many genes associated with dopamine (DA) and norepinephrine (NE) systems influence cognitive deficits of schizophrenia patients, but one key enzyme is dopamine beta-hydroxylase (DBH), which converts DA to NE and whose activity and levels are under strong genetic control. This study examines the association of the 19 bp insertion/deletion (Ins/Del) polymorphism in the 5' flank of the DBH gene with cognitive deficits in first-episode schizophrenic patients (FEP). We assessed the cognitive function in 195 FEP and 304 healthy controls using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). The 19 bp Ins/Del polymorphism of DBH gene was genotyped. Our results showed that the allelic and genotypic frequencies of the 19 bp Ins/Del polymorphism significantly differed between FEP and healthy controls (both p 0.05). Immediate memory abilities significantly differed by genotype (p<0.05) but not genotype×diagnosis. Immediate memory score was lower in FEP with DBH5'-Del/Del genotype (61.3 ± 17.2) than those with DBH5'-Ins/Ins genotype (68.6 ± 16.2; p < 0.05). The 19 bp Del allele was associated with poorer immediate memory performance than the Ins allele in FEP (p < 0.05). However, healthy controls did not show any differences in cognitive function indices between the Ins and Del for either the allele or genotype of the 19 bp Ins/Del polymorphism. Our findings suggest that the DBH5'-Ins/Del polymorphism may play a role in susceptibility to FEP. The DBH5'-Ins/Del polymorphism may also influence immediate memory in FEP. Moreover, FEP had poorer cognitive function than healthy controls in all examined cognitive domains except for the visuospatial/constructional index.

  3. Construction of unmarked bp26 gene-deleted strains of Brucella spp.%布鲁氏菌bp26基因缺失株的构建

    Institute of Scientific and Technical Information of China (English)

    潘文; 王佳莹; 赵明秋; 珺春梅; 易琳; 常艳; 虞红娇; 陈金顶

    2011-01-01

    选择含有反向筛选基因sacB标记的pRE112质粒为自杀载体,利用等位基因交换的方法成功敲除了布鲁氏菌弱毒疫苗S19株、S2株、M5株的bp26基因,构建了具有非杭性基因标记的缺失株S19-△bp26、S2-△bp26、M5-△bp26.将构建的重组自杀质粒pRE-△bp26(缺失了bp26基因的681个碱基)电转化入布鲁氏菌后,经过5μg/mL氯霉素筛选单交换子和70g/L蔗糖筛选同源重组双交换子,用菌落PCR及DNA测序的方法进行验证.结果表明,bp26基因的缺失改造成功,连续传20代后菌落PCR及DNA测序的结果显示突变株具有遗传稳定性.以pRE112自杀质粒为基础构建无杭性基因标记的布鲁氏菌缺失株为布鲁氏菌的基因功能研究莫定了基础,同时△bp26缺失株的构建可为新型布普氏菌疫苗的研制莫定基础.%Three unmarked gene deletion strains of Brucella spp., S19-Δbp26, M5-Δbp26 and S2-Δbp26,were constructed by the allelic exchange introduced by the transformation of the pRE1l2 suicide plasmid containing counter-selection gene sacB.Firstly, the upstream and downstream fragments of bp26 gene were amplified from Brucella spp.genome and then subcloned into suicide plasmid pRE112 to construct the recombinant suicide vector pRE-Δbp26 with 681 bp-deleted bp26 gene fragment.The recombinant suicide vector pREΔbp26 was transformed by electroporation into Brucella spp.and the transformants were selected on TSB-YE plates containing 5 μg/mL chloramphenicol and then 70 g/L sucrose.The successful construction of bp26 gene deletion strains of Brucella spp.were confirmed by the bacterial colony PCR and DNA sequencing.Twenty generations of continuous passage of the S19-Δbp26, M5-Δbp26 and S2-Δbp26 strains showed genetic stability in vitro.The application of pRE112 provided a new suicide plasmid for the construction of unmarked gene deletion strain of Brucella spp.and these strains would be utilized for the study of gene function of Brucella

  4. A fast and easy real-time PCR genotyping method for the HLA-G 14-bp insertion/deletion polymorphism in the 3' untranslated region

    DEFF Research Database (Denmark)

    Djurisic, S; Sørensen, A E; Hviid, T V F

    2012-01-01

    and reliable method to screen for the HLA-G 14-bp insertion/deletion polymorphism using an optimized real-time polymerase chain reaction protocol. The genotyping assay has been validated by comparison with conventional methods. As results can be obtained within a few hours, the assay will have a potential...

  5. A closed-tube assay for genotyping of the 32-bp deletion polymorphism in the chemokine receptor 5 (CCR5) gene

    DEFF Research Database (Denmark)

    Rasmussen, Henrik Berg; Werge, Thomas

    2007-01-01

    We have developed a closed-tube assay for determination of the chemokine receptor type 5 (CCR5) 32-bp deletion allele, which protects against infections with HIV and modulates susceptibility to a variety of inflammatory diseases. This assay utilizes dissociation analysis of amplified products...

  6. Pushing it back. Dating the CCR5–32 bp deletion to the Mesolithic in Sweden and its implications for the Meso\\Neo transition

    Directory of Open Access Journals (Sweden)

    Kerstin Lidén

    2006-12-01

    Full Text Available Genetic variation in the chemokine receptor gene CCR5 has received considerable scientific interest during the last few years. Protection against HIV-infection and AIDS, together with specific geographic distribution are the major reasons for the great interest in CCR5 32bp deletion. The event for the occurrence of this mutation has been postulated by coalescence dating to the 14th century, or 5000 BP. In our prehistoric Swedish samples we show that the frequency of 32pb deletion in CCR5 in the Neolithic population does not deviate from the frequency in a modern Swedish population, and that the deletion existed in Sweden already during the Mesolithic period.

  7. Detection of a new 20-bp insertion/deletion (indel) within sheep PRND gene using mathematical expectation (ME) method.

    Science.gov (United States)

    Li, Jie; Zhu, Xichun; Ma, Lin; Xu, Hongwei; Cao, Xin; Luo, Renyun; Chen, Hong; Sun, Xiuzhu; Cai, Yong; Lan, Xianyong

    2017-03-31

    Prion-related protein doppel gene (PRND), as an essential member of the mammalian prion gene family, is associated with the scrapie susceptibility as well as phenotype traits, so the mutation polymorphism of the PRND has been highly concerned recently, including the single nucleiotide polymorphism and insertion/deletion (indel). Therefore, the objective of present study was to examine this novel indel variants by mathematical expectation (ME) detection method as well as explore its associations with phenotype traits. A novel 20-bp indel was verified in 623 tested individuals representing four diversity sheep breeds. The results showed that three genotypes were detected and the minor allelic frequency was 0.008 (Lanzhou Fat-Tail sheep), 0.084 (Small Tail Han sheep), 0.021(Tong sheep) and 0.083 (Hu sheep), respectively. Comparing with the traditional method of detecting samples one by one, the reaction times with ME method was decreased by 36.22% (STHS), 37.00% (HS), 68.67% (TS) and 83.33% (LFTS), respectively. Besides, this locus were significantly associated to cannon circumference index (P = 0.012) and trunk index (P = 0.037) in the Hu sheep breed. Notably, it was not concordance with the result of DNA sequencing (GCTGTCCCTGCAGGGCTTCT) and dbSNPase of NCBI (NC_443194: g.46184887- 46184906delCTGCTGTCCCTGCAGGGCTT). Consequently, it was the first time to detect the 20-bp indel of sheep PRND gene by ME strategy, which may provide a valuable theoretical basis for marker-assisted selection in sheep genetics and breeding.

  8. Targeted Genes Sequencing Identified a Novel 15 bp Deletion on GJA8 in a Chinese Family with Autosomal Dominant Congenital Cataracts

    Institute of Scientific and Technical Information of China (English)

    Han-Yi Min; Peng-Peng Qiao; Asan; Zhi-Hui Yan; Hui-Feng Jiang; Ya-Ping Zhu; Hui-Qian Du

    2016-01-01

    Background:Congenital cataract (CC) is the leading cause of visual impairment or blindness in children worldwide.Because of highly genetic and clinical heterogeneity,a molecular diagnosis of the lens disease remains a challenge.Methods:In this study,we tested a three-generation Chinese family with autosomal dominant CCs by targeted sequencing of 45 CC genes on next generation sequencing and evaluated the pathogenicity of the detected mutation by protein structure,pedigree validation,and molecular dynamics (MD) simulation.Results:A novel 15 bp deletion on GJA8 (c.426_440delGCTGGAGGGGACCCT or p.143_147delLEGTL) was detected in the family.The deletion,concemed with an in-frame deletion of 5 amino acid residues in a highly evolutionarily conserved region within the cytoplasmic loop domain of the gap junction channel protein connexin 50 (Cx50),was in full cosegregation with the cataract phenotypes in the family but not found in 1100 control exomes.MD simulation revealed that the introduction of the deletion destabilized the Cx50 gap junction channel,indicating the deletion as a dominant-negative mutation.Conclusions:The above results support the pathogenic role of the 15 bp deletion on GJA8 in the Chinese family and demonstrate targeted genes sequencing as a resolution to molecular diagnosis of CCs.

  9. Genotype and phenotype of a new 2-bp deletion of hMSH2 at codon 233.

    Science.gov (United States)

    Müller, A; Beyser, K; Arps, H; Bolander, S; Becker, H; Rüschhoff, J

    2001-08-01

    Germline mutations within mismatch repair genes, such as hMSH2, hMLH1, and hMSH6, have been shown to be the hallmark of the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome. The spectrum of tumors associated with mismatch repair gene defects and the possible relationship between genotype and phenotype are still unclear. Therefore, the spectrum of tumors and the possible genotype-phenotype relationship are still under discussion. Here, we report on a family with a new germline mutation in the hMSH2 gene with a 2-bp deletion at codons 232 and 233 leading to a frame shift and a stop at codon 254. Accordingly, immunohistochemistry revealed loss of hMSH2 expression in colorectal carcinomas of three affected family members. In this one family, there was a high penetrance. Interestingly, mutational screening of the family revealed a high penetrance of the mutation affecting four of five tested people at risk, with a high mortality rate and a trend toward lower age of onset in subsequent generations. Finally, a metachronous breast cancer in one patient turned out to be a tumor unrelated to microsatellite instability phenocopy, i.e., a sporadic tumor unrelated to HNPCC that expressed the hMSH2 gene and did not show any microsatellite instability.

  10. Whole exome sequencing combined with linkage analysis identifies a novel 3 bp deletion in NR5A1.

    Science.gov (United States)

    Eggers, Stefanie; Smith, Katherine R; Bahlo, Melanie; Looijenga, Leendert H J; Drop, Stenvert L S; Juniarto, Zulfa A; Harley, Vincent R; Koopman, Peter; Faradz, Sultana M H; Sinclair, Andrew H

    2015-04-01

    Disorders of sex development (DSDs) encompass a broad spectrum of conditions affecting the development of the gonads and genitalia. The underlying causes for DSDs include gain or loss of function variants in genes responsible for gonad development or steroidogenesis. Most patients with DSD have an unknown genetic etiology and cannot be given an accurate diagnosis. We used whole exome capture and massively parallel sequencing to analyse a large family with 46,XY DSD and 46,XX premature ovarian insufficiency. In addition, we used a recently developed method for linkage analysis using genotypes extracted from the MPS data. This approach identified a unique linkage peak on chromosome 9 and a novel, 3 bp, in-frame deletion in exon six of NR5A1 (steroidogenic factor-1 or SF1) in all affected individuals. We confirmed that the variant disrupts the SF1 protein and its ability to bind and regulate downstream genes. NR5A1 has key roles at multiple points in gonad development and steroidogenic pathways. The variant described here affects the function of SF1 in early testis development and later ovarian function, ultimately leading to the 46,XY DSD and 46,XX premature ovarian insufficiency phenotypes, respectively. This study shows that even at low coverage, whole exome sequencing, when combined with linkage analysis, can be a powerful tool to identify rapidly the disease-causing variant in large pedigrees.

  11. Saethre-Chotzen syndrome and hyper IgE syndrome in a patient with a novel 11 bp deletion of the TWIST gene.

    Science.gov (United States)

    Boeck, A; Kosan, C; Ciznar, P; Kunz, J

    2001-11-15

    Molecular genetic studies in a seven-year-old boy and his mother demonstrated a novel 11 bp deletion in the TWIST gene (127del11), causing Saethre-Chotzen syndrome. The mother had rather mild signs of the Saethre-Chotzen syndrome; however, her son presented with marked acrocephalosyndactyly type 3, leading to craniotomy at three years. He also had recurrent infections and laboratory findings comparable with the hyper IgE syndrome, a rare primary immunodeficiency disorder. It is likely that the 11bp deletion caused the Saethre-Chotzen syndrome in the patient and his mother, and another, not yet identified genetic defect, seen in the patient but not in the mother, is responsible for the hyper IgE phenotype. A combination of these two congenital conditions has not been described to date.

  12. Mitochondrial DNA 4977-bp deletion correlated with reactive oxygen species production and manganese superoxide dismutase expression in gastric tumor cells

    Institute of Scientific and Technical Information of China (English)

    WANG Juan; L(U) You-yong

    2009-01-01

    Background Mitochondrial DNA 4977-bp deletion (△mtDNA4977) was reported in many human neoplasia. However, its biological significance remains to be evaluated and the molecular mechanism needs to be investigated. In this study, we analyzed the frequency of △mtDNA4977 in gastric cancer (GC) cell lines and tissues, as well as reactive oxygen species (ROS) contents and manganese superoxide dismutase (MnSOD) expression levels in GC cell lines to explore its biological significance and molecular mechanism.Methods Semi-quantitative PCR and real-time PCR were used to detect the incidence of △mtDNA4977 in 13 GC cell lines and 272 human gastric tissues (108 GC specimens and the respective adjacent normal tissues, and 56 normal gastric mucosa from non-cancer patients). We further identified intracellular ROS production by flow cytometry and MnSOD expression by semi-quantitative reverse transcription-PCR (RT-PCR) and Western blotting. Statistical analyses were carried out using the Logistic regression analysis and Kaplan-Meier method.Results Based on our earlier study, we optimized the PCR amplification condition by reducing the cycle number. In this study, we systematically documented the high incidence of △mtDNA4977 in GC cell lines (10/13, 76.9%), GC tissues (86/108, 79.6%), matched normal tissues (73/108, 67.6%), and normal gastric mucosa of non-cancer patients (29/56, 51.8%). A significantly higher incidence of mutated △mtDNA4977 was observed in GC tissues with respect to the adjacent normal tissues (79.6% vs 67.6%, P=0.045), and they were both higher than that in normal controls (P <0.05). Most importantly, we linked the △mtDNA4977 mutations with the expression level of MnSOD and ROS contents. The cell lines containing lower expression level of MnSOD was found to have generally higher frequent △mtDNA4977 and more ROS.Conclusion The decreased anti-oxidative ability, which leads to increased ROS contents, is correlated with the mtDNA damage during gastric

  13. Lack of evidence for mutations or deletions in the CDKN2A/p16 and CDKN2B/p15 genes of Brazilian neuroblastoma patients

    Directory of Open Access Journals (Sweden)

    Bassi C.L.

    2004-01-01

    Full Text Available Neuroblastoma, the most common extracranial tumor in childhood, has a wide spectrum of clinical and biological features. The loss of heterozygosity within the 9p21 region has been reported as a prognostic factor. Two tumor suppressor genes located in this region, the CDKN2B/p15 and CDKN2A/p16 (cyclin-dependent kinase inhibitors 2B and 2A, respectively genes, play a critical role in cell cycle progression and are considered to be targets for tumor inactivation. We analyzed CDKN2B/p15 and CDKN2A/p16 gene alterations in 11 patients, who ranged in age from 4 months to 13 years (male/female ratio was 1.2:1. The most frequent stage of the tumor was stage IV (50%, followed by stages II and III (20% and stage I (10%. The samples were submitted to the multiplex PCR technique for homozygous deletion analysis and to single-strand conformation polymorphism and nucleotide sequencing for mutation analysis. All exons of both genes were analyzed, but no deletion was detected. One sample exhibited shift mobility specific for exon 2 in the CDKN2B/p15 gene, not confirmed by DNA sequencing. Homozygous deletions and mutations are not involved in the inactivation mechanism of the CDKN2B/p15 and CDKN2A/p16 genes in neuroblastoma; however, these two abnormalities do not exclude other inactivation pathways. Recent evidence has shown that the expression of these genes is altered in this disease. Therefore, other mechanisms of inactivation, such as methylation of promoter region and unproperly function of proteins, may be considered in order to estimate the real contribution of these genes to neuroblastoma genesis or disease progression.

  14. Decreased peak bone mass is associated with a 3-bp deletion/insertion of the CYP19 intron 4 polymorphism: preliminary data from the GOOS study.

    Science.gov (United States)

    Kastelan, D; Grubic, Z; Kraljevic, I; Duric, K; Kardum, I; Dusek, T; Stingl, K; Giljevic, Z; Kerhin-Brkljacic, V; Suchanek, E; Korsic, M

    2007-06-01

    Finding that estrogen plays an important role in bone homeostasis in men prompted research on relationship of polymorphism at the CYP19 gene and the bone mass. Therefore, influence of 3-bp deletion/insertion polymorphism of CYP19 (TTTA)7 allele on the peak bone mass attainment in males was studied. Fifty-eight unrelated male participants, aged 21-35, were selected depending on the presence of (TTTA)7 (no.=19) or (TTTA)7-3 (no.=39) alleles from the initial cohort of 92 young males. Heterozygotes (TTTA)7/(TTTA)7-3 (no.=13) were not included in the analysis. Serum levels of estradiol, free testosterone, 25-hydroxyvitamin D, bone alkaline phosphatase, osteocalcin, and beta-crosslaps were measured. Bone mass was measured by DXA at the hip and at the spine. (TTTA)7-3 allele was associated with significantly lower femoral neck bone mineral density (BMD) (p=0.02). Logistic regression model indicated strong association of (TTTA)7-3 allele with low BMD in the range of osteopenia/osteoporosis (p=0.014, odds ratio 12.36, confidence intervals 1.65-92.46). In the present study association of 3-bp deletion polymorphism of the (TTTA)7 allele with decreased peak bone mass in males is reported for the first time. However, further studies are necessary to elucidate the functional relevance of this polymorphism.

  15. Sequence analysis for the complete proviral genome of subgroup J Avian Leukosis virus associated with hemangioma: a special 11 bp deletion was observed in U3 region of 3'UTR

    Directory of Open Access Journals (Sweden)

    Zou Nianli

    2011-04-01

    Full Text Available Abstract Background Avian Leukosis virus (ALV of subgroup J (ALV-J belong to retroviruses, which could induce tumors in domestic and wild birds. Myelocytomatosis was the most common neoplasma observed in infected flocks; however, few cases of hemangioma caused by ALV-J were reported in recent year. Results An ALV-J strain SCDY1 associated with hemangioma was isolated and its proviral genomic sequences were determined. The full proviral sequence of SCDY1 was 7489 nt long. Homology analysis of the env, pol and gag gene between SCDY1 and other strains in GenBank were 90.3-94.2%, 96.6-97.6%, and 94.3-96.5% at nucleotide level, respectively; while 85.1-90.7%, 97.4-98.7%, and 96.2-98.4% at amino acid level, respectively. Alignment analysis of the genomic sequence of ALV-J strains by using HPRS-103 as reference showed that a special 11 bp deletion was observed in U3 region of 3'UTR of SCDY1 and another ALV-J strain NHH isolated from case of hemangioma, and the non-functional TM and E element were absent in the genome of SCDY1, but the transcriptional regulatory elements including C/EBP, E2BP, NFAP-1, CArG box and Y box were highly conserved. Phylogenetic analysis revealed that all analyzed ALV-J strains could be separated into four groups, and SCDY1 as well as another strain NHH were included in the same cluster. Conclusion The variation in envelope glycoprotein was higher than other genes. The genome sequence of SCDY1 has a close relationship with that of another ALV-J strain NHH isolated from case of hemangioma. A 11 bp deletion observed in U3 region of 3'UTR of genome of ALV-J isolated from case of hemangioma is interesting, which may be associated with the occurrence of hemangioma.

  16. Activin A induces ovine follicle stimulating hormone beta using -169/-58 bp of its promoter and a simple TATA box

    Directory of Open Access Journals (Sweden)

    Miller William L

    2009-06-01

    Full Text Available Abstract Background Activin A increases production of follicle stimulating hormone (FSH by inducing transcription of its beta subunit (FSHB. This induction has been studied here in LbetaT2 gonadotropes using transient expression of ovine FSHBLuc (-4741 bp of ovine FSHB promoter plus exon/intron 1 linked to Luc. Several sequences between -169/-58 bp of the ovine FSHB proximal promoter are necessary for induction by activin A in LbetaT2 cells, but deletions between -4741/-752 bp decrease induction > 70% suggesting the existence of other important 5' sequences. Induction disappears if a minimal T81 thymidine kinase promoter replaces the ovine FSHB TATA box and 3' exon/intron. The study reported here was designed to determine if sequences outside -169/-58 bp are important for induction of ovine FSHB by activin A. Methods Progressively longer deletions of ovine FSHBLuc were created between -4741/-195 bp. Deletions internal to this region were created also, but replaced with substitute DNA. The ovine FSHB TATA box region (-40/+3 bp was replaced by thymidine kinase and rat prolactin minimal promoters, and substitutions were made in 3' intron/exon sequences. All constructs were tested for basal and activin A-induced expression in LbetaT2 cells. Results Successive 5' deletions progressively lowered fold-induction by activin A from 9.5 to zero, but progressively increased basal expression. Replacing deletions with substitute DNA showed no changes in basal expression or fold-induction. Induction by activin A was supported by the minimal rat prolactin promoter (TATA box but not the thymidine kinase promoter (no TATA box. Replacement mutations in the 3' region did not decrease induction by activin A. Conclusion The data show that specific ovine FSHB sequences 5' to -175 bp or 3' of the transcription start site are not required for induction by activin A. A minimal TATA box promoter supports induction by activin A, but the sequence between the TATA box and

  17. 老龄小鼠耳蜗mtDNA3867bp大片缺失%Cochlear mitochondrial DNA3867bp deletion in aged mice

    Institute of Scientific and Technical Information of China (English)

    张欣欣; 丁大连; 等

    2002-01-01

    Objectives To study the status of cochlear mitochondrial DNA (mtDNA) and to determine the location of mtDNA deletion in aged mice. Methods We detected cochlear mtDNA in 2, 7-10 and 17-19 month old mice by nested polymerase chain reaction (PCR) and DNA sequencing. Results mtDNA3867bp deletions were found in the cochleae of aged mice. The deletion occurred within nt9103-nt12970 and were flanked by 15 base pair direct repeats. Comparing the incidence of mtDNA3867bp deletions, 17-19 month old mice (7/8) were significantly higher than 7-10 month old mice (4/16). The deletion was not observed in 2 month old mice (0/7). The ratio of deleted mtDNA/total mtDNA in 17-19 month old mice was higher than in 7-10 month old mice (P<0.001). Conclusion Cochlear mtDNA 3867bp deletion in aged mice may be related to presbycusis.%目的探讨老龄小鼠耳蜗mtDNA缺失情况,明确老龄小鼠耳蜗mtDNA缺失的位置.方法应用套式PCR和DNA测序技术对不同月龄129/CD1杂交小鼠耳蜗31个(2月龄7个,7-10月龄16个,17-19月龄8个)进行定性及定量检测.结果 1.小鼠耳蜗mtDNA3867bp大片缺失,缺失发生在nt9103-nt12970之间,其两侧nt9089-nt9103和nt12956-nt12970为核苷酸完全相同的15bp重复序列.2. 随着小鼠月龄的增加,耳蜗mtDNA3867bp缺失发生率有明显增加的趋势,2月龄小鼠未发现缺失(0/7);17-19月龄小鼠(7/8)明显高于7-10月龄小鼠(4/16)(P<0.01).3. 缺失mtDNA/总mtDNA比值,17-19月龄小鼠明显高于7-10月龄小鼠(P<0.01).结论老龄小鼠耳蜗出现mtDNA3867bp大片缺失可能与老年性聋发生相关.

  18. Association of large scale 4977-bp “common” deletions in sperm mitochondrial DNA with asthenozoospermia and oligoasthenoteratozoospermia

    OpenAIRE

    Ambulkar, Prafulla S.; Chuadhari, Ajay R.; Pal, Asoke K

    2016-01-01

    OBJECTIVE: To determine the association of large-scale mitochondrial DNA (mtDNA) deletions with abnormal sperm or abnormal flagellar movement of human spermatozoa in asthenozoospermia and oligoasthenoteratozoospermia (OAT) subjects using percoll gradients fractionation and long-range polymerase chain reaction (PCR). DESIGN: We investigated sixty infertile men and thirty normal healthy fertile controls. Of sixty infertile men, 39 were asthenozoospermia and 21 were OAT. MATERIALS AND METHODS: P...

  19. The association between functional HLA-G 14bp insertion/deletion and +3142 C>G polymorphisms and susceptibility to multiple sclerosis.

    Science.gov (United States)

    Ben Fredj, Nadia; Sakly, Kaouthar; Bortolotti, Daria; Aissi, Mouna; Frih-Ayed, Mahbouba; Rotola, Antonella; Caselli, Elisabetta; Cura, Franscesca; Sakly, Nabil; Aouni, Mahjoub; Di Luca, Dario; Rizzo, Roberta

    2016-12-01

    We aimed to investigate two main polymorphisms in the 3' untranslated region (3'UTR) of the HLA-G gene [14bp insertion/deletion (INS/DEL) and +3142 C>G] and to assess their impact on the soluble HLA-G (sHLA-G) production in patients with multiple sclerosis (MS). This study included 60 patients with relasping-remitting (RR) MS and 112 healthy donors (HD). Mutations were identified by PCR and PCR-RFLP, and serum sHLA-G quantification was performed by ELISA. For the 14bp INS/DEL polymorphism, variants frequencies were similar in patients and controls, whereas a significant increased frequency of the +3142 G allele was found in MS patients compared to HD (63.4% vs 52.3%, p=0.04; OR=1.58, 95%CI=1.003-2.48). In addition, an association was found between MS susceptibility and the haplotypes regrouping both studied polymorphisms. Indeed, the 14bp DEL/+3142 G haplotype frequency was significantly increased in MS patients compared to HD (20.8% vs 12.5%, p=0.04, OR=1.84). On the other hand, no associations were detected between both polymorphisms and clinical parameters, except the lower age of disease onset (ADO) in patients with the +3142 C/C genotype. Moreover, our study doesn't show any significant variation of sHLA-G serum levels between patients and controls. Our findings showed that the +3142 C>G, but not the 14bp INS/DEL, polymorphism may constitute a genetic susceptibility factor to MS in the Tunisian population. However, no association was found between the two polymorphisms and sHLA-G serum levels.

  20. The Immature Fiber Mutant Phenotype of Cotton (Gossypium hirsutum Is Linked to a 22-bp Frame-Shift Deletion in a Mitochondria Targeted Pentatricopeptide Repeat Gene

    Directory of Open Access Journals (Sweden)

    Gregory N. Thyssen

    2016-06-01

    Full Text Available Cotton seed trichomes are the most important source of natural fibers globally. The major fiber thickness properties influence the price of the raw material, and the quality of the finished product. The recessive immature fiber (im gene reduces the degree of fiber cell wall thickening by a process that was previously shown to involve mitochondrial function in allotetraploid Gossypium hirsutum. Here, we present the fine genetic mapping of the im locus, gene expression analysis of annotated proteins near the locus, and association analysis of the linked markers. Mapping-by-sequencing identified a 22-bp deletion in a pentatricopeptide repeat (PPR gene that is completely linked to the immature fiber phenotype in 2837 F2 plants, and is absent from all 163 cultivated varieties tested, although other closely linked marker polymorphisms are prevalent in the diversity panel. This frame-shift mutation results in a transcript with two long open reading frames: one containing the N-terminal transit peptide that targets mitochondria, the other containing only the RNA-binding PPR domains, suggesting that a functional PPR protein cannot be targeted to mitochondria in the im mutant. Taken together, these results suggest that PPR gene Gh_A03G0489 is involved in the cotton fiber wall thickening process, and is a promising candidate gene at the im locus. Our findings expand our understanding of the molecular mechanisms that modulate cotton fiber fineness and maturity, and may facilitate the development of cotton varieties with superior fiber attributes.

  1. A 1-bp deletion in Fgf5 causes male-dominant long hair in the Syrian hamster.

    Science.gov (United States)

    Yoshizawa, Yasuhiro; Wada, Kenta; Shimoi, Gaku; Shiomi, Gaku; Kameyama, Yuichi; Wakabayashi, Yuichi; Fukuta, Katsuhiro; Hashizume, Ryoichi

    2015-12-01

    Hair length in mammals is generally regulated by the hair cycle, and its disruption leads to abnormal hair morphogenesis in several species. FGF5, one of the hair cycle regulators, has a role in inducing catagen, and that mutation causes abnormal hair length in both sexes in humans, mice, dogs, and cats. Male-dominant long-haired coat (MALC) is an inbred strain of Syrian hamster exhibiting spontaneous long hair in males. After castration, MALC exhibited significantly shorter hair than the control individuals, but testosterone administration to castrated MALC showed reversion to the original phenotype. Moreover, flutamide administration led to MALC phenotype repression. Histological analysis revealed that hair follicle regression was shown in the wild-type 4 weeks after depilation, but that of MALC remained in the anagen phase. We detected a c.546delG of Fgf5 in MALC (Fgf5malc) that might lead to truncation resulting from a frame shift in FGF5 (p.Arg184GlyfsX6). Additionally, homozygous Fgf5malc was only detected in long-haired (Slc:Syrian×MALC)F2 and (J-2-Nn×MALC)F2 progenies, and all homozygous wild and heterozygous Fgf5malc individuals showed normal hair length. Thus, Fgf5malc leads to male-dominant long hair via a prolonged anagen phase which is affected by testosterone in hamsters. To our knowledge, this report is the first to present the sexual dimorphism of hair length caused by the Fgf5 mutation.

  2. Polypeptone induces dramatic cell lysis in ura4 deletion mutants of fission yeast.

    Directory of Open Access Journals (Sweden)

    Yuzy Matsuo

    Full Text Available Polypeptone is widely excluded from Schizosaccharomyces pombe growth medium. However, the reasons why polypeptone should be avoided have not been documented. Polypeptone dramatically induced cell lysis in the ura4 deletion mutant when cells approached the stationary growth phase, and this phenotype was suppressed by supplementation of uracil. To determine the specificity of this cell lysis phenotype, we created deletion mutants of other genes involved in de novo biosynthesis of uridine monophosphate (ura1, ura2, ura3, and ura5. Cell lysis was not observed in these gene deletion mutants. In addition, concomitant disruption of ura1, ura2, ura3, or ura5 in the ura4 deletion mutant suppressed cell lysis, indicating that cell lysis induced by polypeptone is specific to the ura4 deletion mutant. Furthermore, cell lysis was also suppressed when the gene involved in coenzyme Q biosynthesis was deleted. This is likely because Ura3 requires coenzyme Q for its activity. The ura4 deletion mutant was sensitive to zymolyase, which mainly degrades (1,3-beta-D glucan, when grown in the presence of polypeptone, and cell lysis was suppressed by the osmotic stabiliser, sorbitol. Finally, the induction of cell lysis in the ura4 deletion mutant was due to the accumulation of orotidine-5-monophosphate. Cell wall integrity was dramatically impaired in the ura4 deletion mutant when grown in the presence of polypeptone. Because ura4 is widely used as a selection marker in S. pombe, caution needs to be taken when evaluating phenotypes of ura4 mutants.

  3. Mitochondrial DNA deletion and impairment of mitochondrial biogenesis are mediated by reactive oxygen species in ionizing radiation-induced premature senescence

    Energy Technology Data Exchange (ETDEWEB)

    Eom, Hyeon Soo; Jung, U Hee; Jo, Sung Kee [Radiation Biotechnology Research Division, Korea Atomic Energy Research Institute, Daejeon (Korea, Republic of); Kim, Young Sang [College of Natural Sciences, Chungnam National University, Daejeon (Korea, Republic of)

    2011-09-15

    Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging, and contributes to harmful effects in cultured cells and animal tissues. mtDNA biogenesis genes (NRF-1, TFAM) are essential for the maintenance of mtDNA, as well as the transcription and replication of mitochondrial genomes. Considering that oxidative stress is known to affect mitochondrial biogenesis, we hypothesized that ionizing radiation (IR)-induced reactive oxygen species (ROS) causes mtDNA deletion by modulating the mitochondrial biogenesis, thereby leading to cellular senescence. Therefore, we examined the effects of IR on ROS levels, cellular senescence, mitochondrial biogenesis, and mtDNA deletion in IMR-90 human lung fibroblast cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated at 4 or 8 Gy. Old cells at PD55, and H2O2-treated young cells at PD 39, were compared as a positive control. The IR increased the intracellular ROS level, senescence-associated {beta}-galactosidase (SA-{beta}-gal) activity, and mtDNA common deletion (4977 bp), and it decreased the mRNA expression of NRF-1 and TFAM in IMR-90 cells. Similar results were also observed in old cells (PD 55) and H{sub 2}O{sub 2}-treated young cells. To confirm that a increase in ROS level is essential for mtDNA deletion and changes of mitochondrial biogenesis in irradiated cells, the effects of N-acetylcysteine (NAC) were examined. In irradiated and H{sub 2}O{sub 2}-treated cells, 5 mM NAC significantly attenuated the increases of ROS, mtDNA deletion, and SA-{beta}-gal activity, and recovered from decreased expressions of NRF-1 and TFAM mRNA. These results suggest that ROS is a key cause of IR-induced mtDNA deletion, and the suppression of the mitochondrial biogenesis gene may mediate this process.

  4. Inhibition of HIF-1{alpha} activity by BP-1 ameliorates adjuvant induced arthritis in rats

    Energy Technology Data Exchange (ETDEWEB)

    Shankar, J. [Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago (United States); Thippegowda, P.B., E-mail: btprabha@uic.edu [Department of Pharmacology, (M/C 868), College of Medicine, University of Illinois at Chicago, 835 S. Wolcott Ave., Chicago, IL 60612 (United States); Kanum, S.A. [Department of Chemistry, Yuvaraj' s College, University of Mysore, Mysore (India)

    2009-09-18

    Rheumatoid arthritis (RA) is a chronic inflammatory, angiogenic disease. Inflamed synovitis is a hallmark of RA which is hypoxic in nature. Vascular endothelial growth factor (VEGF), one of the key regulators of angiogenesis, is overexpressed in the pathogenesis of RA. VEGF expression is regulated by hypoxia-inducible factor-1{alpha} (HIF-1{alpha}), a master regulator of homeostasis which plays a pivotal role in hypoxia-induced angiogenesis. In this study we show that synthetic benzophenone analogue, 2-benzoyl-phenoxy acetamide (BP-1) can act as a novel anti-arthritic agent in an experimental adjuvant induced arthritis (AIA) rat model by targeting VEGF and HIF-1{alpha}. BP-1 administered hypoxic endothelial cells and arthritic animals clearly showed down regulation of VEGF expression. Further, BP-1 inhibits nuclear translocation of HIF-1{alpha}, which in turn suppresses transcription of the VEGF gene. These results suggest a further possible clinical application of the BP-1 derivative as an anti-arthritic agent in association with conventional chemotherapeutic agents.

  5. Recognition of edible oil by using BP neural network and laser induced fluorescence spectrum

    Science.gov (United States)

    Mu, Tao-tao; Chen, Si-ying; Zhang, Yin-chao; Guo, Pan; Chen, He; Zhang, Hong-yan; Liu, Xiao-hua; Wang, Yuan; Bu, Zhi-chao

    2013-09-01

    In order to accomplish recognition of the different edible oil we set up a laser induced fluorescence spectrum system in the laboratory based on Laser induced fluorescence spectrum technology, and then collect the fluorescence spectrum of different edible oil by using that system. Based on this, we set up a fluorescence spectrum database of different cooking oil. It is clear that there are three main peak position of different edible oil from fluorescence spectrum chart. Although the peak positions of all cooking oil were almost the same, the relative intensity of different edible oils was totally different. So it could easily accomplish that oil recognition could take advantage of the difference of relative intensity. Feature invariants were extracted from the spectrum data, which were chosen from the fluorescence spectrum database randomly, before distinguishing different cooking oil. Then back propagation (BP) neural network was established and trained by the chosen data from the spectrum database. On that basis real experiment data was identified by BP neural network. It was found that the overall recognition rate could reach as high as 83.2%. Experiments showed that the laser induced fluorescence spectrum of different cooking oil was very different from each other, which could be used to accomplish the oil recognition. Laser induced fluorescence spectrum technology, combined BP neural network,was fast, high sensitivity, non-contact, and high recognition rate. It could become a new technique to accomplish the edible oil recognition and quality detection.

  6. Antibodies with higher bactericidal activity induced by a Neisseria gonorrhoeae Rmp deletion mutant strain.

    Directory of Open Access Journals (Sweden)

    Guocai Li

    Full Text Available Neisseria gonorrhoeae (N. gonorrhoeae outer membrane protein reduction modifiable protein (Rmp has strong immunogenicity. However, anti-Rmp antibodies block rather than preserve the antibacterial effects of protective antibodies, which hampers the development of vaccines for gonococcal infections. We herein constructed an Rmp deletion mutant strain of N. gonorrhoeae by gene homologous recombination. The 261-460 nucleotide residues of Rmp gene amplified from N. gonorrhoeae WHO-A strain were replaced with a kanamycin-resistant Kan gene amplified from pET-28a. The resultant hybridized DNA was transformed into N. gonorrhoeae WHO-A strain. PCR was used to screen the colonies in which wild-type Rmp gene was replaced with a mutant gene fragment. Western blotting revealed that the Rmp deletion mutant strain did not express Rmp protein. Rmp deletion did not alter the morphological and Gram staining properties of the mutant strain that grew slightly more slowly than the wild-type one. Rmp gene mutated stably throughout 25 generations of passage. Antibody-mediated complement-dependent cytotoxicity assay indicated that the antibodies induced by the mutant strain had evidently higher bactericidal activities than those induced by the wild-type strain. Further modification of the Rmp deletion mutant strain is still required in the development of novel live attenuated vaccines for gonorrhea by Opa genes deletion or screening of phenotypic variant strains that do not express Opa proteins.

  7. Antibodies with higher bactericidal activity induced by a Neisseria gonorrhoeae Rmp deletion mutant strain.

    Science.gov (United States)

    Li, Guocai; Xie, Rushan; Zhu, Xiaoping; Mao, Yanli; Liu, Shuangxi; Jiao, Hongmei; Yan, Hua; Xiong, Kun; Ji, Mingchun

    2014-01-01

    Neisseria gonorrhoeae (N. gonorrhoeae) outer membrane protein reduction modifiable protein (Rmp) has strong immunogenicity. However, anti-Rmp antibodies block rather than preserve the antibacterial effects of protective antibodies, which hampers the development of vaccines for gonococcal infections. We herein constructed an Rmp deletion mutant strain of N. gonorrhoeae by gene homologous recombination. The 261-460 nucleotide residues of Rmp gene amplified from N. gonorrhoeae WHO-A strain were replaced with a kanamycin-resistant Kan gene amplified from pET-28a. The resultant hybridized DNA was transformed into N. gonorrhoeae WHO-A strain. PCR was used to screen the colonies in which wild-type Rmp gene was replaced with a mutant gene fragment. Western blotting revealed that the Rmp deletion mutant strain did not express Rmp protein. Rmp deletion did not alter the morphological and Gram staining properties of the mutant strain that grew slightly more slowly than the wild-type one. Rmp gene mutated stably throughout 25 generations of passage. Antibody-mediated complement-dependent cytotoxicity assay indicated that the antibodies induced by the mutant strain had evidently higher bactericidal activities than those induced by the wild-type strain. Further modification of the Rmp deletion mutant strain is still required in the development of novel live attenuated vaccines for gonorrhea by Opa genes deletion or screening of phenotypic variant strains that do not express Opa proteins.

  8. Wilson's disease caused by alternative splicing and Alu exonization due to a homozygous 3039-bp deletion spanning from intron 1 to exon 2 of the ATP7B gene.

    Science.gov (United States)

    Mameli, Eva; Lepori, Maria Barbara; Chiappe, Francesca; Ranucci, Giusy; Di Dato, Fabiola; Iorio, Raffaele; Loudianos, Georgios

    2015-09-15

    We describe a case of Wilson's disease (WD) diagnosed at 5 years after routine biochemical test showed increased aminotransferases. Mutation analysis of the ATP7B gene revealed a 3039-bp deletion in the homozygous state spanning from the terminal part of intron 1 to nt position 368 of exon 2. This deletion results in the activation of 3 cryptic splice sites: an AG acceptor splice site in nt positions 578-579 producing a different breakpoint and removing the first 577 nts of exon 2, an acceptor and a donor splice site in nt positions 20363-4 and 20456-7, respectively, in intron 1, resulting in the activation of a 94-bp cryptic Alu exon being incorporated into the mature transcript. The resulting alternative transcript contains a TAG stop codon in the first amino acid position of the cryptic exon, likely producing a truncated, non-functional protein. This study shows that intron exonization can also occur in humans through naturally occurring gross deletions. The results suggest that the combination of DNA and RNA analyses can be used for molecular characterization of gross ATP7B deletions, thus improving genetic counseling and diagnosis of WD. Moreover these studies help to better establish new molecular mechanisms producing Wilson's disease.

  9. [A Simple and Efficient Method of Inducing Targeted Deletions in the Drosophila Genome].

    Science.gov (United States)

    Kravchuk, O I; Mikhailov, V S; Savitsky, M Yu

    2015-11-01

    Deletion mutagenesis is one of the most efficient approaches to studying gene function. However, conventional methods of inducing targeted mutations in the drosophila genome are time- and labor-consuming. This work proposes a new, simple, and effective method of producing drosophila mutants with gene deletions. The method involves the insertion of I-Scel and I-CreI recognition sites and a fragment homologous to the target sequence into the chromosome region of interest by means of an attB-containing construct, the induction of double-strand DNA breaks by the appropriate meganuclease, and their repair by homologous recombination. The procedure results in a deletion extending from the attP-site to the target locus. A cassette was designed to enable single-step construct production for the deletion of any given genomic region. A set of markers facilitates the selection of recombination events. The efficacy of the proposed technique was confirmed by the induction of a 47-kb deletion containing the qtc gene.

  10. Glandular epithelial AR inactivation enhances PTEN deletion-induced uterine pathology.

    Science.gov (United States)

    Choi, Jaesung Peter; Zheng, Yu; Handelsman, David J; Simanainen, Ulla

    2016-05-01

    Phosphatase and tensin homolog (PTEN) deletion induces uterine pathology, whereas androgen actions via androgen receptor (AR) support uterine growth and therefore may modify uterine cancer risk. We hypothesized that the androgen actions mediated via uterine glandular epithelial AR could modify PTEN deletion-induced uterine pathology. To test our hypothesis, we developed uterine glandular epithelium-specific PTEN and/or AR knockout mouse models comparing the uterine pathology among wild-type (WT), glandular epithelium-specific AR inactivation (ugeARKO), PTEN deletion (ugePTENKO), and the combined PTEN and AR knockout (ugePTENARKO) female mice. The double knockout restricted to glandular epithelium showed that AR inactivation enhanced PTEN deletion-induced uterine pathology with development of intraepithelial neoplasia by 20 weeks of age. In ugePTENARKO, 6/10 (60%) developed intraepithelial neoplasia, whereas 3/10 (30%) developed only glandular hyperplasia in ugePTENKO uterus. No uterine pathology was observed in WT (n=8) and ugeARKO (n=7) uteri. Uterine weight was significantly (P=0.002) increased in ugePTENARKO (374±97 mg (mean±s.e.)) compared with WT (97±6 mg), ugeARKO (94±12 mg), and ugePTENKO (205±33 mg). Estrogen receptor alpha (ERα) and P-AKT expression was modified by uterine pathology but did not differ between ugePTENKO and ugePTENARKO, suggesting that its expressions are not directly affected by androgens. However, progesterone receptor (PR) expression was reduced in ugePTENARKO compared to ugePTENKO uterus, suggesting that PR expression could be regulated by glandular epithelial AR inactivation. In conclusion, glandular epithelial AR inactivation (with persistent stromal AR action) enhanced PTEN deletion-induced uterine pathology possibly by downregulating PR expression in the uterus.

  11. Mitochondrial DNA deletion and impairment of mitochondrial biogenesis by reactive oxygen species in ionizing radiation-induced premature senescence

    Energy Technology Data Exchange (ETDEWEB)

    Eom, Hyeon Soo; Jung, U Hee; Jo, Sung Kee [Korea Atomic Energy Research Institute, Daejeon (Korea, Republic of)

    2011-10-15

    The aim of this study was to determine whether an increase of ROS level in cellular senescence induced by IR could mediate mtDNA deletion via impairment of mitochondria biogenesis in IMR-90 human lung fibroblast cells. Our results showed that IR induced cellular senescence, intracellular ROS, and mtDNA deletion, and in particular, suppressed the expression of mitochondrial biogenesis genes (NRF-1, TFAM). Furthermore, these IR-induced events were abolished using a potent antioxidant, NAC, which suggests that ROS is a key cause of mtDNA deletion in IR-induced cellular senescence, and that the alteration of mitochondrial biogenesis may mediate these processes

  12. Effects of bpV(pic) and bpV(phen) on H9c2 cardiomyoblasts during both hypoxia/reoxygenation and H2O2-induced injuries.

    Science.gov (United States)

    Tian, Youqing; Daoud, Abdelkader; Shang, Jing

    2012-03-01

    Reactive oxygen species (ROS) are involved in myocardial injury. ROS are known to inactivate lipid phosphatase and tension homolog on chromosome 10 (PTEN), an enzyme that increases apoptosis in neonatal cardiomyocytes. BpV(pic) and bpV(phen), two bisperoxovanadium molecules and PTEN inhibitors, may be involved in limiting myocardial infarction. To compare the protective effects of bpV(pic) and bpV(phen) on ROS-induced cardiomyocyte injury and their possible mechanisms, we selected two popular models of hypoxia/reoxygenation (H/R) and H2O2-induced injury in H9c2 cardiomyoblasts to investigate their effects against injury. We found that pre-treatment with bpV(pic) and bpV(phen) increased the viability and protected the morphology of H9c2 cells under the conditions of H/R and H2O2 by inhibiting LDH release, apoptosis and caspases 3/8/9 activities. However, their respective inhibitory abilities in the two models were different, suggesting that the quantity of ROS from the two models might be different. However, the conflict between ROS and PTEN may affect the action of bpV(pic) and bpV(phen). Taken together, the results demonstrate that bpV(pic) and bpV(phen) have inhibitory effects on oxidative stress-induced cardiomyocyte injury that may be partially modulated by the action of ROS on PTEN.

  13. A nine-nucleotide deletion and splice variation in the coding region of the interferon induced ISG12 gene

    DEFF Research Database (Denmark)

    Smidt, Kamille; Hansen, Lise Lotte; Søgaard, T Max M;

    2003-01-01

    distributed between ISG12 and ISG12-S in breast carcinoma cells, in cancer cell lines and in cervical cytobrush material with neoplastic lesions. In addition, we have found a nine-nucleotide deletion situated in exon 4 of the ISG12 gene. This deletion leads to a three-amino-acid deletion (AMA) in the putative...... inducible splice variant of ISG12 lacking exon 2 leading to a putative truncated protein isoform of Mr 7400, ISG12-S. In cells from blood and cervical cytobrush material from healthy women, the level of ISG12-S expression was higher than ISG12 expression, whereas the expression pattern was more evenly...

  14. CtBP1/BARS is an activator of phospholipase D1 necessary for agonist-induced macropinocytosis.

    Science.gov (United States)

    Haga, Yuki; Miwa, Noriko; Jahangeer, Saleem; Okada, Taro; Nakamura, Shun-ichi

    2009-05-06

    Vesicular trafficking such as macropinocytosis is a dynamic process that requires coordinated interactions between specialized proteins and lipids. A recent report suggests the involvement of CtBP1/BARS in epidermal growth factor (EGF)-induced macropinocytosis. Detailed mechanisms as to how lipid remodelling is regulated during macropinocytosis are still undefined. Here, we show that CtBP1/BARS is a physiological activator of PLD1 required in agonist-induced macropinocytosis. EGF-induced macropinocytosis was specifically blocked by 1-butanol but not by 2-butanol. In addition, stimulation of cells by serum or EGF resulted in the association of CtBP1/BARS with PLD1. Finally, CtBP1/BARS activated PLD1 in a synergistic manner with other PLD activators, including ADP-ribosylation factors as demonstrated by in vitro and intact cell systems. The present results shed light on the molecular basis of how the 'fission protein' CtBP1/BARS controls vesicular trafficking events including macropinocytosis.

  15. Increased 4E-BP1 Expression Protects against Diet-Induced Obesity and Insulin Resistance in Male Mice

    Directory of Open Access Journals (Sweden)

    Shih-Yin Tsai

    2016-08-01

    Full Text Available Obesity is a major risk factor driving the global type II diabetes pandemic. However, the molecular factors linking obesity to disease remain to be elucidated. Gender differences are apparent in humans and are also observed in murine models. Here, we link these differences to expression of eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1, which, upon HFD feeding, becomes significantly reduced in the skeletal muscle and adipose tissue of male but not female mice. Strikingly, restoring 4E-BP1 expression in male mice protects them against HFD-induced obesity and insulin resistance. Male 4E-BP1 transgenic mice also exhibit reduced white adipose tissue accumulation accompanied by decreased circulating levels of leptin and triglycerides. Importantly, transgenic 4E-BP1 male mice are also protected from aging-induced obesity and metabolic decline on a normal diet. These results demonstrate that 4E-BP1 is a gender-specific suppressor of obesity that regulates insulin sensitivity and energy metabolism.

  16. [Repression of the enzyme inducible syntheses in Escherichia coli K12 mutant with a deleted ptsH gene].

    Science.gov (United States)

    Gershanovich, V N; Il'ina, T S; Rusina, O Iu; Iurovitskaia, N V; Bol'shakova, T N

    1977-01-01

    The genome of lambda phage with thermosensitive repressor was integrated into the pts region of the E. coli chromosome. Such a lysogenic culture behaves as a pts mutant at 30 degrees. Heating of cells of this strain leads to the induction of lambda prophage and formation of deletions in the pts region. A mutant with a deletion covering ptsH gene was isolated after prophage induction. The deletion nature of pts mutation was confirmed in genetic and biochemical experiments. It was shown that the deletion is small and does not involve ptsI and lig genes. The isolated deltaptsH mutant possesses all characteristics of pts mutants: pleiotropic impairment of transport and utilization of a number of carbohydrates, repression of the enzyme inducible synthesis and resistance to catabolite repression with glucose. These data (together with earlier ones) allow us to conclude that the phosphorylated form of HPr is involved (in direct of indirect manner/ in activation of DNA transcription.

  17. Differential roles for Bim and Nur77 in thymocyte clonal deletion induced by ubiquitous self-antigen.

    Science.gov (United States)

    Hu, Qian Nancy; Baldwin, Troy A

    2015-03-15

    Negative selection, primarily mediated through clonal deletion of self-reactive thymocytes, is critical for establishing self-tolerance and preventing autoimmunity. Recent studies suggest that the molecular mechanisms of negative selection differ depending on the thymic compartment and developmental stage at which thymocytes are deleted. Using the physiological HY(cd4) TCR transgenic model of negative selection against ubiquitous self-antigen, we previously found that one of the principal mediators implicated in clonal deletion, Bim, is required for caspase-3 activation but is ultimately dispensable for negative selection. On the basis of these data, we hypothesized that Nur77, another molecule thought to be a key mediator of clonal deletion, could be responsible for Bim-independent deletion. Despite comparable Nur77 induction in thymocytes during negative selection, Bim deficiency resulted in an accumulation of high-affinity-signaled thymocytes as well as impairment in caspase-mediated and caspase-independent cell death. Although these data suggested that Bim may be required for Nur77-mediated cell death, we found that transgenic Nur77 expression was sufficient to induce apoptosis independently of Bim. However, transgenic Nur77-induced apoptosis was significantly inhibited in the context of TCR signaling, suggesting that endogenous Nur77 could be similarly regulated during negative selection. Although Nur77 deficiency alone did not alter positive or negative selection, combined deficiency in Bim and Nur77 impaired clonal deletion efficiency and significantly increased positive selection efficiency. Collectively, these data shed light on the different roles for Bim and Nur77 during ubiquitous Ag-mediated clonal deletion and highlight potential differences from their reported roles in tissue-restricted Ag-mediated clonal deletion.

  18. Identification and examination of a novel 9-bp insert/deletion polymorphism on porcine SFTPA1 exon 2 associated with acute lung injury using an oleic acid-acute lung injury model.

    Science.gov (United States)

    Zhang, Yuebo; Zhang, Longchao; Wang, Ligang; Qiao, Lijuan; Liang, Jing; Yan, Hua; Zhao, Kebin; Liu, Xin; Wang, Lixian

    2015-06-01

    The pulmonary surfactant-associated protein (SFTPA1, SP-A) gene has been studied as a candidate gene for lung disease resistance in humans and livestock. The objective of the present study was to identify polymorphisms of the porcine SFTPA1 gene coding region and its association with acute lung injury (ALI). Through DNA sequencing and the PCR-single-strand conformation polymorphism method, a novel 9-bp nucleotide insertion (+) or deletion (-) was detected on exon 2 of SFTPA1, which causes a change in three amino acids, namely, alanine (Ala), glycine (Gly) and proline (Pro). Individuals of three genotypes (-/-, +/- and +/+) were divided into equal groups from 60 Rongchang pigs that were genotyped. These pigs were selected for participation in the oleic acid (OA)-ALI model by 1-h and 3-h injections of OA, and there were equal numbers of pigs in the control and injection groups. The lung water content, a marker for acute lung injury, was measured in this study; there is a significant correlation between high lung water content and the presence of the 9-bp indel polymorphism (P polymorphism causing altered expression of the gene. The individuals with the -/- genotype showed lower lung water content than the +/+ genotype pigs, which suggests that polymorphism could be a potential marker for lung disease-resistant pig breeding and that pig can be a potential animal model for human lung disease resistance in future studies.

  19. Resistance to discodermolide, a microtubule-stabilizing agent and senescence inducer, is 4E-BP1–dependent

    OpenAIRE

    Chao, Suzan K.; Lin, Juan; Brouwer-Visser, Jurriaan; Smith, Amos B.; Horwitz, Susan Band; McDaid, Hayley M.

    2010-01-01

    Discodermolide is a microtubule-stabilizing agent that induces accelerated cell senescence. A discodermolide-resistant cell line, AD32, was generated from the human lung cancer cell line A549. We hypothesize that the major resistance mechanism in these cells is escape from accelerated senescence. AD32 cells have decreased levels of 4E-BP1 mRNA and protein, relative to the parental discodermolide-sensitive A549 cells. Lentiviral-mediated re-expression of wild-type 4E-BP1 in AD32 cells increase...

  20. Deletion of Rb1 induces both hyperproliferation and cell death in murine germinal center B cells.

    Science.gov (United States)

    He, Zhiwen; O'Neal, Julie; Wilson, William C; Mahajan, Nitin; Luo, Jun; Wang, Yinan; Su, Mack Y; Lu, Lan; Skeath, James B; Bhattacharya, Deepta; Tomasson, Michael H

    2016-03-01

    The retinoblastoma gene (RB1) has been implicated as a tumor suppressor in multiple myeloma (MM), yet its role remains unclear because in the majority of cases with 13q14 deletions, un-mutated RB1 remains expressed from the retained allele. To explore the role of Rb1 in MM, we examined the functional consequences of single- and double-copy Rb1 loss in germinal center B cells, the cells of origin of MM. We generated mice without Rb1 function in germinal center B cells by crossing Rb1(Flox/Flox) with C-γ-1-Cre (Cγ1) mice expressing the Cre recombinase in class-switched B cells in a p107(-/-) background to prevent p107 from compensating for Rb1 loss (Cγ1-Rb1(F/F)-p107(-/-)). All mice developed normally, but B cells with two copies of Rb1 deleted (Cγ1-Rb1(F/F)-p107(-/-)) exhibited increased proliferation and cell death compared with Cγ1-Rb1(+/+)-p107(-/-) controls ex vivo. In vivo, Cγ1-Rb1(F/F)-p107(-/-) mice had a lower percentage of splenic B220+ cells and reduced numbers of bone marrow antigen-specific secreting cells compared with control mice. Our data indicate that Rb1 loss induces both cell proliferation and death in germinal center B cells. Because no B-cell malignancies developed after 1 year of observation, our data also suggest that Rb1 loss is not sufficient to transform post-germinal center B cells and that additional, specific mutations are likely required to cooperate with Rb1 loss to induce malignant transformation.

  1. SH3BP2 gain-of-function mutation exacerbates inflammation and bone loss in a murine collagen-induced arthritis model.

    Directory of Open Access Journals (Sweden)

    Tomoyuki Mukai

    Full Text Available OBJECTIVE: SH3BP2 is a signaling adapter protein which regulates immune and skeletal systems. Gain-of-function mutations in SH3BP2 cause cherubism, characterized by jawbone destruction. This study was aimed to examine the role of SH3BP2 in inflammatory bone loss using a collagen-induced arthritis (CIA model. METHODS: CIA was induced in wild-type (Sh3bp2(+/+ and heterozygous P416R SH3BP2 cherubism mutant knock-in (Sh3bp2(KI/+ mice, an SH3BP2 gain-of-function model. Severity of the arthritis was determined by assessing the paw swelling and histological analyses of the joints. Micro-CT analysis was used to determine the levels of bone loss. Inflammation and osteoclastogenesis in the joints were evaluated by quantitating the gene expression of inflammatory cytokines and osteoclast markers. Furthermore, involvement of the T- and B-cell responses was determined by draining lymph node cell culture and measurement of the serum anti-mouse type II collagen antibody levels, respectively. Finally, roles of the SH3BP2 mutation in macrophage activation and osteoclastogenesis were determined by evaluating the TNF-α production levels and osteoclast formation in bone marrow-derived M-CSF-dependent macrophage (BMM cultures. RESULTS: Sh3bp2(KI/+ mice exhibited more severe inflammation and bone loss, accompanying an increased number of osteoclasts. The mRNA levels for TNF-α and osteoclast marker genes were higher in the joints of Sh3bp2(KI/+ mice. Lymph node cell culture showed that lymphocyte proliferation and IFN-γ and IL-17 production were comparable between Sh3bp2(+/+ and Sh3bp2(KI/+ cells. Serum anti-type II collagen antibody levels were comparable between Sh3bp2(+/+ and Sh3bp2(KI/+ mice. In vitro experiments showed that TNF-α production in Sh3bp2(KI/+ BMMs is elevated compared with Sh3bp2(+/+ BMMs and that RANKL-induced osteoclastogenesis is enhanced in Sh3bp2(KI/+ BMMs associated with increased NFATc1 nuclear localization. CONCLUSION: Gain-of-function of

  2. Method for identifying mutagenic agents which induce large, multilocus deletions in DNA

    Energy Technology Data Exchange (ETDEWEB)

    Bradley, W.E.C.; Belouchi, A.; Dewyse, P.

    1993-07-13

    A method of identifying a mutagenic agent is described which includes a large, multilocus deletions in DNA in mammalian cells comprising: (i) exposing a class III heterozygous CHO cell line to a potential mutagenic agent under investigation, and allowing any mutation of the cell line to proceed, said cell line being characterized in that a restriction fragment length variation exists in on mutation it becomes resistant to 2,6-diaminopurine and in that the DNA sequence adjacent to the two alleles of the APRT gene such that the DNA sequence adjacent to one of the two alleles can be digested with the enzyme BclI but the DNA sequence variation adjacent to the other of the two alleles cannot be digested with BclI, (ii) isolating induced mutations of the cell line deficient in APRT function, (iii) isolating DNA from the induced mutants, (iv) digesting the isolated DNA with BclI enzyme to produce digested fragments including a 19 kb fragment and any 2 kb fragment, which fragments hybridize with the labeled probe derived from DNA fragment PDI, (v) separating any digested fragments, (vi) transferring the separated fragments of (v) to a solid support, (vii) hybridizing the supported separated fragments with a labeled probe derived from the clone DNA fragment PD 1, (viii) determining fragments having undergone loss of the 2 kb band identified by the probe, as an identification of parent mutants in which the loss occurred, and (ix) evaluating the mutating ability of the potential mutagenic agent.

  3. Resistance to discodermolide, a microtubule-stabilizing agent and senescence inducer, is 4E-BP1-dependent.

    Science.gov (United States)

    Chao, Suzan K; Lin, Juan; Brouwer-Visser, Jurriaan; Smith, Amos B; Horwitz, Susan Band; McDaid, Hayley M

    2011-01-01

    Discodermolide is a microtubule-stabilizing agent that induces accelerated cell senescence. A discodermolide-resistant cell line, AD32, was generated from the human lung cancer cell line A549. We hypothesize that the major resistance mechanism in these cells is escape from accelerated senescence. AD32 cells have decreased levels of 4E-BP1 mRNA and protein, relative to the parental discodermolide-sensitive A549 cells. Lentiviral-mediated re-expression of wild-type 4E-BP1 in AD32 cells increased the proliferation rate and reverted resistance to discodermolide via restoration of discodermolide-induced accelerated senescence. Consistent with this, cell growth and response to discodermolide was confirmed in vivo using tumor xenograft models. Furthermore, reintroduction of a nonphosphorylatable mutant (Thr-37/46 Ala) of 4E-BP1 was able to partially restore sensitivity and enhance proliferation in AD32 cells, suggesting that these effects are independent of phosphorylation by mTORC1. Microarray profiling of AD32-resistant cells versus sensitive A549 cells, and subsequent unbiased gene ontology analysis, identified molecular pathways and functional groupings of differentially expressed mRNAs implicated in overcoming discodermolide-induced senescence. The most statistically significant classes of differentially expressed genes included p53 signaling, G2/M checkpoint regulation, and genes involved in the role of BRCA1 in the DNA damage response. Consistent with this, p53 protein expression was up-regulated and had increased nuclear localization in AD32 cells relative to parental A549 cells. Furthermore, the stability of p53 was enhanced in AD32 cells. Our studies propose a role for 4E-BP1 as a regulator of discodermolide-induced accelerated senescence.

  4. Protective Role of Aldose Reductase Deletion in an Animal Model of Oxygen-Induced Retinopathy

    Directory of Open Access Journals (Sweden)

    Zhongjie Fu

    2011-05-01

    Full Text Available Retinopathy of prematurity (ROP is a common disease occurred in premature babies. Both vascular abnormality and neural dysfunction of the retina were reported, and oxidative stress was involved. Previously, it has been showed that deficiency of aldose reductase (AR, the rate-limiting enzyme in polyol pathway, lowered oxidative stress. Here, the effect of AR deletion on neonatal retinal injury was investigated by using a mouse model of ROP (oxygen-induced retinopathy, OIR. Seven-day-old pups were exposed to 75% oxygen for 5 days and then returned to room air. The vascular changes and neuronal/glial responses were examined and compared between wild-type and AR-deficient OIR mice. Significantly reduced vaso-obliterated area, blood vessel leakage, and early revascularization were observed in AR-deficient OIR mice. Moreover, reduced amacrine cells and less distorted strata were observed in AR-deficient OIR mice. Less astrocytic immunoreactivity and reduced Müller cell gliosis were also observed in AR-deficient mice. After OIR, nitrotyrosine immunoreactivity and poly (ADP-ribose (PAR translocation, which are two oxidative stress markers, were decreased in AR-deficient mice. Significant decrease in VEGF, pho-Erk1/2, pho-Akt, and pho-I?B expression was found in AR-deficient OIR retinae. Thus, these observations suggest that the deficiency of aldose reductase may protect the retina in the OIR model.

  5. Enhancement of DNA vaccine-induced immune responses by a 72-bp element from SV40 enhancer

    Institute of Scientific and Technical Information of China (English)

    LI Hai-shan; XU Jian-qing; HONG Kun-xue; SHAO Yi-ming; LIU Yong; LI Ding-feng; ZHANG Ran-ran; TANG Hai-li; ZHANG Yu-wei; HUANG Wei; LIU Ying; PENG Hong

    2007-01-01

    Background Although DNA vaccine is considered as the next generation of vaccine, most DNA vaccine candidates are still suffering from the relatively weak immunogenicity despite the increased dosage of plasmid DNA administered. In order to enhance the immune responses elicited by a codon-optimized HIV gag DNA vaccine, a modified plasmid vector pDRVI1.0 and a booster immunization with replicating Tiantan vaccinia (RTV) strain expressing the same gene were employed.Methods Vector pDRVI1.0 was constructed through inserting the 72-bp element from the SV40 enhancer, which was reported promoting nuclear transport of plasmid DNA, to the upstream of cytomegalovirus enhancer/promoter region of the plasmid vector pVR1012. Gene expression levels from expression plasmids based on pDRVI1.0 and pVR1012 were tested. Humoral and cellular immune responses induced by DNA vaccine alone or DNA prime-RTV boost regimen were determined in mice.Results It was shown that the 72-bp element significantly enhanced the gene expression level in non-dividing cells.gag-specific humoral and cellular immune responses induced by DNA vaccination were both significantly improved, while the Th1/Th2 balance was not obviously affected by the 72-bp element. RTV boosting further significantly enhanced DNA vaccine-primed antibody and T cell responses in a Th1-biased manner.Conclusions The 72-bp SV40 enhancer element should be included in the DNA vaccine vector and RTV strain is a very efficient live vector for boosting immunization.

  6. Large mitochondrial DNA deletions in ultraviolet B-induced cutaneous photodamage%UVB诱导皮肤细胞光损伤过程中线粒体DNA大片段缺失突变的研究

    Institute of Scientific and Technical Information of China (English)

    王懿娜; 方红; 彭国平; 鲁海峰

    2009-01-01

    Objective To analyze the association between mtDNA mutations and photodamagc after ultraviolet B (UVB) irradiation. Methods Primary human skin fibroblasts (HSF) and primary human epi- dermal keratinocytes of adult (HEKa) were irradiated by sub-lethal doses of UVB thrice a day for 4-5 days. Thereafter, genomic DNA was extracted from irradiated cells and conventional PCR was applied to detect the frequency rates of 4977 bp and 3895 bp mtDNA deletion. To quantitatively analyze the mutation levels, SYBR Green real-time PCR method was performed. Results In both cell lines, the frequency rates and relative copy number of deletions increased with the cumulative doses of UVB exposure (P<0.05). The prevalence rate of 3895 bp deletion peaked 53.3% and and relative copy number reached (49.63±4.38)×10-5, showing a more intense response to the accumulation of UVB radiation than 4977 bp deletion. In HSF, the minimum cumu- lative dose of UVB radiation was 150 mJ/cm2 for the induction of 3895 bp deletion, and 200 mJ/cm2 for the induction of 4977 bp deletion. It seemed that mtDNA deletion was more readily to be induced by UVB radia- tion in HSF than in HEKa. Conclusions The development and accumulation of mtDNA mutation are intimately related with cumulated UVB dose received by skin cells, and the 3895 bp deletion is more reliable in moni- toring the photodamage caused by UV than 4977 bp deletion. Therefore, the 3895 bp deletion may serve as a biomarker for the detection of photodamagc in skin cells. HSF appear to have an increased susceptibility to UVB radiation, which results in a higher frequency and level of mtDNA mutations compared with HEKa.%目的 探讨UVB照射后,线粒体DNA(mtDNA)突变与皮肤细胞光损伤之间的关系.方法 用UVB小剂量、多次照射人皮肤原代成纤维细胞(HSF)和成人原代角质形成细胞(HEKa),诱导其相对活性下降,分别提取基因组DNA,以普通PCR检测mtDNA中的4977 bp缺失和3895 bp缺失突变的发生频率,

  7. PCR detection of retinoblastoma gene deletions in radiation-induced mouse lung adenocarcinomas

    Energy Technology Data Exchange (ETDEWEB)

    Churchill, M.E.; Gemmell, M.A.; Woloschak, G.E.

    1994-05-01

    From 1971--1986, Argonne National Laboratory conducted a series of large-scale studies of tumor incidence in 40,000 BCF{sub 1} mice irradiated with {sup 60}Co {gamma}-rays or JANUS fission-spectrum neutrons. Polymerase chain reaction (PCR) technique was used to detect deletions in the mouse retinoblastoma (mRb) gene. Six mRb gene exon fragments were amplified in a 40-cycle, 3-temperature PCR protocol. Absence of any of these fragments on a Southern blot indicated a deletion of that portion of the mRb gene. Tumors chosen for analysis were lung adenocarcinomas that were judged to be the cause of death in post-mortem analyses. Spontaneous tumors as well as those from irradiated mice were analyzed for mRb deletions. In all normal mouse tissues studies all six mRb exon fragments were present on Southern blots. Tumors in six neutron-irradiated mice also had no mRb deletions. However, 1 of 6 tumors from {gamma}-irradiated mice and 6 of 18 spontaneous tumors from unirradiated mice showed a deletion in one or both mRb alleles. All deletions detected were in the 5{prime} region of the mRb gene.

  8. Deletion of autophagy inducer RB1CC1 results in degeneration of the retinal pigment epithelium.

    Science.gov (United States)

    Yao, Jingyu; Jia, Lin; Khan, Naheed; Lin, Chengmao; Mitter, Sayak K; Boulton, Michael E; Dunaief, Joshua L; Klionsky, Daniel J; Guan, Jun-Lin; Thompson, Debra A; Zacks, David N

    2015-01-01

    Autophagy regulates cellular homeostasis and response to environmental stress. Within the retinal pigment epithelium (RPE) of the eye, the level of autophagy can change with both age and disease. The purpose of this study is to determine the relationship between reduced autophagy and age-related degeneration of the RPE. The gene encoding RB1CC1/FIP200 (RB1-inducible coiled-coil 1), a protein essential for induction of autophagy, was selectively knocked out in the RPE by crossing Best1-Cre mice with mice in which the Rb1cc1 gene was flanked with Lox-P sites (Rb1cc1(flox/flox)). Ex vivo and in vivo analyses, including western blot, immunohistochemistry, transmission electron microscopy, fundus photography, optical coherence tomography, fluorescein angiography, and electroretinography were performed to assess the structure and function of the retina as a function of age. Deletion of Rb1cc1 resulted in multiple autophagy defects within the RPE including decreased conversion of LC3-I to LC3-II, accumulation of autophagy-targeted precursors, and increased numbers of mitochondria. Age-dependent degeneration of the RPE occurred, with formation of atrophic patches, subretinal migration of activated microglial cells, subRPE deposition of inflammatory and oxidatively damaged proteins, subretinal drusenoid deposits, and occasional foci of choroidal neovascularization. There was secondary loss of photoreceptors overlying the degenerated RPE and reduction in the electroretinogram. These observations are consistent with a critical role of autophagy in the maintenance of normal homeostasis in the aging RPE, and indicate that disruption of autophagy leads to retinal phenotypes associated with age-related degeneration.

  9. A composite six bp in-frame deletion in the melanocortin 1 receptor (MC1R gene is associated with the Japanese brindling coat colour in rabbits (Oryctolagus cuniculus

    Directory of Open Access Journals (Sweden)

    Russo Vincenzo

    2010-07-01

    Full Text Available Abstract Background In the domestic rabbit (Oryctolagus cuniculus, classical genetic studies have identified five alleles at the Extension locus: ED (dominant black, ES (steel, weaker version of ED, E (wild type, normal extension of black, eJ(Japanese brindling, mosaic distribution of black and yellow and e (non-extension of black, yellow/red with white belly. Sequencing almost the complete coding sequence (CDS of the rabbit MC1R gene, we recently identified two in-frame deletions associated with dominant black (c.280_285del6; alleles ED or ES and recessive red (c.304_333del30; allele e coat colours. It remained to characterize the eJallele whose phenotypic effect is similar to the Orange and Sex-linked yellow loci of cat and Syrian hamster. Results We sequenced the whole CDS in 25 rabbits of different coat colours including 10 Japanese and 10 Rhinelander (tricolour rabbits and identified another 6 bp-in frame deletion flanked by a G > A transition in 5' (c.[124G>A;125_130del6] that was present in all animals with Japanese brindling coat colour and pattern. These mutations eliminate two amino acids in the first transmembrane domain and, in addition, cause an amino acid substitution at position 44 of the wild type sequence. Genotyping 371 rabbits of 31 breeds with different coat colour this allele (eJ was present in homozygous state in Japanese, Rhinelander and Dutch tricolour rabbits only (except one albino rabbit. Rabbits with eJ/eJ genotype were non fixed at the non-agouti mutation we previously identified in the ASIP gene. Segregation in F1 and F2 families confirmed the order of dominance already determined by classical genetic experiments with a possible dose effect evident comparing eJ/eJ and eJ/e animals. MC1R mRNA was expressed in black hair skin regions only. Conclusions The c.[124A;125_130del6] allele may be responsible for a MC1R variant determining eumelanin production in the black areas. However, the mechanism determining the

  10. A large deletion/insertion-induced frameshift mutation of the androgen receptor gene in a family with a familial complete androgen insensitivity syndrome.

    Science.gov (United States)

    Cong, Peikuan; Ye, Yinghui; Wang, Yue; Lu, Lingping; Yong, Jing; Yu, Ping; Joseph, Kimani Kagunda; Jin, Fan; Qi, Ming

    2012-06-01

    Androgen insensitivity syndrome (AIS) is an X-linked recessive genetic disorder with a normal 46, XY karyotype caused by abnormality of the androgen receptor (AR) gene. One Chinese family consisting of the proband and 5 other members with complete androgen insensitivity syndrome (CAIS) was investigated. Mutation analysis by DNA sequencing on all 8 exons and flanking intron regions of the AR gene revealed a unique large deletion/insertion mutation in the family. A 287 bp deletion and 77 bp insertion (c.933_1219delins77) mutation at codon 312 resulted in a frameshift which caused a premature stop (p.Phe312Aspfs*7) of polypeptide formation. The proband's mother and grandmother were heterozygous for the mutant allele. The proband's father, uncle and grandfather have the normal allele. From the pedigree constructed from mutational analysis of the family, it is revealed that the probably pathogenic mutation comes from the maternal side.

  11. PCR detection of retinoblastoma gene deletions in radiation-induced mouse lung adenocarcinomas

    Energy Technology Data Exchange (ETDEWEB)

    Churchill, M.E.; Gemmell, M.A.; Woloschak, G.E.

    1993-04-01

    From 1971 to 1986, Argonne National Laboratory conducted a series of large-scale studies of tumor incidence in 40,000 BCF{sub 1} mice irradiated with {sup 60}Co {gamma} rays or JANUS fission-spectrum neutrons; normal and tumor tissues from mice in these studies were preserved in paraffin blocks. A polymerase chain reaction (PCR) technique has been developed to detect deletions in the mouse retinoblastoma (mRb) gene in the paraffin-embedded tissues. Microtomed sections were used as the DNA source in PCR reaction mixtures. Six mRb gene exon fragments were amplified in a 40-cycle, 3-temperature PCR protocol. The absence of any of these fragments (relative to control PCR products) on a Southern blot indicated a deletion of that portion of the mRb gene. The tumors chosen for analysis were lung adenocarcinomas that were judged to be the cause of death in post-mortem analyses. Spontaneous tumors as well as those from irradiated mice (569 cGy of {sup 60}Co {gamma} rays or 60 cGy of JANUS neutrons, doses that have been found to have approximately equal biological effectiveness in the BCF, mouse) were analyzed for mRb deletions. In all normal mouse tissues studies, all six mRb exon fragments were present on Southem blots. Tumors in six neutron-irradiated mice also had no mRb deletions. However, I of 6 tumors from {gamma}-irradiated mice and 6 of 18 spontaneous tumors from unirradiated mice had a deletion in one or both mRb alleles. All deletions detected were in the 5{prime} region of the mRb gene.

  12. PCR detection of retinoblastoma gene deletions in radiation-induced mouse lung adenocarcinomas

    Energy Technology Data Exchange (ETDEWEB)

    Churchill, M.E.; Gemmell, M.A.; Woloschak, G.E.

    1993-01-01

    From 1971 to 1986, Argonne National Laboratory conducted a series of large-scale studies of tumor incidence in 40,000 BCF[sub 1] mice irradiated with [sup 60]Co [gamma] rays or JANUS fission-spectrum neutrons; normal and tumor tissues from mice in these studies were preserved in paraffin blocks. A polymerase chain reaction (PCR) technique has been developed to detect deletions in the mouse retinoblastoma (mRb) gene in the paraffin-embedded tissues. Microtomed sections were used as the DNA source in PCR reaction mixtures. Six mRb gene exon fragments were amplified in a 40-cycle, 3-temperature PCR protocol. The absence of any of these fragments (relative to control PCR products) on a Southern blot indicated a deletion of that portion of the mRb gene. The tumors chosen for analysis were lung adenocarcinomas that were judged to be the cause of death in post-mortem analyses. Spontaneous tumors as well as those from irradiated mice (569 cGy of [sup 60]Co [gamma] rays or 60 cGy of JANUS neutrons, doses that have been found to have approximately equal biological effectiveness in the BCF, mouse) were analyzed for mRb deletions. In all normal mouse tissues studies, all six mRb exon fragments were present on Southem blots. Tumors in six neutron-irradiated mice also had no mRb deletions. However, I of 6 tumors from [gamma]-irradiated mice and 6 of 18 spontaneous tumors from unirradiated mice had a deletion in one or both mRb alleles. All deletions detected were in the 5[prime] region of the mRb gene.

  13. Gene deletion of glutathione S-transferase theta: correlation with induced genetic damage and potential role in endogenous mutagenesis.

    Science.gov (United States)

    Wiencke, J K; Pemble, S; Ketterer, B; Kelsey, K T

    1995-01-01

    Genetic traits that confer increased susceptibility to DNA and chromosomal damage from reactive epoxide and peroxides could be important individual risk factors in the development of human cancers. To provide an index of individual sensitivity to expoxides, we previously studied sister chromatid exchange (SCE) induction in peripheral blood lymphocytes and identified a trait involving sensitivity to chromosomal damage by monoepoxybutene and diepoxybutane (DEB), both potential carcinogenic metabolites of 1,3-butadiene. Individuals sensitive to DEB induction of SCEs also had an increased number of background or "spontaneous" SCEs. The present investigation was conducted to test whether a newly described deletion polymorphism in the glutathione S-transferase class theta (GSTT1) was significantly associated with the previously described inherited chromosomal sensitivity to DEB. The background and DEB-induced SCE frequencies in peripheral blood lymphocytes from 78 healthy volunteers were determined with the use of fluorescence plus Giemsa staining. The presence or absence of the homozygous deletion of the GSTT1 gene was determined for each participant using PCR methods. In the present study, we report a close correlation of the DEB sensitivity trait with the novel polymorphism in GSTT1. The GSTT1 polymorphism was also highly associated with the background frequencies of SCE. These studies raise the possibility that DBE is a substrate for GST-theta. Individuals who carry a homozygous deletion of the GSTT1 gene may be at increased risk for genotoxic damage from environmental or occupational 1,3-butadiene exposures. The association of the GSTT1 deletion polymorphism with increases in background SCEs indicates that substrates for this isozyme are encountered commonly in the environment or are endogenous in nature.(ABSTRACT TRUNCATED AT 250 WORDS)

  14. Molecular analysis of two mouse dilute locus deletion mutations: Spontaneous dilute lethal20J and radiation-induced dilute prenatal lethal Aa2 alleles

    Energy Technology Data Exchange (ETDEWEB)

    Strobel, M.C.; Seperack, P.K.; Copeland, N.G.; Jenkins, N.A. (National Cancer Institute-Frederick Cancer Research Facility, MD (USA))

    1990-02-01

    The dilute (d) coat color locus of mouse chromosome 9 has been identified by more than 200 spontaneous and mutagen-induced recessive mutations. With the advent of molecular probes for this locus, the molecular lesion associated with different dilute alleles can be recognized and precisely defined. In this study, two dilute mutations, dilute-lethal20J (dl20J) and dilute prenatal lethal Aa2, have been examined. Using a dilute locus genomic probe in Southern blot analysis, we detected unique restriction fragments in dl20J and Aa2 DNA. Subsequent analysis of these fragments showed that they represented deletion breakpoint fusion fragments. DNA sequence analysis of each mutation-associated deletion breakpoint fusion fragment suggests that both genomic deletions were generated by nonhomologous recombination events. The spontaneous dl20J mutation is caused by an interstitial deletion that removes a single coding exon of the dilute gene. The correlation between this discrete deletion and the expression of all dilute-associated phenotypes in dl20J homozygotes defines the dl20J mutation as a functional null allele of the dilute gene. The radiation-induced Aa2 allele is a multilocus deletion that, by complementation analysis, affects both the dilute locus and the proximal prenatal lethal-3 (pl-3) functional unit. Molecular analysis of the Aa2 deletion breakpoint fusion fragment has provided access to a previously undefined gene proximal to d. Initial characterization of this new gene suggests that it may represent the genetically defined pl-3 functional unit.

  15. Tph2 gene deletion enhances amphetamine-induced hypermotility: effect of 5-HT restoration and role of striatal noradrenaline release.

    Science.gov (United States)

    Carli, Mirjana; Kostoula, Chrysaugi; Sacchetti, Giuseppina; Mainolfi, Pierangela; Anastasia, Alessia; Villani, Claudia; Invernizzi, Roberto William

    2015-11-01

    Variants of tryptophan hydroxylase-2 (Tph2), the gene encoding enzyme responsible for the synthesis of brain serotonin (5-HT), have been associated with neuropsychiatric disorders, substance abuse and addiction. This study assessed the effect of Tph2 gene deletion on motor behavior and found that motor activity induced by 2.5 and 5 mg/kg amphetamine was enhanced in Tph2(-/-) mice. Using the in vivo microdialysis technique we found that the ability of amphetamine to stimulate noradrenaline (NA) release in the striatum was reduced by about 50% in Tph2(-/-) mice while the release of dopamine (DA) was not affected. Tph2 deletion did not affect the release of NA and DA in the prefrontal cortex. The role of endogenous 5-HT in enhancing the effect of amphetamine was confirmed showing that treatment with the 5-HT precursor 5-hydroxytryptophan (10 mg/kg) restored tissue and extracellular levels of brain 5-HT and the effects of amphetamine on striatal NA release and motor activity in Tph2(-/-) mice. Treatment with the NA precursor dihydroxyphenylserine (400 mg/kg) was sufficient to restore the effect of amphetamine on striatal NA release and motor activity in Tph2(-/-) mice. These findings indicate that amphetamine-induced hyperactivity is attenuated by endogenous 5-HT through the inhibition of striatal NA release. Tph2(-/-) mice may be a useful preclinical model to assess the role of 5-HT-dependent mechanisms in the action of psychostimulants. Acute sensitivity to the motor effects of amphetamine has been associated to increased risk of psychostimulant abuse. Here, we show that deletion of Tph2, the gene responsible for brain 5-HT synthesis, enhances the motor effect of amphetamine in mice through the inhibition of striatal NA release. This suggests that Tph2(-/-) mice is a useful preclinical model to assess the role of 5-HT-dependent mechanisms in psychostimulants action. Tph2, tryptophan hydroxylase-2.

  16. Adipocyte-specific deletion of Ip6k1 reduces diet-induced obesity by enhancing AMPK-mediated thermogenesis

    Science.gov (United States)

    Zhu, Qingzhang; Ghoshal, Sarbani; Rodrigues, Ana; Gao, Su; Asterian, Alice; Kamenecka, Theodore M.; Barrow, James C.

    2016-01-01

    Enhancing energy expenditure (EE) is an attractive strategy to combat obesity and diabetes. Global deletion of Ip6k1 protects mice from diet-induced obesity (DIO) and insulin resistance, but the tissue-specific mechanism by which IP6K1 regulates body weight is unknown. Here, we have demonstrated that IP6K1 regulates fat accumulation by modulating AMPK-mediated adipocyte energy metabolism. Cold exposure led to downregulation of Ip6k1 in murine inguinal and retroperitoneal white adipose tissue (IWAT and RWAT) depots. Adipocyte-specific deletion of Ip6k1 (AdKO) enhanced thermogenic EE, which protected mice from high-fat diet–induced weight gain at ambient temperature (23°C), but not at thermoneutral temperature (30°C). AdKO-induced increases in thermogenesis also protected mice from cold-induced decreases in body temperature. UCP1, PGC1α, and other markers of browning and thermogenesis were elevated in IWAT and RWAT of AdKO mice. Cold-induced activation of sympathetic signaling was unaltered, whereas AMPK was enhanced, in AdKO IWAT. Moreover, beige adipocytes from AdKO IWAT displayed enhanced browning, which was diminished by AMPK depletion. Furthermore, we determined that IP6 and IP6K1 differentially regulate upstream kinase-mediated AMPK stimulatory phosphorylation in vitro. Finally, treating mildly obese mice with the IP6K inhibitor TNP enhanced thermogenesis and inhibited progression of DIO. Thus, IP6K1 regulates energy metabolism via a mechanism that could potentially be targeted in obesity. PMID:27701146

  17. 63. Study on the deletions of the FHIT gene mRNA in murine lung cancer induced by Coal Tar Pitch

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    in liquid nitrogen. The murine cDNA sequence was found in GenBank. The primers were devised by Primer Devising software. The targeted DNA fragment was amplified by nested-PCR. The expected length of product was 694bp. Results: ①The diet habit and activities of mice in experimental group were normal, the weights of the mice in the experimental groups were 32.83±5.40 gram and 38.34±5.47 gram in 12th weeks and 24th weeks respectively. There were significant loss compared to the control group mice. The index of lung and body in experimental group was increased significantly compared to control group. ②The main histology type of lung cancer induced by CTP fume was carcinoid (87.5%). In experimental group, there were 2 cases of carcinoid occurred (2/16) in 12th week, whereas there were 5 cases and 1 case of adenocarcinoma occurred in 24th weeks. However, there was no any cancer occurred in control group. ③Deletions of FHIT transcripts were found in the tissue of precancerous lesion, tumor lesion and its adjacent tissues. Nested-PCR results show that 52% PCR products exhibited aberrant bands in the exposure group. Among 8 mice with tumors, aberrant bands were shown in 4 carcinoids mice, 5 of 7 precancerous specimens showed aberrant bands. Except for the wild-type 694bp band, there were one or two aberrant bands, which were shorter than normal band. The length of deletions was 100bp or so. Aberrant transcriptions were not detected in control group. Conclusions: ①The main histological type of lung cancer induced by CTP was carcinoid. This finding indicates that the CTP fume can specifically cause mouse carcinoid. ②Aberrant FHIT transcripts were detected consistently, from precancerous lesion to tumor specimen, which suggests that abnormality of FHIT gene transcript is an early and frequent molecular genetic event and this change can last to the occurrence of tumor. The finding is valuable for early diagnosis.

  18. EXPRESSION CHANGES OF NUCLEAR FACTOR κBp65 AND CYCLIND1 IN 4-NITROQUINOLINE 1-OXIDE-INDUCED RAT TONGUE CARCINOGENESIS

    Institute of Scientific and Technical Information of China (English)

    GE shu-yun; Zhou zeng-tong

    2006-01-01

    Objective To observe the different expression of NF-κBp65 and cyclinD1 during oral carcinogenesis and to analyze the relationship between the abnormal expression of NF-κBp65 , cyclinD1, and the occurrence and development of oral carcinogenesis. Methods The streptavidin-biotin-peroxidase (S-P) immunohistochemical method was employed to detect the expression of NF-κBp65 and cyclinD1 protein in 38 rat tongue carcinogenesis specimens induced by 4-nitroquinoline 1-oxide. Results With the progress of tongue carcinogenesis, the expression of NF-κBp65, cyclinD1 was up-regulated. In normal, mild epithelial dysplasia, moderate epithelial dysplasia,severe epithelial dysplasia, carcinoma in situ and squamous cell carcinoma ( SCC) , the positive rate of NF-κBp65was 20%, 20%, 50%, 62.5%, 50% and 83.33%, respectively. There was significant differences between normal and SCC ( P<0.05); while the level of cyclinD1 was 20%, 60%, 62.5%, 87. 5%, 100% and 83.33%, respectively. There was significant differences between normal and severe epithelial dysplasia, carcinoma in situ and SCC ( P<0.01 or P<0.05). There was a significant correlation between the increased levels of NF-κBp65, cyclinD1 and histopathological grade. The positive expression of NF-κBp65 was also associated with cyclinD1 in SCC (r=0.7353, P<0.05). Conclusion The up-expression of NF-κBp65 and cyclinD1 protein may be correlated to the occurrence and the development of oral carcinoma; activated NF-κB plays an important role in the overexpression of cyclinD1. Furthermore, NF-κB and cyclinD1 may be the useful biomarker of oral precancerous lesion.

  19. SH3BP2 cherubism mutation potentiates TNF-α-induced osteoclastogenesis via NFATc1 and TNF-α-mediated inflammatory bone loss.

    Science.gov (United States)

    Mukai, Tomoyuki; Ishida, Shu; Ishikawa, Remi; Yoshitaka, Teruhito; Kittaka, Mizuho; Gallant, Richard; Lin, Yi-Ling; Rottapel, Robert; Brotto, Marco; Reichenberger, Ernst J; Ueki, Yasuyoshi

    2014-12-01

    Cherubism (OMIM# 118400) is a genetic disorder with excessive jawbone resorption caused by mutations in SH3 domain binding protein 2 (SH3BP2), a signaling adaptor protein. Studies on the mouse model for cherubism carrying a P416R knock-in (KI) mutation have revealed that mutant SH3BP2 enhances tumor necrosis factor (TNF)-α production and receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation in myeloid cells. TNF-α is expressed in human cherubism lesions, which contain a large number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells, and TNF-α plays a critical role in inflammatory bone destruction in homozygous cherubism mice (Sh3bp2(KI/KI) ). The data suggest a pathophysiological relationship between mutant SH3BP2 and TNF-α-mediated bone loss by osteoclasts. Therefore, we investigated whether P416R mutant SH3BP2 is involved in TNF-α-mediated osteoclast formation and bone loss. Here, we show that bone marrow-derived M-CSF-dependent macrophages (BMMs) from the heterozygous cherubism mutant (Sh3bp2(KI/+) ) mice are highly responsive to TNF-α and can differentiate into osteoclasts independently of RANKL in vitro by a mechanism that involves spleen tyrosine kinase (SYK) and phospholipase Cγ2 (PLCγ2) phosphorylation, leading to increased nuclear translocation of NFATc1. The heterozygous cherubism mutation exacerbates bone loss with increased osteoclast formation in a mouse calvarial TNF-α injection model as well as in a human TNF-α transgenic mouse model (hTNFtg). SH3BP2 knockdown in RAW264.7 cells results in decreased TRAP-positive multinucleated cell formation. These findings suggest that the SH3BP2 cherubism mutation can cause jawbone destruction by promoting osteoclast formation in response to TNF-α expressed in cherubism lesions and that SH3BP2 is a key regulator for TNF-α-induced osteoclastogenesis. Inhibition of SH3BP2 expression in osteoclast progenitors could be a potential strategy for

  20. Live cell detection of chromosome 2 deletion and Sfpi1/PU1 loss in radiation-induced mouse acute myeloid leukaemia.

    Science.gov (United States)

    Olme, C-H; Finnon, R; Brown, N; Kabacik, S; Bouffler, S D; Badie, C

    2013-10-01

    The CBA/H mouse model of radiation-induced acute myeloid leukaemia (rAML) has been studied for decades to bring to light the molecular mechanisms associated with multistage carcinogenesis. A specific interstitial deletion of chromosome 2 found in a high proportion of rAML is recognised as the initiating event. The deletion leads to the loss of Sfpi, a gene essential for haematopoietic development. Its product, the transcription factor PU.1 acts as a tumour suppressor in this model. Although the deletion can be detected early following ionising radiation exposure by cytogenetic techniques, precise characterisation of the haematopoietic cells carrying the deletion and the study of their fate in vivo cannot be achieved. Here, using a genetically engineered C57BL/6 mouse model expressing the GFP fluorescent molecule under the control of the Sfpi1 promoter, which we have bred onto the rAML-susceptible CBA/H strain, we demonstrate that GFP expression did not interfere with X-ray induced leukaemia incidence and that GFP fluorescence in live leukaemic cells is a surrogate marker of radiation-induced chromosome 2 deletions with or without point mutations on the remaining allele of the Sfpi1 gene. This study presents the first experimental evidence for the detection of this leukaemia initiating event in live leukemic cells.

  1. Microhomology-mediated deletion and gene conversion in African trypanosomes.

    Science.gov (United States)

    Glover, Lucy; Jun, Junho; Horn, David

    2011-03-01

    Antigenic variation in African trypanosomes is induced by DNA double-strand breaks (DSBs). In these protozoan parasites, DSB repair (DSBR) is dominated by homologous recombination (HR) and microhomology-mediated end joining (MMEJ), while non-homologous end joining (NHEJ) has not been reported. To facilitate the analysis of chromosomal end-joining, we established a system whereby inter-allelic repair by HR is lethal due to loss of an essential gene. Analysis of intrachromosomal end joining in individual DSBR survivors exclusively revealed MMEJ-based deletions but no NHEJ. A survey of microhomologies typically revealed sequences of between 5 and 20 bp in length with several mismatches tolerated in longer stretches. Mean deletions were of 54 bp on the side closest to the break and 284 bp in total. Break proximity, microhomology length and GC-content all favored repair and the pattern of MMEJ described above was similar at several different loci across the genome. We also identified interchromosomal gene conversion involving HR and MMEJ at different ends of a duplicated sequence. While MMEJ-based deletions were RAD51-independent, one-sided MMEJ was RAD51 dependent. Thus, we describe the features of MMEJ in Trypanosoma brucei, which is analogous to micro single-strand annealing; and RAD51 dependent, one-sided MMEJ. We discuss the contribution of MMEJ pathways to genome evolution, subtelomere recombination and antigenic variation.

  2. Mitochondrial Ferritin Deletion Exacerbates β-Amyloid-Induced Neurotoxicity in Mice

    Directory of Open Access Journals (Sweden)

    Peina Wang

    2017-01-01

    Full Text Available Mitochondrial ferritin (FtMt is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV with Aβ25–35 to establish an Alzheimer’s disease model. Knockout of Ftmt significantly exacerbated Aβ25–35-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected in Ftmt knockout mice treated with Aβ25–35. In conclusion, this study demonstrated that the neurological impairment induced by Aβ25–35 was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress.

  3. Mitochondrial Ferritin Deletion Exacerbates β-Amyloid-Induced Neurotoxicity in Mice

    Science.gov (United States)

    Wang, Peina; Wu, Qiong; Wu, Wenyue; Li, Haiyan; Guo, Yuetong; Yu, Peng; Gao, Guofen; Shi, Zhenhua; Zhao, Baolu

    2017-01-01

    Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with Aβ25–35 to establish an Alzheimer's disease model. Knockout of Ftmt significantly exacerbated Aβ25–35-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected in Ftmt knockout mice treated with Aβ25–35. In conclusion, this study demonstrated that the neurological impairment induced by Aβ25–35 was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress.

  4. UNC5B receptor deletion exacerbates DSS-induced colitis in mice by increasing epithelial cell apoptosis.

    Science.gov (United States)

    Ranganathan, Punithavathi; Jayakumar, Calpurnia; Li, Dean Y; Ramesh, Ganesan

    2014-07-01

    The netrin-1 administration or overexpression is known to protect colon from acute colitis. However, the receptor that mediates netrin-1 protective activities in the colon during colitis remains unknown. We tested the hypothesis that UNC5B receptor is a critical mediator of protective function of netrin-1 in dextran sodium sulfate (DSS)-induced colitis using mice with partial deletion of UNC5B receptor. DSS colitis was performed in mice with partial genetic UNC5B deficiency (UNC5B(+/-) mice) or wild-type mice to examine the role of endogenous UNC5B. These studies were supported by in vitro models of DSS-induced apoptosis in human colon epithelial cells. WT mice developed colitis in response to DSS feeding as indicated by reduction in bw, reduction in colon length and increase in colon weight. These changes were exacerbated in heterozygous UNC5B knockout mice treated with DSS. Periodic Acid-Schiff stained section shows damages in colon epithelium and mononuclear cell infiltration in WT mice, which was further increased in UNC5B heterozygous knockout mice. This was associated with large increase in inflammatory mediators such as cytokine and chemokine expression and extensive apoptosis of epithelial cells in heterozygous knockout mice as compared to WT mice. Overexpression of UNC5B human colon epithelial cells suppressed DSS-induced apoptosis and caspase-3 activity. Moreover, DSS induced large amount of netrin-1 and shRNA mediated knockdown of netrin-1 induction exacerbated DSS-induced epithelial cell apoptosis. Our results suggest that UNC5B is a critical mediator of cell survival in response to stress in colon.

  5. Deletion of IFT20 in early stage T lymphocyte differentiation inhibits the development of collagen-induced arthritis

    Institute of Scientific and Technical Information of China (English)

    Xue Yuan; Lee Ann Garrett-Sinha; Debanjan Sarkar; Shuying Yang

    2014-01-01

    IFT20 is the smallest member of the intraflagellar transport protein (IFT) complex B. It is involved in cilia formation. Studies of IFT20 have been confined to ciliated cells. Recently, IFT20 was found to be also expressed in non-ciliated T cells and have functions in immune synapse formation and signaling in vitro. However, how IFT20 regulates T-cell development and activation in vivo is still unknown. We deleted the IFT20 gene in early and later stages of T-cell development by crossing IFT20flox/flox (IFT20f/f) mice with Lck-Cre and CD4-Cre transgenic mice, and investigated the role of IFT20 in T-cell maturation and in the development of T cell-mediated collagen-induced arthritis (CIA). We found that both Lck-Cre/IFT20f/f and CD4-Cre/IFT20f/f mice were indistinguishable from their wild-type littermates in body size, as well as in the morphology and weight of the spleen and thymus. However, the number of CD4-and CD8-positive cells was significantly lower in thymus and spleen in Lck-Cre/IFT20f/f mice. Meanwhile, the incidence and severity of CIA symptoms were significantly decreased, and inflammation in the paw was significantly inhibited in Lck-Cre/IFT20f/f mice compared to Lck-Cre/IFT201/1 littermates. Deletion IFT20 in more mature T cells of CD4-Cre/IFT20f/f mice had only mild effects on the development of T cells and CIA. The expression of IL-1b, IL-6 and TGF-b1 were significantly downregulated in the paw of Lck-Cre/IFT20f/f mice, but just slight decreased in CD4-Cre/IFT20f/f mice. These results demonstrate that deletion of IFT20 in the early stage of T-cell development inhibited CIA development through regulating T-cell development and the expression of critical cytokines.

  6. Deletion of miR-150 Exacerbates Retinal Vascular Overgrowth in High-Fat-Diet Induced Diabetic Mice.

    Science.gov (United States)

    Shi, Liheng; Kim, Andy Jeesu; Chang, Richard Cheng-An; Chang, Janet Ya-An; Ying, Wei; Ko, Michael L; Zhou, Beiyan; Ko, Gladys Yi-Ping

    2016-01-01

    Diabetic retinopathy (DR) is the leading cause of blindness among American adults above 40 years old. The vascular complication in DR is a major cause of visual impairment, making finding therapeutic targets to block pathological angiogenesis a primary goal for developing DR treatments. MicroRNAs (miRs) have been proposed as diagnostic biomarkers and potential therapeutic targets for various ocular diseases including DR. In diabetic animals, the expression levels of several miRs, including miR-150, are altered. The expression of miR-150 is significantly suppressed in pathological neovascularization in mice with hyperoxia-induced retinopathy. The purpose of this study was to investigate the functional role of miR-150 in the development of retinal microvasculature complications in high-fat-diet (HFD) induced type 2 diabetic mice. Wild type (WT) and miR-150 null mutant (miR-150-/-) male mice were given a HFD (59% fat calories) or normal chow diet. Chronic HFD caused a decrease of serum miR-150 in WT mice. Mice on HFD for 7 months (both WT and miR-150-/-) had significant decreases in retinal light responses measured by electroretinograms (ERGs). The retinal neovascularization in miR-150-/--HFD mice was significantly higher compared to their age matched WT-HFD mice, which indicates that miR-150 null mutation exacerbates chronic HFD-induced neovascularization in the retina. Overexpression of miR-150 in cultured endothelial cells caused a significant reduction of vascular endothelial growth factor receptor 2 (VEGFR2) protein levels. Hence, deletion of miR-150 significantly increased the retinal pathological angiogenesis in HFD induced type 2 diabetic mice, which was in part through VEGFR2.

  7. Myeloperoxidase Deletion Prevents High-Fat Diet–Induced Obesity and Insulin Resistance

    OpenAIRE

    Wang, Qilong; Xie, Zhonglin; Zhang, Wencheng; Zhou, Jun; Wu, Yue; Zhang, Miao; Zhu, Huaiping; Zou, Ming-hui

    2014-01-01

    Activation of myeloperoxidase (MPO), a heme protein primarily expressed in granules of neutrophils, is associated with the development of obesity. However, whether MPO mediates high-fat diet (HFD)-induced obesity and obesity-associated insulin resistance remains to be determined. Here, we found that consumption of an HFD resulted in neutrophil infiltration and enhanced MPO expression and activity in epididymal white adipose tissue, with an increase in body weight gain and impaired insulin sig...

  8. Deletion of the Men1 Gene Prevents Streptozotocin-Induced Hyperglycemia in Mice

    Directory of Open Access Journals (Sweden)

    Yuqing Yang

    2010-01-01

    Full Text Available Diabetes ultimately results from an inadequate number of functional beta cells in the islets of Langerhans. Enhancing proliferation of functional endogenous beta cells to treat diabetes remains underexplored. Here, we report that excision of the Men1 gene, whose loss-of-function mutation leads to inherited multiple endocrine neoplasia type 1 (MEN1, rendered resistant to streptozotocin-induced hyperglycemia in a tamoxifen-inducible and temporally controlled Men1 excision mouse model as well as in a tissue-specific Men1 excision mouse model. Men1 excision prevented mice from streptozotocin-induced hyperglycemia mainly through increasing the number of functional beta cells. BrdU incorporation by beta cells, islet size, and circulating insulin levels were significantly increased in Men1-excised mice. Membrane localization of glucose transporter 2 was largely preserved in Men1-excised beta cells, but not in Men1-expressing beta cells. Our findings suggest that repression of menin, a protein encoded by the Men1 gene, might be a valuable means to maintain or increase the number of functional endogenous beta cells to prevent or ameliorate diabetes.

  9. Tau Deletion Prevents Stress-Induced Dendritic Atrophy in Prefrontal Cortex: Role of Synaptic Mitochondria.

    Science.gov (United States)

    Lopes, Sofia; Teplytska, Larysa; Vaz-Silva, Joao; Dioli, Chrysoula; Trindade, Rita; Morais, Monica; Webhofer, Christian; Maccarrone, Giuseppina; Almeida, Osborne F X; Turck, Christoph W; Sousa, Nuno; Sotiropoulos, Ioannis; Filiou, Michaela D

    2016-04-12

    Tau protein in dendrites and synapses has been recently implicated in synaptic degeneration and neuronal malfunction. Chronic stress, a well-known inducer of neuronal/synaptic atrophy, triggers hyperphosphorylation of Tau protein and cognitive deficits. However, the cause-effect relationship between these events remains to be established. To test the involvement of Tau in stress-induced impairments of cognition, we investigated the impact of stress on cognitive behavior, neuronal structure, and the synaptic proteome in the prefrontal cortex (PFC) of Tau knock-out (Tau-KO) and wild-type (WT) mice. Whereas exposure to chronic stress resulted in atrophy of apical dendrites and spine loss in PFC neurons as well as significant impairments in working memory in WT mice, such changes were absent in Tau-KO animals. Quantitative proteomic analysis of PFC synaptosomal fractions, combined with transmission electron microscopy analysis, suggested a prominent role for mitochondria in the regulation of the effects of stress. Specifically, chronically stressed animals exhibit Tau-dependent alterations in the levels of proteins involved in mitochondrial transport and oxidative phosphorylation as well as in the synaptic localization of mitochondria in PFC. These findings provide evidence for a causal role of Tau in mediating stress-elicited neuronal atrophy and cognitive impairment and indicate that Tau may exert its effects through synaptic mitochondria.

  10. Myeloperoxidase deletion prevents high-fat diet-induced obesity and insulin resistance.

    Science.gov (United States)

    Wang, Qilong; Xie, Zhonglin; Zhang, Wencheng; Zhou, Jun; Wu, Yue; Zhang, Miao; Zhu, Huaiping; Zou, Ming-Hui

    2014-12-01

    Activation of myeloperoxidase (MPO), a heme protein primarily expressed in granules of neutrophils, is associated with the development of obesity. However, whether MPO mediates high-fat diet (HFD)-induced obesity and obesity-associated insulin resistance remains to be determined. Here, we found that consumption of an HFD resulted in neutrophil infiltration and enhanced MPO expression and activity in epididymal white adipose tissue, with an increase in body weight gain and impaired insulin signaling. MPO knockout (MPO(-/-)) mice were protected from HFD-enhanced body weight gain and insulin resistance. The MPO inhibitor 4-aminobenzoic acid hydrazide reduced peroxidase activity of neutrophils and prevented HFD-enhanced insulin resistance. MPO deficiency caused high body temperature via upregulation of uncoupling protein-1 and mitochondrial oxygen consumption in brown adipose tissue. Lack of MPO also attenuated HFD-induced macrophage infiltration and expression of proinflammatory cytokines. We conclude that activation of MPO in adipose tissue contributes to the development of obesity and obesity-associated insulin resistance. Inhibition of MPO may be a potential strategy for prevention and treatment of obesity and insulin resistance.

  11. Targeted deletion of Nrf2 reduces urethane-induced lung tumor development in mice.

    Directory of Open Access Journals (Sweden)

    Alison K Bauer

    Full Text Available Nrf2 is a key transcription factor that regulates cellular redox and defense responses. However, permanent Nrf2 activation in human lung carcinomas promotes pulmonary malignancy and chemoresistance. We tested the hypothesis that Nrf2 has cell survival properties and lack of Nrf2 suppresses chemically-induced pulmonary neoplasia by treating Nrf2(+/+ and Nrf2(-/- mice with urethane. Airway inflammation and injury were assessed by bronchoalveolar lavage analyses and histopathology, and lung tumors were analyzed by gross and histologic analysis. We used transcriptomics to assess Nrf2-dependent changes in pulmonary gene transcripts at multiple stages of neoplasia. Lung hyperpermeability, cell death and apoptosis, and inflammatory cell infiltration were significantly higher in Nrf2(-/- mice compared to Nrf2(+/+ mice 9 and 11 wk after urethane. Significantly fewer lung adenomas were found in Nrf2(-/- mice than in Nrf2(+/+ mice at 12 and 22 wk. Nrf2 modulated expression of genes involved cell-cell signaling, glutathione metabolism and oxidative stress response, and immune responses during early stage neoplasia. In lung tumors, Nrf2-altered genes had roles in transcriptional regulation of cell cycle and proliferation, carcinogenesis, organismal injury and abnormalities, xenobiotic metabolism, and cell-cell signaling genes. Collectively, Nrf2 deficiency decreased susceptibility to urethane-induced lung tumorigenesis in mice. Cell survival properties of Nrf2 were supported, at least in part, by reduced early death of initiated cells and heightened advantage for tumor cell expansion in Nrf2(+/+ mice relative to Nrf2(-/- mice. Our results were consistent with the concept that Nrf2 over-activation is an adaptive response of cancer conferring resistance to anti-cancer drugs and promoting malignancy.

  12. Deletion of glutathione peroxidase-2 inhibits azoxymethane-induced colon cancer development.

    Directory of Open Access Journals (Sweden)

    Mike F Müller

    Full Text Available The selenoprotein glutathione peroxidase-2 (GPx2 appears to have a dual role in carcinogenesis. While it protected mice from colon cancer in a model of inflammation-triggered carcinogenesis (azoxymethane and dextran sodium sulfate treatment, it promoted growth of xenografted tumor cells. Therefore, we analyzed the effect of GPx2 in a mouse model mimicking sporadic colorectal cancer (azoxymethane-treatment only. GPx2-knockout (KO and wild-type (WT mice were adjusted to an either marginally deficient (-Se, adequate (+Se, or supranutritional (++Se selenium status and were treated six times with azoxymethane (AOM to induce tumor development. In the -Se and ++Se groups, the number of tumors was significantly lower in GPx2-KO than in respective WT mice. On the +Se diet, the number of dysplastic crypts was reduced in GPx2-KO mice. This may be explained by more basal and AOM-induced apoptotic cell death in GPx2-KO mice that eliminates damaged or pre-malignant epithelial cells. In WT dysplastic crypts GPx2 was up-regulated in comparison to normal crypts which might be an attempt to suppress apoptosis. In contrast, in the +Se groups tumor numbers were similar in both genotypes but tumor size was larger in GPx2-KO mice. The latter was associated with an inflammatory and tumor-promoting environment as obvious from infiltrated inflammatory cells in the intestinal mucosa of GPx2-KO mice even without any treatment and characterized as low-grade inflammation. In WT mice the number of tumors tended to be lowest in +Se compared to -Se and ++Se feeding indicating that selenium might delay tumorigenesis only in the adequate status. In conclusion, the role of GPx2 and presumably also of selenium depends on the cancer stage and obviously on the involvement of inflammation.

  13. PHO13 deletion-induced transcriptional activation prevents sedoheptulose accumulation during xylose metabolism in engineered Saccharomyces cerevisiae.

    Science.gov (United States)

    Xu, Haiqing; Kim, Sooah; Sorek, Hagit; Lee, Youngsuk; Jeong, Deokyeol; Kim, Jungyeon; Oh, Eun Joong; Yun, Eun Ju; Wemmer, David E; Kim, Kyoung Heon; Kim, Soo Rin; Jin, Yong-Su

    2016-03-01

    The deletion of PHO13 (pho13Δ) in Saccharomyces cerevisiae, encoding a phosphatase enzyme of unknown specificity, results in the transcriptional activation of genes related to the pentose phosphate pathway (PPP) such as TAL1 encoding transaldolase. It has been also reported that the pho13Δ mutant of S. cerevisiae expressing a heterologous xylose pathway can metabolize xylose efficiently compared to its parental strain. However, the interaction between the pho13Δ-induced transcriptional changes and the phenotypes of xylose fermentation was not understood. Thus we investigated the global metabolic changes in response to pho13Δ when cells were exponentially growing on xylose. Among the 134 intracellular metabolites that we identified, the 98% reduction of sedoheptulose was found to be the most significant change in the pho13Δ mutant as compared to its parental strain. Because sedoheptulose-7-phosphate (S7P), a substrate of transaldolase, reduced significantly in the pho13Δ mutant as well, we hypothesized that limited transaldolase activity in the parental strain might cause dephosphorylation of S7P, leading to carbon loss and inefficient xylose metabolism. Mutants overexpressing TAL1 at different degrees were constructed, and their TAL1 expression levels and xylose consumption rates were positively correlated. Moreover, as TAL1 expression levels increased, intracellular sedoheptulose concentration dropped significantly. Therefore, we concluded that TAL1 upregulation, preventing the accumulation of sedoheptulose, is the most critical mechanism for the improved xylose metabolism by the pho13Δ mutant of engineered S. cerevisiae.

  14. ADAR1 deletion induces NFκB and interferon signaling dependent liver inflammation and fibrosis.

    Science.gov (United States)

    Ben-Shoshan, Shirley Oren; Kagan, Polina; Sultan, Maya; Barabash, Zohar; Dor, Chen; Jacob-Hirsch, Jasmine; Harmelin, Alon; Pappo, Orit; Marcu-Malina, Victoria; Ben-Ari, Ziv; Amariglio, Ninette; Rechavi, Gideon; Goldstein, Itamar; Safran, Michal

    2016-06-30

    Adenosine deaminase acting on RNA (ADAR) 1 binds and edits double-stranded (ds) RNA secondary structures found mainly within untranslated regions of many transcripts. In the current research, our aim was to study the role of ADAR1 in liver homeostasis. As previous studies show a conserved immunoregulatory function for ADAR1 in mammalians, we focused on its role in preventing chronic hepatic inflammation and the associated activation of hepatic stellate cells to produce extracellular matrix and promote fibrosis. We show that hepatocytes specific ADAR1 knock out (KO) mice display massive liver damage with multifocal inflammation and fibrogenesis. The bioinformatics analysis of the microarray gene-expression datasets of ADAR1 KO livers reveled a type-I interferons signature and an enrichment for immune response genes compared to control littermate livers. Furthermore, we found that in vitro silencing of ADAR1 expression in HepG2 cells leads to enhanced transcription of NFκB target genes, foremost of the pro-inflammatory cytokines IL6 and IL8. We also discovered immune cell-independent paracrine signaling among ADAR1-depleted HepG2 cells and hepatic stellate cells, leading to the activation of the latter cell type to adopt a profibrogenic phenotype. This paracrine communication dependent mainly on the production and secretion of the cytokine IL6 induced by ADAR1 silencing in hepatocytes. Thus, our findings shed a new light on the vital regulatory role of ADAR1 in hepatic immune homeostasis, chiefly its inhibitory function on the crosstalk between the NFκB and type-I interferons signaling cascades, restraining the development of liver inflammation and fibrosis.

  15. Neuronal deletion of caspase 8 protects against brain injury in mouse models of controlled cortical impact and kainic acid-induced excitotoxicity.

    Directory of Open Access Journals (Sweden)

    Maryla Krajewska

    Full Text Available Acute brain injury is an important health problem. Given the critical position of caspase 8 at the crossroads of cell death pathways, we generated a new viable mouse line (Ncasp8(-/-, in which the gene encoding caspase 8 was selectively deleted in neurons by cre-lox system.Caspase 8 deletion reduced rates of neuronal cell death in primary neuronal cultures and in whole brain organotypic coronal slice cultures prepared from 4 and 8 month old mice and cultivated up to 14 days in vitro. Treatments of cultures with recombinant murine TNFα (100 ng/ml or TRAIL (250 ng/mL plus cyclohexamide significantly protected neurons against cell death induced by these apoptosis-inducing ligands. A protective role of caspase 8 deletion in vivo was also demonstrated using a controlled cortical impact (CCI model of traumatic brain injury (TBI and seizure-induced brain injury caused by kainic acid (KA. Morphometric analyses were performed using digital imaging in conjunction with image analysis algorithms. By employing virtual images of hundreds of brain sections, we were able to perform quantitative morphometry of histological and immunohistochemical staining data in an unbiased manner. In the TBI model, homozygous deletion of caspase 8 resulted in reduced lesion volumes, improved post-injury motor performance, superior learning and memory retention, decreased apoptosis, diminished proteolytic processing of caspases and caspase substrates, and less neuronal degeneration, compared to wild type, homozygous cre, and caspase 8-floxed control mice. In the KA model, Ncasp8(-/- mice demonstrated superior survival, reduced seizure severity, less apoptosis, and reduced caspase 3 processing. Uninjured aged knockout mice showed improved learning and memory, implicating a possible role for caspase 8 in cognitive decline with aging.Neuron-specific deletion of caspase 8 reduces brain damage and improves post-traumatic functional outcomes, suggesting an important role for this

  16. Effects of Ginkgo biloba Extract on Inflammatory Mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6) in TNBS-Induced Colitis in Rats

    OpenAIRE

    Yan-Hong Zhou; Jie-Ping Yu; Yi-Fei Liu; Xiao-Jun Teng; Mei Ming; Peng Lv; Ping An; Shi-Quan Liu; Hong-Gang Yu

    2006-01-01

    Inflammatory mediators play a criticial role in ulcerative colitis immune and inflammatory processes. The aim of the study was to investigate the effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6) in TNBS-induced colitis in rats. Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid (TNBS, 150 mg/kg). EGB in doses of (50, 100, 200 mg/kg) was administered for 4 weeks to protect colitis. The results showed that ...

  17. Midkine Regulates BP through Cytochrome P450-Derived Eicosanoids.

    Science.gov (United States)

    Sato, Yuka; Sato, Waichi; Maruyama, Shoichi; Wilcox, Christopher S; Falck, John R; Masuda, Tomohiro; Kosugi, Tomoki; Kojima, Hiroshi; Maeda, Kayaho; Furuhashi, Kazuhiro; Ando, Masahiko; Imai, Enyu; Matsuo, Seiichi; Kadomatsu, Kenji

    2015-08-01

    The effects of endothelium-derived hyperpolarizing factors have been attributed to cytochrome P450-derived epoxyeicosatrienoic acids (EETs), but the regulation and role of EETs in endothelial dysfunction remain largely unexplored. Hypertension is a primary risk factor for renal dysfunction, which is frequently accompanied by various systemic diseases induced by endothelial dysfunction in the microcirculation. We previously reported that the endothelial growth factor midkine (MK) enhances hypertension in a model of CKD. Here, we investigated the hypothesis that MK regulates EET activity and thereby BP. MK gene-deleted mice were resistant to hypertension and developed less glomerulosclerosis and proteinuria after administration of a nitric oxide synthase (NOS) inhibitor in the setting of uninephrectomy. The hypertension observed in uninephrectomized wild-type mice after NOS inhibition was ameliorated by anti-MK antibody. MK-deficient mice produced higher amounts of EETs, and EETs dominantly regulated BP in these mice. Furthermore, MK administration to MK-deficient mice recapitulated the BP control observed in wild-type mice. EETs also dominantly regulated renal blood flow, which may influence renal function, in MK-deficient mice. Taken together, these results suggest that the MK/EET pathway is physiologically engaged in BP control and could be a target for the treatment of hypertension complicated by endothelial dysfunction.

  18. Deletion of the Mitochondrial Flavoprotein Apoptosis Inducing Factor (AIF) Induces β-Cell Apoptosis and Impairs β-Cell Mass

    Science.gov (United States)

    Schulthess, Fabienne T.; Katz, Sophie; Ardestani, Amin; Kawahira, Hiroshi; Georgia, Senta; Bosco, Domenico; Bhushan, Anil; Maedler, Kathrin

    2009-01-01

    Background Apoptosis is a hallmark of β-cell death in both type 1 and type 2 diabetes mellitus. Understanding how apoptosis contributes to β-cell turnover may lead to strategies to prevent progression of diabetes. A key mediator of apoptosis, mitochondrial function, and cell survival is apoptosis inducing factor (AIF). In the present study, we investigated the role of AIF on β-cell mass and survival using the Harlequin (Hq) mutant mice, which are hypomorphic for AIF. Methodology/Principal Findings Immunohistochemical evaluation of pancreata from Hq mutant mice displayed much smaller islets compared to wild-type mice (WT). Analysis of β-cell mass in these mice revealed a greater than 4-fold reduction in β-cell mass together with an 8-fold increase in β-cell apoptosis. Analysis of cell cycle dynamics, using BrdU pulse as a marker for cells in S-phase, did not detect significant differences in the frequency of β-cells in S-phase. In contrast, double staining for phosphorylated Histone H3 and insulin showed a 3-fold increase in β-cells in the G2 phase in Hq mutant mice, but no differences in M-phase compared to WT mice. This suggests that the β-cells from Hq mutant mice are arrested in the G2 phase and are unlikely to complete the cell cycle. β-cells from Hq mutant mice display increased sensitivity to hydrogen peroxide-induced apoptosis, which was confirmed in human islets in which AIF was depleted by siRNA. AIF deficiency had no effect on glucose stimulated insulin secretion, but the impaired effect of hydrogen peroxide on β-cell function was potentiated. Conclusions/Significance Our results indicate that AIF is essential for maintaining β-cell mass and for oxidative stress response. A decrease in the oxidative phosphorylation capacity may counteract the development of diabetes, despite its deleterious effects on β-cell survival. PMID:19197367

  19. Deletion of the mitochondrial flavoprotein apoptosis inducing factor (AIF induces beta-cell apoptosis and impairs beta-cell mass.

    Directory of Open Access Journals (Sweden)

    Fabienne T Schulthess

    Full Text Available BACKGROUND: Apoptosis is a hallmark of beta-cell death in both type 1 and type 2 diabetes mellitus. Understanding how apoptosis contributes to beta-cell turnover may lead to strategies to prevent progression of diabetes. A key mediator of apoptosis, mitochondrial function, and cell survival is apoptosis inducing factor (AIF. In the present study, we investigated the role of AIF on beta-cell mass and survival using the Harlequin (Hq mutant mice, which are hypomorphic for AIF. METHODOLOGY/PRINCIPAL FINDINGS: Immunohistochemical evaluation of pancreata from Hq mutant mice displayed much smaller islets compared to wild-type mice (WT. Analysis of beta-cell mass in these mice revealed a greater than 4-fold reduction in beta-cell mass together with an 8-fold increase in beta-cell apoptosis. Analysis of cell cycle dynamics, using BrdU pulse as a marker for cells in S-phase, did not detect significant differences in the frequency of beta-cells in S-phase. In contrast, double staining for phosphorylated Histone H3 and insulin showed a 3-fold increase in beta-cells in the G2 phase in Hq mutant mice, but no differences in M-phase compared to WT mice. This suggests that the beta-cells from Hq mutant mice are arrested in the G2 phase and are unlikely to complete the cell cycle. beta-cells from Hq mutant mice display increased sensitivity to hydrogen peroxide-induced apoptosis, which was confirmed in human islets in which AIF was depleted by siRNA. AIF deficiency had no effect on glucose stimulated insulin secretion, but the impaired effect of hydrogen peroxide on beta-cell function was potentiated. CONCLUSIONS/SIGNIFICANCE: Our results indicate that AIF is essential for maintaining beta-cell mass and for oxidative stress response. A decrease in the oxidative phosphorylation capacity may counteract the development of diabetes, despite its deleterious effects on beta-cell survival.

  20. Effects of Ginkgo biloba Extract on Inflammatory Mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6 in TNBS-Induced Colitis in Rats

    Directory of Open Access Journals (Sweden)

    Yan-Hong Zhou

    2006-01-01

    Full Text Available Inflammatory mediators play a criticial role in ulcerative colitis immune and inflammatory processes. The aim of the study was to investigate the effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6 in TNBS-induced colitis in rats. Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid (TNBS, 150 mg/kg. EGB in doses of (50, 100, 200 mg/kg was administered for 4 weeks to protect colitis. The results showed that EGB could significantly ameliorate macroscopic and histological damage, evidently elevate the activities of SOD and reduce the contents of MDA, inhibit the protein and mRNA expressions of TNF-α, NF-κBp65, and IL-6 in the colon tissues of experimental colitis in a dose-dependent manner compared with the model group. We concluded that the probable mechanisms of EGB ameliorated inflammatory injury in TNBS-induced colitis in rats by its modulation of inflammatory mediators and antioxidation.

  1. Deletion of inducible nitric-oxide synthase in leptin-deficient mice improves brown adipose tissue function.

    Directory of Open Access Journals (Sweden)

    Sara Becerril

    Full Text Available BACKGROUND: Leptin and nitric oxide (NO on their own participate in the control of non-shivering thermogenesis. However, the functional interplay between both factors in this process has not been explored so far. Therefore, the aim of the present study was to analyze the impact of the absence of the inducible NO synthase (iNOS gene in the regulation of energy balance in ob/ob mice. METHODS AND FINDINGS: Double knockout (DBKO mice simultaneously lacking the ob and iNOS genes were generated, and the expression of molecules involved in the control of brown fat cell function was analyzed by real-time PCR, western-blot and immunohistochemistry. Twelve week-old DBKO mice exhibited reduced body weight (p<0.05, decreased amounts of total fat pads (p<0.05, lower food efficiency rates (p<0.05 and higher rectal temperature (p<0.05 than ob/ob mice. Ablation of iNOS also improved the carbohydrate and lipid metabolism of ob/ob mice. DBKO showed a marked reduction in the size of brown adipocytes compared to ob/ob mutants. In this sense, in comparison to ob/ob mice, DBKO rodents showed an increase in the expression of PR domain containing 16 (Prdm16, a transcriptional regulator of brown adipogenesis. Moreover, iNOS deletion enhanced the expression of mitochondria-related proteins, such as peroxisome proliferator-activated receptor gamma coactivator-1 alpha (Pgc-1alpha, sirtuin-1 (Sirt-1 and sirtuin-3 (Sirt-3. Accordingly, mitochondrial uncoupling proteins 1 and 3 (Ucp-1 and Ucp-3 were upregulated in brown adipose tissue (BAT of DBKO mice as compared to ob/ob rodents. CONCLUSION: Ablation of iNOS improved the energy balance of ob/ob mice by decreasing food efficiency through an increase in thermogenesis. These effects may be mediated, in part, through the recovery of the BAT phenotype and brown fat cell function improvement.

  2. Mitochondrial DNA deletions in patients with chronic suppurative otitis media.

    Science.gov (United States)

    Tatar, Arzu; Tasdemir, Sener; Sahin, Ibrahim; Bozoglu, Ceyda; Erdem, Haktan Bagis; Yoruk, Ozgur; Tatar, Abdulgani

    2016-09-01

    The aim of this study was to investigate the 4977 and 7400 bp deletions of mitochondrial DNA in patients with chronic suppurative otitis media and to indicate the possible association of mitochondrial DNA deletions with chronic suppurative otitis media. Thirty-six patients with chronic suppurative otitis media were randomly selected to assess the mitochondrial DNA deletions. Tympanomastoidectomy was applied for the treatment of chronic suppurative otitis media, and the curettage materials including middle ear tissues were collected. The 4977 and 7400 bp deletion regions and two control regions of mitochondrial DNA were assessed by using the four pair primers. DNA was extracted from middle ear tissues and peripheral blood samples of the patients, and then polymerase chain reactions (PCRs) were performed. PCR products were separated in 2 % agarose gel. Seventeen of 36 patients had the heterozygote 4977 bp deletion in the middle ear tissue but not in peripheral blood. There wasn't any patient who had the 7400 bp deletion in mtDNA of their middle ear tissue or peripheral blood tissue. The patients with the 4977 bp deletion had a longer duration of chronic suppurative otitis media and a higher level of hearing loss than the others (p media and the reactive oxygen species can cause the mitochondrial DNA deletions and this may be a predisposing factor to sensorineural hearing loss in chronic suppurative otitis media. An antioxidant drug as a scavenger agent may be used in long-term chronic suppurative otitis media.

  3. Alu Sx repeat-induced homozygous deletion of the StAR gene causes lipoid congenital adrenal hyperplasia.

    Science.gov (United States)

    Eiden-Plach, Antje; Nguyen, Huy-Hoang; Schneider, Ursula; Hartmann, Michaela F; Bernhardt, Rita; Hannemann, Frank; Wudy, Stefan A

    2012-05-01

    Lipoid congenital adrenal hyperplasia (Lipoid CAH) is the most severe form of the autosomal recessive disorder CAH. A general loss of the steroid biosynthetic activity caused by defects in the StAR gene manifests as life-threatening primary adrenal insufficiency. We report a case of Lipoid CAH caused by a so far not described homozygous deletion of the complete StAR gene and provide diagnostic results based on a GC-MS steroid metabolomics and molecular genetic analysis. The patient presented with postnatal hypoglycemia, vomiting, adynamia, increasing pigmentation and hyponatremia. The constellation of urinary steroid metabolites suggested Lipoid CAH and ruled out all other forms of CAH or defects of aldosterone biosynthesis. After treatment with sodium supplementation, hydrocortisone and fludrocortisone the child fully recovered. Molecular genetic analysis demonstrated a homozygous 12.1 kb deletion in the StAR gene locus. The breakpoints of the deletion are embedded into two typical genomic repetitive Alu Sx elements upstream and downstream of the gene leading to the loss of all exons and regulatory elements. We established deletion-specific and intact allele-specific PCR methods and determined the StAR gene status of all available family members over three generations. This analysis revealed that one of the siblings, who died a few weeks after birth, carried the same genetic defect. Since several Alu repeats at the StAR gene locus increase the probability of deletions, patients with typical symptoms of lipoid CAH lacking evidence for the presence of both StAR alleles should be analyzed carefully for this kind of disorder.

  4. Golgi membrane fission requires the CtBP1-S/BARS-induced activation of lysophosphatidic acid acyltransferase δ.

    Science.gov (United States)

    Pagliuso, Alessandro; Valente, Carmen; Giordano, Lucia Laura; Filograna, Angela; Li, Guiling; Circolo, Diego; Turacchio, Gabriele; Marzullo, Vincenzo Manuel; Mandrich, Luigi; Zhukovsky, Mikhail A; Formiggini, Fabio; Polishchuk, Roman S; Corda, Daniela; Luini, Alberto

    2016-07-12

    Membrane fission is an essential cellular process by which continuous membranes split into separate parts. We have previously identified CtBP1-S/BARS (BARS) as a key component of a protein complex that is required for fission of several endomembranes, including basolateral post-Golgi transport carriers. Assembly of this complex occurs at the Golgi apparatus, where BARS binds to the phosphoinositide kinase PI4KIIIβ through a 14-3-3γ dimer, as well as to ARF and the PKD and PAK kinases. We now report that, when incorporated into this complex, BARS binds to and activates a trans-Golgi lysophosphatidic acid (LPA) acyltransferase type δ (LPAATδ) that converts LPA into phosphatidic acid (PA); and that this reaction is essential for fission of the carriers. LPA and PA have unique biophysical properties, and their interconversion might facilitate the fission process either directly or indirectly (via recruitment of proteins that bind to PA, including BARS itself).

  5. Deleting exon 55 from the nebulin gene induces severe muscle weakness in a mouse model for nemaline myopathy

    OpenAIRE

    Ottenheijm, Coen A. C.; Buck, Danielle; de Winter, Josine M; Ferrara, Claudia; Piroddi, Nicoletta; Tesi, Chiara; Jasper, Jeffrey R.; Malik, Fady I.; Meng, Hui; Stienen, Ger J. M.; Beggs, Alan H.; Labeit, Siegfried; Poggesi, Corrado; Lawlor, Michael W.; Granzier, Henk

    2013-01-01

    Nebulin—a giant sarcomeric protein—plays a pivotal role in skeletal muscle contractility by specifying thin filament length and function. Although mutations in the gene encoding nebulin (NEB) are a frequent cause of nemaline myopathy, the most common non-dystrophic congenital myopathy, the mechanisms by which mutations in NEB cause muscle weakness remain largely unknown. To better understand these mechanisms, we have generated a mouse model in which Neb exon 55 is deleted (NebΔExon55) to repl...

  6. Sperm mitochondrial DNA deletion in Iranian infertiles with asthenozoospermia.

    Science.gov (United States)

    Bahrehmand Namaghi, I; Vaziri, H

    2017-04-01

    Asthenozoospermia is an important cause of male infertility. The mutations in sperm mitochondrial DNA (mtDNA) result in either functionless or malfunctioning some proteins, subsequently affecting sperm motility leading to asthenozoospermia. The purpose of this study was to investigate sperm mtDNA 4,977-bp deletion in infertile men with low sperm motility/immotile spermatozoa compared to healthy subjects with high sperm motility. Semen samples of 256 asthenozoospermic infertiles and 200 controls from northern Iran were collected. After extraction of spermatozoa total DNA, Gap-polymerase chain reaction (Gap-PCR) was performed. The deletion was observed in 85.93% of patients with asthenozoospermia compared with 14% in controls [OR = 37.5397, 95% confidence interval = 12.937-108.9276, p asthenozoospermia-induced infertility in the population examined. Large-scale mtDNA deletions in spermatozoa may induce bioenergetic disorders. Nevertheless, to validate our results broader research may be needed.

  7. Characterization of FeDREB1 promoter involved in cold- and drought-inducible expression from common buckwheat (Fagopyrum esculentum).

    Science.gov (United States)

    Fang, Z W; Xu, X Y; Gao, J F; Wang, P K; Liu, Z X; Feng, B L

    2015-07-17

    C-repeat-binding factor (CBF)/dehydration-responsive element (DREB) transcription factors play key roles in plant stress responses. However, little information is available on the regulation of CBF/DREB expression. In this study, we isolated and characterized the FeDREB1 promoter sequence from the common buckwheat accession Xinong 9976. To identify the upstream region of the FeDREB1 gene required for promoter activity, we constructed a series of FeDREB1 promoter deletion derivatives. Each deletion construct was analyzed through Agrobacterium-mediated transient transformation in tobacco leaves treated with 4°C cold or drought stress. Promoter-beta-glucuronidase fusion assays revealed that the pCD1 (-270 bp) deletion in the upstream region of FeDREB1 could activate expression of the GUS gene at 4°C. The pCD1 (-270 bp), pCD2 (-530 bp), and pCD3 (-904 bp) deletion induced low-level GUS expression under drought stress. However, the pCD4 (-1278 bp) deletion clearly activated GUS gene expression. Our results suggest that sections pCD1 (-270 bp) and pCD4 (-1278 bp) in the FeDREB1 gene promoter are new sources of induced promoters for adversity-resistance breeding in plant genetic engineering.

  8. Nitric Oxide-Dependent Oxidative Stress Induced Mitochondrial DNA Overproliferation and Deletion in the Context of Cancer and Alzheimer Disease

    Directory of Open Access Journals (Sweden)

    Gjumrakch Aliev

    2015-03-01

    Full Text Available Oxidative stress initiates mitochondrial DNA overproliferation and/or deletion of the organ and/or tissues, especially the mitochondrial energy demands, have been implicated in the pathogenesis of several diseases, including Alzheimer disease (AD, tumor growth, and metastasis. The present study has determined if an intimate, i.e. causal, relationship between oxidative stress and mitochondrial damage and/or vascular lesions occurs before the development of human AD, in animal models that mimic human neurodegenerative diseases and human colorectal carcinoid cancer or primary malignant brain cancer. In situ hybridization and ultrastructural analysis of the mitochondria (mitochondria with electron dense matrix, mitochondrial-derived lysosomes showed that mitochondria with the abnormal structures and lipofuscin appear to be features of hippocampal damaged neurons in human AD, aged Tg (+ mice, 2 and 3 vessel occlusion model of the brain hypoperfusion, and malignant primary and metastatic cancer. The abnormal mitochondria appeared to be a permanent feature in all cellular compartments; in situ hybridization analysis with mouse and human mtDNA probes found a large amount of deleted mtDNA in human AD and in all models that mimic human AD (mice, rats etc. hippocampus and cancer tissues compared to aged controls. The majority of these mtDNA deletions were found in mitochondrial-derived lysosomes in regions closely associated with lipofuscin and/or tumor growth regions. In situ hybridization with a chimeric cDNA probe for the 5kb common deletion indicated that the 5kb mtDNA is increased at least 3 and 4 fold respectively in AD and malignant tumor cases as compared to controls. Only hippocampal and cortical vulnerable neurons as well as malignant cancer tissues showed immunopositive staining for RNA oxidation markers visualized by using 8-OHG-staining, NOSs, and all oxidative stress markers. The mitochondrial DNA overproliferation and deletion detected by

  9. Altered Actions of Memantine and NMDA-Induced Currents in a New Grid2-Deleted Mouse Line

    Directory of Open Access Journals (Sweden)

    Ayako Kumagai

    2014-12-01

    Full Text Available Memantine is a non-competitive antagonist of the N-methyl-D-aspartate (NMDA receptor, and is an approved drug for the treatment of moderate-to-severe Alzheimer’s disease. We identified a mouse strain with a naturally occurring mutation and an ataxic phenotype that presents with severe leg cramps. To investigate the phenotypes of these mutant mice, we screened several phenotype-modulating drugs and found that memantine (10 mg/kg disrupted the sense of balance in the mutants. Moreover, the mutant mice showed an attenuated optokinetic response (OKR and impaired OKR learning, which was also observed in wild-type mice treated with memantine. Microsatellite analyses indicated that the Grid2 gene-deletion is responsible for these phenotypes. Patch-clamp analysis showed a relatively small change in NMDA-dependent current in cultured granule cells from Grid2 gene-deleted mice, suggesting that GRID2 is important for correct NMDA receptor function. In general, NMDA receptors are activated after the activation of non-NMDA receptors, such as AMPA receptors, and AMPA receptor dysregulation also occurs in Grid2 mutant mice. Indeed, the AMPA treatment enhanced memantine susceptibility in wild-type mice, which was indicated by balance sense and OKR impairments. The present study explores a new role for GRID2 and highlights the adverse effects of memantine in different genetic backgrounds.

  10. Deletion of the thymidine kinase gene induces complete attenuation of the Georgia isolate of African swine fever virus.

    Science.gov (United States)

    Sanford, B; Holinka, L G; O'Donnell, V; Krug, P W; Carlson, J; Alfano, M; Carrillo, C; Wu, Ping; Lowe, Andre; Risatti, G R; Gladue, D P; Borca, M V

    2016-02-02

    African swine fever virus (ASFV) is the etiological agent of a contagious and often lethal viral disease of domestic pigs. There are no vaccines to control Africa swine fever (ASF). Experimental vaccines have been developed using genetically modified live attenuated ASFVs obtained by specifically deleting virus genes involved in virulence, including the thymidine kinase (TK) gene. TK has been shown to be involved in the virulence of several viruses, including ASFV. Here we report the construction of a recombinant virus (ASFV-G/V-ΔTK) obtained by deleting the TK gene in a virulent strain of ASFV Georgia adapted to replicate in Vero cells (ASFV-G/VP30). ASFV-G/P-ΔTK demonstrated decreased replication both in primary swine macrophage cell cultures and in Vero cells compared with ASFV-G/VP30. In vivo, intramuscular administration of up to 10(6) TCID50 of ASFV-G/V-ΔTK does not result in ASF disease. However, these animals are not protected when challenged with the virulent parental Georgia strain.

  11. Tis7 deletion reduces survival and induces intestinal anastomotic inflammation and obstruction in high-fat diet-fed mice with short bowel syndrome.

    Science.gov (United States)

    Garcia, Amy M; Wakeman, Derek; Lu, Jianyun; Rowley, Christopher; Geisman, Taylor; Butler, Catherine; Bala, Shashi; Swietlicki, Elzbieta A; Warner, Brad W; Levin, Marc S; Rubin, Deborah C

    2014-09-15

    Effective therapies are limited for patients with parenteral nutrition-dependent short bowel syndrome. We previously showed that intestinal expression of the transcriptional coregulator tetradecanoyl phorbol acetate-induced sequence 7 (tis7) is markedly increased during the adaptive response following massive small bowel resection and tis7 plays a role in normal gut lipid metabolism. Here, we further explore the functional implications of tis7 deletion in intestinal lipid metabolism and the adaptive response following small bowel resection. Intestinal tis7 transgenic (tis7(tg)), tis7(-/-), and wild-type (WT) littermates were subjected to 50% small bowel resection. Mice were fed a control or a high-saturated-fat (42% energy) diet for 21 days. Survival, body weight recovery, lipid absorption, mucosal lipid analysis, and the morphometric adaptive response were analyzed. Quantitative real-time PCR was performed to identify tis7 downstream gene targets. Postresection survival was markedly reduced in high-fat, but not control, diet-fed tis7(-/-) mice. Decreased survival was associated with anastomotic inflammation and intestinal obstruction postresection. High-fat, but not control, diet-fed tis7(-/-) mice had increased intestinal IL-6 expression. Intestinal lipid trafficking was altered in tis7(-/-) compared with WT mice postresection. In contrast, high-fat diet-fed tis7(tg) mice had improved survival postresection compared with WT littermates. High-fat diet feeding in the setting of tis7 deletion resulted in postresection anastomotic inflammation and small bowel obstruction. Tolerance of a calorie-rich, high-fat diet postresection may require tis7 and its target genes. The presence of luminal fat in the setting of tis7 deletion promotes an intestinal inflammatory response postresection.

  12. Molecular analysis of the Retinoic Acid Induced 1 gene (RAI1) in patients with suspected Smith-Magenis syndrome without the 17p11.2 deletion.

    Science.gov (United States)

    Vilboux, Thierry; Ciccone, Carla; Blancato, Jan K; Cox, Gerald F; Deshpande, Charu; Introne, Wendy J; Gahl, William A; Smith, Ann C M; Huizing, Marjan

    2011-01-01

    Smith-Magenis syndrome (SMS) is a complex neurobehavioral disorder characterized by multiple congenital anomalies. The syndrome is primarily ascribed to a ∼3.7 Mb de novo deletion on chromosome 17p11.2. Haploinsufficiency of multiple genes likely underlies the complex clinical phenotype. RAI1 (Retinoic Acid Induced 1) is recognized as a major gene involved in the SMS phenotype. Extensive genetic and clinical analyses of 36 patients with SMS-like features, but without the 17p11.2 microdeletion, yielded 10 patients with RAI1 variants, including 4 with de novo deleterious mutations, and 6 with novel missense variants, 5 of which were familial. Haplotype analysis showed two major RAI1 haplotypes in our primarily Caucasian cohort; the novel RAI1 variants did not occur in a preferred haplotype. RNA analysis revealed that RAI1 mRNA expression was significantly decreased in cells of patients with the common 17p11.2 deletion, as well as in those with de novo RAI1 variants. Expression levels varied in patients with familial RAI1 variants and in non-17p11.2 deleted patients without identified RAI1 defects. No correlation between SNP haplotype and RAI1 expression was found. Two clinical features, ocular abnormalities and polyembolokoilomania (object insertion), were significantly correlated with decreased RAI1 expression. While not significantly correlated, the presence of hearing loss, seizures, hoarse voice, childhood onset of obesity and specific behavioral aspects and the absence of immunologic abnormalities and cardiovascular or renal structural anomalies, appeared to be specific for the de novo RAI1 subgroup. Recognition of the combination of these features will assist in referral for RAI1 analysis of patients with SMS-like features without detectable microdeletion of 17p11.2. Moreover, RAI1 expression emerged as a genetic target for development of therapeutic interventions for SMS.

  13. Molecular analysis of the Retinoic Acid Induced 1 gene (RAI1 in patients with suspected Smith-Magenis syndrome without the 17p11.2 deletion.

    Directory of Open Access Journals (Sweden)

    Thierry Vilboux

    Full Text Available Smith-Magenis syndrome (SMS is a complex neurobehavioral disorder characterized by multiple congenital anomalies. The syndrome is primarily ascribed to a ∼3.7 Mb de novo deletion on chromosome 17p11.2. Haploinsufficiency of multiple genes likely underlies the complex clinical phenotype. RAI1 (Retinoic Acid Induced 1 is recognized as a major gene involved in the SMS phenotype. Extensive genetic and clinical analyses of 36 patients with SMS-like features, but without the 17p11.2 microdeletion, yielded 10 patients with RAI1 variants, including 4 with de novo deleterious mutations, and 6 with novel missense variants, 5 of which were familial. Haplotype analysis showed two major RAI1 haplotypes in our primarily Caucasian cohort; the novel RAI1 variants did not occur in a preferred haplotype. RNA analysis revealed that RAI1 mRNA expression was significantly decreased in cells of patients with the common 17p11.2 deletion, as well as in those with de novo RAI1 variants. Expression levels varied in patients with familial RAI1 variants and in non-17p11.2 deleted patients without identified RAI1 defects. No correlation between SNP haplotype and RAI1 expression was found. Two clinical features, ocular abnormalities and polyembolokoilomania (object insertion, were significantly correlated with decreased RAI1 expression. While not significantly correlated, the presence of hearing loss, seizures, hoarse voice, childhood onset of obesity and specific behavioral aspects and the absence of immunologic abnormalities and cardiovascular or renal structural anomalies, appeared to be specific for the de novo RAI1 subgroup. Recognition of the combination of these features will assist in referral for RAI1 analysis of patients with SMS-like features without detectable microdeletion of 17p11.2. Moreover, RAI1 expression emerged as a genetic target for development of therapeutic interventions for SMS.

  14. CCAAT/enhancer binding protein {beta} deletion increases mitochondrial function and protects mice from LXR-induced hepatic steatosis

    Energy Technology Data Exchange (ETDEWEB)

    Rahman, Shaikh M., E-mail: rmizanoor@hotmail.com [Department of Pediatrics, School of Medicine, University of Colorado Denver, Aurora, CO 80045 (United States); Choudhury, Mahua; Janssen, Rachel C.; Baquero, Karalee C. [Department of Pediatrics, School of Medicine, University of Colorado Denver, Aurora, CO 80045 (United States); Miyazaki, Makoto [Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Denver, Aurora, CO 80045 (United States); Friedman, Jacob E. [Department of Pediatrics, School of Medicine, University of Colorado Denver, Aurora, CO 80045 (United States); Department of Biochemistry and Molecular Genetics, School of Medicine, University of Colorado Denver, Aurora, CO 80045 (United States)

    2013-01-04

    Highlights: Black-Right-Pointing-Pointer LXR agonist activation increases liver TG accumulation by increasing lipogenesis. Black-Right-Pointing-Pointer C/EBP{beta}{sup -/-} mouse prevents LXR activation-mediated induction of hepatic lipogenesis. Black-Right-Pointing-Pointer C/EBP{beta} deletion increases mitochondrial transport chain function. Black-Right-Pointing-Pointer Beneficial effects of LXR activation on liver cholesterol metabolism did not change. Black-Right-Pointing-Pointer C/EBP{beta} inhibition might have important therapeutic potential. -- Abstract: Drugs designed specifically to activate liver X receptors (LXRs) have beneficial effects on lowering cholesterol metabolism and inflammation but unfortunately lead to severe hepatic steatosis. The transcription factor CCAAT/enhancer binding protein beta (C/EBP{beta}) is an important regulator of liver gene expression but little is known about its involvement in LXR-based steatosis and cholesterol metabolism. The present study investigated the role of C/EBP{beta} expression in LXR agonist (T0901317)-mediated alteration of hepatic triglyceride (TG) and lipogenesis in mice. C/EBP{beta} deletion in mice prevented LXR agonist-mediated induction of lipogenic gene expression in liver in conjunction with significant reduction of liver TG accumulation. Surprisingly, C/EBP{beta}{sup -/-} mice showed a major increase in liver mitochondrial electron chain function compared to WT mice. Furthermore, LXR activation in C/EBP{beta}{sup -/-} mice increased the expression of liver ATP-binding cassette transporter ABCG1, a gene implicated in cholesterol efflux and reducing blood levels of total and LDL-cholesterol. Together, these findings establish a central role for C/EBP{beta} in the LXR-mediated steatosis and mitochondrial function, without impairing the influence of LXR activation on lowering LDL and increasing HDL-cholesterol. Inactivation of C/EBP{beta} might therefore be an important therapeutic strategy to prevent LXR

  15. Inducible and targeted deletion of the ERK5 MAP kinase in adult neurogenic regions impairs adult neurogenesis in the olfactory bulb and several forms of olfactory behavior.

    Directory of Open Access Journals (Sweden)

    Yung-Wei Pan

    Full Text Available Although adult-born neurons in the subventricular zone (SVZ and olfactory bulb (OB have been extensively characterized at the cellular level, their functional impact on olfactory behavior is still highly controversial with many conflicting results reported in the literature. Furthermore, signaling mechanisms regulating adult SVZ/OB neurogenesis are not well defined. Here we report that inducible and targeted deletion of erk5, a MAP kinase selectively expressed in the adult neurogenic regions of the adult brain, impairs adult neurogenesis in the SVZ and OB of transgenic mice. Although erk5 deletion had no effect on olfactory discrimination among discrete odorants in the habituation/dishabituation assay, it reduced short-term olfactory memory as well as detection sensitivity to odorants and pheromones including those evoking aggression and fear. Furthermore, these mice show impaired acquisition of odor-cued associative olfactory learning, a novel phenotype that had not been previously linked to adult neurogenesis. These data suggest that ERK5 MAP kinase is a critical kinase signaling pathway regulating adult neurogenesis in the SVZ/OB, and provide strong evidence supporting a functional role for adult neurogenesis in several distinct forms of olfactory behavior.

  16. GD2-specific CAR T Cells Undergo Potent Activation and Deletion Following Antigen Encounter but can be Protected From Activation-induced Cell Death by PD-1 Blockade.

    Science.gov (United States)

    Gargett, Tessa; Yu, Wenbo; Dotti, Gianpietro; Yvon, Eric S; Christo, Susan N; Hayball, John D; Lewis, Ian D; Brenner, Malcolm K; Brown, Michael P

    2016-06-01

    Chimeric antigen receptor (CAR) T cells have shown great promise in the treatment of hematologic malignancies but more variable results in the treatment of solid tumors and the persistence and expansion of CAR T cells within patients has been identified as a key correlate of antitumor efficacy. Lack of immunological "space", functional exhaustion, and deletion have all been proposed as mechanisms that hamper CAR T-cell persistence. Here we describe the events following activation of third-generation CAR T cells specific for GD2. CAR T cells had highly potent immediate effector functions without evidence of functional exhaustion in vitro, although reduced cytokine production reversible by PD-1 blockade was observed after longer-term culture. Significant activation-induced cell death (AICD) of CAR T cells was observed after repeated antigen stimulation, and PD-1 blockade enhanced both CAR T-cell survival and promoted killing of PD-L1(+) tumor cell lines. Finally, we assessed CAR T-cell persistence in patients enrolled in the CARPETS phase 1 clinical trial of GD2-specific CAR T cells in the treatment of metastatic melanoma. Together, these data suggest that deletion also occurs in vivo and that PD-1-targeted combination therapy approaches may be useful to augment CAR T-cell efficacy and persistence in patients.

  17. Deficiency in Either 4E-BP1 or 4E-BP2 Augments Innate Antiviral Immune Responses

    Science.gov (United States)

    Nehdi, Atef; Sean, Polen; Linares, Izzar; Colina, Rodney; Jaramillo, Maritza; Alain, Tommy

    2014-01-01

    Genetic deletion of both 4E-BP1 and 4E-BP2 was found to protect cells against viral infections. Here we demonstrate that the individual loss of either 4E-BP1 or 4E-BP2 in mouse embryonic fibroblasts (MEFs) is sufficient to confer viral resistance. shRNA-mediated silencing of 4E-BP1 or 4E-BP2 renders MEFs resistant to viruses, and compared to wild type cells, MEFs knockout for either 4E-BP1 or 4E-BP2 exhibit enhanced translation of Irf-7 and consequently increased innate immune response to viruses. Accordingly, the replication of vesicular stomatitis virus, encephalomyocarditis virus, influenza virus and Sindbis virus is markedly suppressed in these cells. Importantly, expression of either 4E-BP1 or 4E-BP2 in double knockout or respective single knockout cells diminishes their resistance to viral infection. Our data show that loss of 4E-BP1 or 4E-BP2 potentiates innate antiviral immunity. These results provide further evidence for translational control of innate immunity and support targeting translational effectors as an antiviral strategy. PMID:25531441

  18. Deletion of TRPC6 Attenuates NMDA Receptor-Mediated Ca2+ Entry and Ca2+-Induced Neurotoxicity Following Cerebral Ischemia and Oxygen-Glucose Deprivation

    Science.gov (United States)

    Chen, Jin; Li, Zhaozhong; Hatcher, Jeffery T.; Chen, Qing-Hui; Chen, Li; Wurster, Robert D.; Chan, Sic L.; Cheng, Zixi

    2017-01-01

    Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na+ and Ca2+ and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca2+ levels ([Ca2+]i), we found that OGD induced a significant higher increase in glutamate-evoked Ca2+ influx compared to untreated control and such an increase was reduced by TRPC6 deletion. Enhancement of TRPC6 expression using AdCMV-TRPC6-GFP infection in WT neurons increased [Ca2+]i in response to glutamate application compared to AdCMV-GFP control. Inhibition of N-methyl-d-aspartic acid receptor (NMDAR) with MK801 decreased TRPC6-dependent increase of [Ca2+]i in TRPC6 infected cells, indicating that such a Ca2+ influx was NMDAR dependent. Furthermore, TRPC6-dependent Ca2+ influx was blunted by blockade of Na+ entry in TRPC6 infected cells. Finally, OGD-enhanced Ca2+ influx was reduced, but not completely blocked, in the presence of voltage-dependent Na+ channel blocker tetrodotoxin (TTX) and dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) blocker CNQX. Altogether, we concluded that I/R-induced brain damage was, in part, due to upregulation of TRPC6 in cortical neurons. We postulate that overexpression of TRPC6 following I/R may induce neuronal death partially through TRPC6-dependent Na+ entry which activated NMDAR, thus leading to a damaging Ca2+ overload. These findings may provide a potential target for future intervention in stroke-induced brain damage.

  19. Alzheimer's disease presenilin-1 exon 9 deletion and L250S mutations sensitize SH-SY5Y neuroblastoma cells to hyperosmotic stress-induced apoptosis

    DEFF Research Database (Denmark)

    Tanii, H; Ankarcrona, M; Flood, F

    2000-01-01

    mutation-related increases in number of apoptotic cells at 24 h following high glucose treatment were not accompanied by significant differences in cell viability at this time-point. Our results indicate that PS1......Mutations in the presenilin-1 (PS1) and presenilin-2 (PS2) genes account for the majority of early-onset familial Alzheimer's disease cases. Recent studies suggest that presenilin gene mutations predispose cells to apoptosis by mechanisms involving altered calcium homeostasis and oxidative damage....... In the present study, we determined whether PS1 mutations also sensitize cells to hyperosmotic stress-induced apoptosis. For this, we established SH-SY5Y neuroblastoma cell lines stably transfected with wild-type PS1 or either the PS1 exon 9 deletion (deltaE9) or PS1 L250S mutants. Cultured cells were exposed...

  20. Tanshinone IIA induced cell death via miR30b-p53-PTPN11/SHP2 signaling pathway in human hepatocellular carcinoma cells.

    Science.gov (United States)

    Ren, Xuanqi; Wang, Cui; Xie, Binbin; Hu, Linfeng; Chai, Hui; Ding, Lei; Tang, Lihua; Xia, Yongliang; Dou, Xiaobing

    2017-02-05

    Tanshinone IIA, a multi-pharmaceutical compound from traditional Chinese herb, has been reported to have anti-hepatocarcinomic (HCC) properties through cell death induction. Apart from the typical p53-dependent pathway, mechanisms of the anti-carcinogenic role of Tanshinone remain scarce. In an effort to explore the mechanism behind Tanshinone IIA, we detected the upstream of the p53 and the potential novel pathway. Tanshinone IIA dose-dependently initiated HepG2 cell apoptosis and cell cycle arrest at the G1 checkpoint. In the miR30 family, only the transcription of miR30b was downregulated by Tanshinone IIA, which subsequently upregulated both the genomic and protein levels of p53. Further, we screened that PTPN11 and Tp53 are the two critical genomes involved in the pharmacology of Tanshinone IIA. Building upon LASAGNA-search and kinetics binding assay, p53 was found to be a potential transcription factor for PTPN11. Concomitant with the expression of p53, Tanshinone IIA stimulated both PTPN11 and its encoded protein SHP2. Inhibition miR30b attenuated the Tanshinone IIA-induced cytotoxicity, level of p53 and PTPN11 in HepG2 cells. Finally, the apoptotic molecules such as Bax/Bcl2, cleavage caspase 3 and the cell cycle regulation factors including p21, cyclin D1, and CDK6 were changed by Tanshinone IIA. Several cytotoxic endpoints induced by Tanshinone IIA were also checked in Hep3B cells. This study confirmed that Tanshinone IIA may induce hepatoma cell death through the miR30b-p53- PTPN11/SHP2 pathway. With regard to the complicated tumorigenesis of HCC and the multi-targets of Tanshinone IIA, our results propose developing Tanshinone IIA for clinic therapy and the interference of HCC.

  1. Visible Light-Responsive Platinum-Containing Titania Nanoparticle-Mediated Photocatalysis Induces Nucleotide Insertion, Deletion and Substitution Mutations

    Directory of Open Access Journals (Sweden)

    Der-Shan Sun

    2016-12-01

    Full Text Available Conventional photocatalysts are primarily stimulated using ultraviolet (UV light to elicit reactive oxygen species and have wide applications in environmental and energy fields, including self-cleaning surfaces and sterilization. Because UV illumination is hazardous to humans, visible light-responsive photocatalysts (VLRPs were discovered and are now applied to increase photocatalysis. However, fundamental questions regarding the ability of VLRPs to trigger DNA mutations and the mutation types it elicits remain elusive. Here, through plasmid transformation and β-galactosidase α-complementation analyses, we observed that visible light-responsive platinum-containing titania (TiO2 nanoparticle (NP-mediated photocatalysis considerably reduces the number of Escherichia coli transformants. This suggests that such photocatalytic reactions cause DNA damage. DNA sequencing results demonstrated that the DNA damage comprises three mutation types, namely nucleotide insertion, deletion and substitution; this is the first study to report the types of mutations occurring after photocatalysis by TiO2-VLRPs. Our results may facilitate the development and appropriate use of new-generation TiO2 NPs for biomedical applications.

  2. Global deletion of MGL in mice delays lipid absorption and alters energy homeostasis and diet-induced obesity

    Science.gov (United States)

    Douglass, John D.; Zhou, Yin Xiu; Wu, Amy; Zadrogra, John A.; Gajda, Angela M.; Lackey, Atreju I.; Lang, Wensheng; Chevalier, Kristen M.; Sutton, Steven W.; Zhang, Sui-Po; Flores, Christopher M.; Connelly, Margery A.; Storch, Judith

    2015-01-01

    Monoacylglycerol lipase (MGL) is a ubiquitously expressed enzyme that catalyzes the hydrolysis of monoacylglycerols (MGs) to yield FFAs and glycerol. MGL contributes to energy homeostasis through the mobilization of fat stores and also via the degradation of the endocannabinoid 2-arachidonoyl glycerol. To further examine the role of MG metabolism in energy homeostasis, MGL−/− mice were fed either a 10% (kilocalories) low-fat diet (LFD) or a 45% (kilocalories) high-fat diet (HFD) for 12 weeks. Profound increases of MG species in the MGL−/− mice compared with WT control mice were found. Weight gain over the 12 weeks was blunted in both diet groups. MGL−/− mice were leaner than WT mice at both baseline and after 12 weeks of LFD feeding. Circulating lipids were decreased in HFD-fed MGL−/− mice, as were the levels of several plasma peptides involved in glucose homeostasis and energy balance. Interestingly, MGL−/− mice had markedly reduced intestinal TG secretion following an oral fat challenge, suggesting delayed lipid absorption. Overall, the results indicate that global MGL deletion leads to systemic changes that produce a leaner phenotype and an improved serum metabolic profile. PMID:25842377

  3. Genetic deletion of low density lipoprotein receptor impairs sterol-induced mouse macrophage ABCA1 expression. A new SREBP1-dependent mechanism.

    Science.gov (United States)

    Zhou, Xiaoye; He, Wei; Huang, Zhiping; Gotto, Antonio M; Hajjar, David P; Han, Jihong

    2008-01-25

    Low density lipoprotein receptor (LDLR) mutations cause familial hypercholesterolemia and early atherosclerosis. ABCA1 facilitates free cholesterol efflux from peripheral tissues. We investigated the effects of LDLR deletion (LDLR(-/-)) on ABCA1 expression. LDLR(-/-) macrophages had reduced basal levels of ABCA1, ABCG1, and cholesterol efflux. A high fat diet increased cholesterol in LDLR(-/-) macrophages but not wild type cells. A liver X receptor (LXR) agonist induced expression of ABCA1, ABCG1, and cholesterol efflux in both LDLR(-/-) and wild type macrophages, whereas expression of LXRalpha or LXRbeta was similar. Interestingly, oxidized LDL induced more ABCA1 in wild type macrophages than LDLR(-/-) cells. LDL induced ABCA1 expression in wild type cells but inhibited it in LDLR(-/-) macrophages in a concentration-dependent manner. However, lipoproteins regulated ABCG1 expression similarly in LDLR(-/-) and wild type macrophages. Cholesterol or oxysterols induced ABCA1 expression in wild type macrophages but had little or inhibitory effects on ABCA1 expression in LDLR(-/-) macrophages. Active sterol regulatory element-binding protein 1a (SREBP1a) inhibited ABCA1 promoter activity in an LXRE-dependent manner and decreased both macrophage ABCA1 expression and cholesterol efflux. Expression of ABCA1 in animal tissues was inversely correlated to active SREBP1. Oxysterols inactivated SREBP1 in wild type macrophages but not in LDLR(-/-) cells. Oxysterol synergized with nonsteroid LXR ligand induced ABCA1 expression in wild type macrophages but blocked induction in LDLR(-/-) cells. Taken together, our studies suggest that LDLR is critical in the regulation of cholesterol efflux and ABCA1 expression in macrophage. Lack of the LDLR impairs sterol-induced macrophage ABCA1 expression by a sterol regulatory element-binding protein 1-dependent mechanism that can result in reduced cholesterol efflux and lipid accumulation in macrophages under hypercholesterolemic conditions.

  4. Analysis on the Frequency of 9 bp Deletion of mtDNA and on Polymorphisim of Y-choromosome DYS287 Sites in Uighur Population in Eight Geographical Regions of Xinjiang%新疆8个地域维吾尔族群线粒体DNA V-区9bp缺失频率与Y-染色体DYS287位点多态性研究

    Institute of Scientific and Technical Information of China (English)

    木耶塞尔·伊斯马依力; 古丽娜·艾山; 马合木提·哈力克

    2011-01-01

    In order to study the frequency of 9 bp deletion of mtDNA V region and polymorphisim of Y-choromosome DYS287 sites among Uighur population in eight geographical regions of Xinjiang. We used the polymorphism of DYS287 sites in Y choromosome and the defeciency frequency of chromosome DNA 9 bp region by PCR directly sequensing method and by PCR combining with agarose gel electro-pho-resis respectively. The results showed: Among 240 unrelated modren Uighur individuals who come from Kashgar, Khotan, Kuqa, and Qarqan, Hulja, Hami, Turpan, and Lopnur in Xinjiang, the frequency of 9 bp deletion of mtDNA value as 4% , 3.1% , 3% , 4% , 4. 5% , 4% , 3% , 4%. Polymorphisim of Y-choromosome DYS 287 sites of 180 modern Uighur male individuals all appears as YAP - , none shows YAP +. The results suggest that Uighur groups in different parts of Xinjiang show very low frequency in their 9 bp deletion of mtDNA, 9 bp deletion is not a modern Uighur matrilineal genetic structure of transfer, Uighurs in different region of Xinjiang share same 9 bp deletion of mtDNA. Paternal genetic structure is simple, YAP + is not a modern Uighur population genetic characteristics of the male line. So, some conclusions can be given: with collecting frequency of 9 bp deletion of mtDNA and polymorphisim of Y-choromosome DYS 287 sites of Uighur population in different regions of Xinjiang, conduct analysis genetic relationship of Uighur population in different region of Xinjiang and Forensic identification provide some background informations about origin relationship Uighur groupsin different regions.%为研究新疆8个地域维吾尔族群体的线粒体DNA 9 bp序列缺失频率与Y染色体DYS287位点多态性,分别采用PCR扩增直接测序法和PCR结合琼脂糖凝胶电泳检测法对群线粒体DNA 9 bp缺失频率与Y-染色体DYS287位点多态性进行分析.结果表明在新疆的喀什、和田、库车、且木、哈密、吐鲁番、伊梨和尉梨县的240个无关现代维

  5. Residual virulence and immunogenicity of CGV26 and CGV2631 B. melitensis Rev. 1 deletion mutant strains in sheep after subcutaneous or conjunctival vaccination.

    Science.gov (United States)

    Guilloteau, Laurence A; Laroucau, Karine; Olivier, Michel; Grillo, Maria Jesus; Marin, Clara M; Verger, Jean-Michel; Blasco, Jose-Maria

    2006-04-24

    The CGV26 and CGV2631 strains are novel engineered Brucella melitensis Rev.1 mutant strains deleted for the bp26 gene or for both bp26 and omp31 genes, respectively, coding for proteins of diagnostic significance. The residual virulence and immunogenicity of both mutants were compared to the parental Rev.1 strain in sheep after subcutaneous or conjunctival vaccination. The deletion of the bp26 gene or both bp26 and omp31 genes had no significant effect on the intracellular survival of the Rev.1 strain in ovine macrophage cultures. The kinetics of infection induced by both mutants in sheep was similar to the Rev.1 strain, and inoculation by the subcutaneous route produced wider and more generalized infections than the conjunctival route. All strains were cleared from lymph nodes and organs within 3 months after inoculation. The CGV26 and CGV2631 mutants induced both specific systemic antibody response and lymphoproliferation in sheep. The kinetics of the responses induced by the mutants was quite similar to that of the parental Rev.1 strain, except for the intensity of the lymphoproliferative response, which was attenuated for the CGV2631 mutant. In conclusion, the residual virulence of both CGV26 and CGV2631 mutants in sheep was similar to that of the parental Rev.1 vaccine strain. These mutants induced also significant specific antibody and cell-mediated immunity in sheep and are suitable to be evaluated as potential vaccine candidates against B. melitensis and B. ovis infections in sheep.

  6. LGALS3BP, lectin galactoside-binding soluble 3 binding protein, induces vascular endothelial growth factor in human breast cancer cells and promotes angiogenesis.

    Science.gov (United States)

    Piccolo, Enza; Tinari, Nicola; Semeraro, Daniela; Traini, Sara; Fichera, Imma; Cumashi, Albana; La Sorda, Rossana; Spinella, Francesca; Bagnato, Anna; Lattanzio, Rossano; D'Egidio, Maurizia; Di Risio, Annalisa; Stampolidis, Pavlos; Piantelli, Mauro; Natoli, Clara; Ullrich, Axel; Iacobelli, Stefano

    2013-01-01

    Elevated serum or tissue levels of lectin galactoside-binding soluble 3 binding protein (LGALS3BP) have been associated with short survival and development of metastasis in a variety of human cancers. However, the role of LGALS3BP, particularly in the context of tumor-host relationships, is still missing. Here, we show that LGALS3BP knockdown in MDA-MB-231 human breast cancer cells leads to a decreased adhesion to fibronectin, a reduced transendothelial migration and, more importantly, a reduced expression of vascular endothelial growth factor (VEGF). Production of VEGF, that was restored by exposure of silenced cells to recombinant LGALS3BP, required an intact PI3k/Akt signaling. Furthermore, we show that LGALS3BP was able to directly stimulate HUVEC tubulogenesis in a VEGF-independent, galectin-3-dependent manner. Immunohistochemical analysis of human breast cancer tissues revealed a correlation among LGALS3BP expression, VEGF expression, and blood vessel density. We propose that in addition to its prometastatic role, LGALS3BP secreted by breast cancer cells functions critically as a pro-angiogenic factor through a dual mechanism, i.e by induction of tumor VEGF and stimulation of endothelial cell tubulogenesis.

  7. Genetic deletion of IL-25 (IL-17E) confers resistance to dextran sulfate sodium-induced colitis in mice

    Science.gov (United States)

    IL-25 is emerging as a key regulator of inflammation in the intestinal mucosa because of its ability to promote Th2 while suppressing Th1 and Th17 cytokine responses. We investigated the contribution of endogenous IL-25 to DSS-induced colitis in mice. Mice were exposed to DSS in drinking water ad li...

  8. Adenosine A2A receptor blockade or deletion diminishes fibrocyte accumulation in the skin in a murine model of scleroderma, bleomycin-induced fibrosis.

    Science.gov (United States)

    Katebi, Majid; Fernandez, Patricia; Chan, Edwin S L; Cronstein, Bruce N

    2008-10-01

    Peripheral blood fibrocytes are a newly identified circulating leukocyte subpopulation that migrates into injured tissue where it may display fibroblast-like properties and participate in wound healing and fibrosis of skin and other organs. Previous studies in our lab demonstrated that A(2A) receptor-deficient and A(2A) antagonist-treated mice were protected from developing bleomycin-induced dermal fibrosis, thus the aim of this study was to determine whether the adenosine A(2A) receptor regulates recruitment of fibrocytes to the dermis in this bleomycin-induced model of dermal fibrosis. Sections of skin from normal mice and bleomycin-treated wild type, A(2A) knockout and A(2A) antagonist-treated mice were stained for Procollagen alpha2 Type I and CD34 and the double stained cells, fibrocytes, were counted in the tissue sections. There were more fibrocytes in the dermis of bleomycin-treated mice than normal mice and the increase was abrogated by deletion or blockade of adenosine A(2A) receptors. Because fibrocytes play a central role in tissue fibrosis these results suggest that diminished adenosine A(2A) receptor-mediated recruitment of fibrocytes into tissue may play a role in the pathogenesis of fibrosing diseases of the skin. Moreover, these results provide further evidence that adenosine A(2A) receptors may represent a new target for the treatment of such fibrosing diseases as scleroderma or nephrogenic fibrosing dermopathy.

  9. Partial deletion of ROCK2 protects mice from high-fat diet-induced cardiac insulin resistance and contractile dysfunction.

    Science.gov (United States)

    Soliman, Hesham; Nyamandi, Vongai; Garcia-Patino, Marysol; Varela, Julia Nogueira; Bankar, Girish; Lin, Guorong; Jia, Zhengping; MacLeod, Kathleen M

    2015-07-01

    Obesity is associated with cardiac insulin resistance and contractile dysfunction, which contribute to the development of heart failure. The RhoA-Rho kinase (ROCK) pathway has been reported to modulate insulin resistance, but whether it is implicated in obesity-induced cardiac dysfunction is not known. To test this, wild-type (WT) and ROCK2(+/-) mice were fed normal chow or a high-fat diet (HFD) for 17 wk. Whole body insulin resistance, determined by an insulin tolerance test, was observed in HFD-WT, but not HFD-ROCK2(+/-), mice. The echocardiographically determined myocardial performance index, a measure of global systolic and diastolic function, was significantly increased in HFD-WT mice, indicating a deterioration of cardiac function. However, no change in myocardial performance index was found in hearts from HFD-ROCK2(+/-) mice. Speckle-tracking-based strain echocardiography also revealed regional impairment in left ventricular wall motion in hearts from HFD-WT, but not HFD-ROCK2(+/-), mice. Activity of ROCK1 and ROCK2 was significantly increased in hearts from HFD-WT mice, and GLUT4 expression was significantly reduced. Insulin-induced phosphorylation of insulin receptor substrate (IRS) Tyr(612), Akt, and AS160 was also impaired in these hearts, while Ser(307) phosphorylation of IRS was increased. In contrast, the increase in ROCK2, but not ROCK1, activity was prevented in hearts from HFD-ROCK2(+/-) mice, and cardiac levels of TNFα were reduced. This was associated with normalization of IRS phosphorylation, downstream insulin signaling, and GLUT4 expression. These data suggest that increased activation of ROCK2 contributes to obesity-induced cardiac dysfunction and insulin resistance and that inhibition of ROCK2 may constitute a novel approach to treat this condition.

  10. Col2CreERT2, A MOUSE MODEL FOR A CHONDROCYTE-SPECIFIC AND INDUCIBLE GENE DELETION

    OpenAIRE

    2014-01-01

    In 2007 and 2008, we published two articles reporting a tamoxifen (TM)-inducible, chondrocyte-specific gene-targeting mouse model in which the expression of CreERT2 is driven by the type II collagen promoter (Col2CreERT2). The fusion protein is specifically expressed and translocated into the nucleus upon TM administration, which in turn triggers gene recombination. Since then, this animal model has become a powerful tool to study the molecular mechanism of skeletal development and degenerati...

  11. Col2CreERT2, a mouse model for a chondrocyte-specific and inducible gene deletion

    Directory of Open Access Journals (Sweden)

    M Chen

    2014-10-01

    Full Text Available In 2007 and 2008, we published two articles reporting a tamoxifen (TM-inducible, chondrocyte-specific gene-targeting mouse model in which the expression of CreERT2 is driven by the type II collagen promoter (Col2CreERT2. The fusion protein is specifically expressed and translocated into the nucleus upon TM administration, which in turn triggers gene recombination. Since then, this animal model has become a powerful tool to study the molecular mechanism of skeletal development and degenerative cartilage diseases, including knee joint osteoarthritis (OA, temporomandibular joint (TMJ OA, and intervertebral disc (IVD degeneration. In this review article, we summarise the application of Col2CreERT2 mice and discuss the potential usage of this animal model in a broad spectrum of cartilage development and molecular pathology studies.

  12. Epithelium-specific deletion of TGF-β receptor type II protects mice from bleomycin-induced pulmonary fibrosis.

    Science.gov (United States)

    Li, Min; Krishnaveni, Manda Sai; Li, Changgong; Zhou, Beiyun; Xing, Yiming; Banfalvi, Agnes; Li, Aimin; Lombardi, Vincent; Akbari, Omid; Borok, Zea; Minoo, Parviz

    2011-01-01

    Idiopathic pulmonary fibrosis (IPF) is a chronic fibroproliferative pulmonary disorder for which there are currently no treatments. Although the etiology of IPF is unknown, dysregulated TGF-β signaling has been implicated in its pathogenesis. Recent studies also suggest a central role for abnormal epithelial repair. In this study, we sought to elucidate the function of epithelial TGF-β signaling via TGF-β receptor II (TβRII) and its contribution to fibrosis by generating mice in which TβRII was specifically inactivated in mouse lung epithelium. These mice, which are referred to herein as TβRIINkx2.1-cre mice, were used to determine the impact of TβRII inactivation on (a) embryonic lung morphogenesis in vivo; and (b) the epithelial cell response to TGF-β signaling in vitro and in a bleomycin-induced, TGF-β-mediated mouse model of pulmonary fibrosis. Although postnatally viable with no discernible abnormalities in lung morphogenesis and epithelial cell differentiation, TβRIINkx2.1-cre mice developed emphysema, suggesting a requirement for epithelial TβRII in alveolar homeostasis. Absence of TβRII increased phosphorylation of Smad2 and decreased, but did not entirely block, phosphorylation of Smad3 in response to endogenous/physiologic TGF-β. However, TβRIINkx2.1-cre mice exhibited increased survival and resistance to bleomycin-induced pulmonary fibrosis. To our knowledge, these findings are the first to demonstrate a specific role for TGF-β signaling in the lung epithelium in the pathogenesis of pulmonary fibrosis.

  13. The 15q11.2 BP1–BP2 Microdeletion Syndrome: A Review

    Directory of Open Access Journals (Sweden)

    Devin M. Cox

    2015-02-01

    Full Text Available Patients with the 15q11.2 BP1–BP2 microdeletion can present with developmental and language delay, neurobehavioral disturbances and psychiatric problems. Autism, seizures, schizophrenia and mild dysmorphic features are less commonly seen. The 15q11.2 BP1–BP2 microdeletion involving four genes (i.e., TUBGCP5, CYFIP1, NIPA1, NIPA2 is emerging as a recognized syndrome with a prevalence ranging from 0.57%–1.27% of patients presenting for microarray analysis which is a two to four fold increase compared with controls. Review of clinical features from about 200 individuals were grouped into five categories and included developmental (73% and speech (67% delays; dysmorphic ears (46% and palatal anomalies (46%; writing (60% and reading (57% difficulties, memory problems (60% and verbal IQ scores ≤75 (50%; general behavioral problems, unspecified (55% and abnormal brain imaging (43%. Other clinical features noted but not considered as common were seizures/epilepsy (26%, autism spectrum disorder (27%, attention deficit disorder (ADD/attention deficit hyperactivity disorder (ADHD (35%, schizophrenia/paranoid psychosis (20% and motor delay (42%. Not all individuals with the deletion are clinically affected, yet the collection of findings appear to share biological pathways and presumed genetic mechanisms. Neuropsychiatric and behavior disturbances and mild dysmorphic features are associated with genomic imbalances of the 15q11.2 BP1–BP2 region, including microdeletions, but with an apparent incomplete penetrance and variable expressivity.

  14. A neuron-specific deletion of the microRNA-processing enzyme DICER induces severe but transient obesity in mice.

    Directory of Open Access Journals (Sweden)

    Géraldine M Mang

    Full Text Available MicroRNAs (miRNAs are small, non-coding RNA molecules that regulate gene expression post-transcriptionally. MiRNAs are implicated in various biological processes associated with obesity, including adipocyte differentiation and lipid metabolism. We used a neuronal-specific inhibition of miRNA maturation in adult mice to study the consequences of miRNA loss on obesity development. Camk2a-CreERT2 (Cre+ and floxed Dicer (Dicerlox/lox mice were crossed to generate tamoxifen-inducible conditional Dicer knockouts (cKO. Vehicle- and/or tamoxifen-injected Cre+;Dicerlox/lox and Cre+;Dicer+/+ served as controls. Four cohorts were used to a measure body composition, b follow food intake and body weight dynamics, c evaluate basal metabolism and effects of food deprivation, and d assess the brain transcriptome consequences of miRNA loss. cKO mice developed severe obesity and gained 18 g extra weight over the 5 weeks following tamoxifen injection, mainly due to increased fat mass. This phenotype was highly reproducible and observed in all 38 cKO mice recorded and in none of the controls, excluding possible effects of tamoxifen or the non-induced transgene. Development of obesity was concomitant with hyperphagia, increased food efficiency, and decreased activity. Surprisingly, after reaching maximum body weight, obese cKO mice spontaneously started losing weight as rapidly as it was gained. Weight loss was accompanied by lowered O2-consumption and respiratory-exchange ratio. Brain transcriptome analyses in obese mice identified several obesity-related pathways (e.g. leptin, somatostatin, and nemo-like kinase signaling, as well as genes involved in feeding and appetite (e.g. Pmch, Neurotensin and in metabolism (e.g. Bmp4, Bmp7, Ptger1, Cox7a1. A gene cluster with anti-correlated expression in the cerebral cortex of post-obese compared to obese mice was enriched for synaptic plasticity pathways. While other studies have identified a role for miRNAs in obesity, we

  15. Mice with a targeted deletion of the type 2 deiodinase are insulin resistant and susceptible to diet induced obesity.

    Directory of Open Access Journals (Sweden)

    Alessandro Marsili

    Full Text Available BACKGROUND: The type 2 iodothyronine deiodinase (D2 converts the pro-hormone thyroxine into T3 within target tissues. D2 is essential for a full thermogenic response of brown adipose tissue (BAT, and mice with a disrupted Dio2 gene (D2KO have an impaired response to cold. BAT is also activated by overfeeding. METHODOLOGY/PRINCIPAL FINDINGS: After 6-weeks of HFD feeding D2KO mice gained 5.6% more body weight and had 28% more adipose tissue. Oxygen consumption (V0(2 was not different between genotypes, but D2KO mice had an increased respiratory exchange ratio (RER, suggesting preferential use of carbohydrates. Consistent with this, serum free fatty acids and β-hydroxybutyrate were lower in D2KO mice on a HFD, while hepatic triglycerides were increased and glycogen content decreased. Neither genotype showed glucose intolerance, but D2KO mice had significantly higher insulin levels during GTT independent of diet. Accordingly, during ITT testing D2KO mice had a significantly reduced glucose uptake, consistent with insulin resistance. Gene expression levels in liver, muscle, and brown and white adipose tissue showed no differences that could account for the increased weight gain in D2KO mice. However, D2KO mice have higher PEPCK mRNA in liver suggesting increased gluconeogenesis, which could also contribute to their apparent insulin resistance. CONCLUSIONS/SIGNIFICANCE: We conclude that the loss of the Dio2 gene has significant metabolic consequences. D2KO mice gain more weight on a HFD, suggesting a role for D2 in protection from diet-induced obesity. Further, D2KO mice appear to have a greater reliance on carbohydrates as a fuel source, and limited ability to mobilize and to burn fat. This results in increased fat storage in adipose tissue, hepatic steatosis, and depletion of liver glycogen in spite of increased gluconeogenesis. D2KO mice are also less responsive to insulin, independent of diet-induced obesity.

  16. Filler DNA is associated with spontaneous deletions in maize.

    OpenAIRE

    Wessler, S; Tarpley, A; Purugganan, M.; Spell, M; Okagaki, R.

    1990-01-01

    We have determined the structure of five spontaneous deletions within the maize waxy (Wx) gene. Of these, four were found in spontaneous wx mutants (wx-B, wx-B1, wx-B6, wx-C4) and include exon sequences; the fifth is restricted to an intron and represents a restriction fragment length polymorphism of a nonmutant allele (Wx-W23). The deletions, which range in size from 60 to 980 base pairs (bp), cluster in a G+C-rich region of approximately 1000 bp that is capable of forming stable secondary s...

  17. Skin-specific deletion of stearoyl-CoA desaturase-1 alters skin lipid composition and protects mice from high fat diet-induced obesity.

    Science.gov (United States)

    Sampath, Harini; Flowers, Matthew T; Liu, Xueqing; Paton, Chad M; Sullivan, Ruth; Chu, Kiki; Zhao, Minghui; Ntambi, James M

    2009-07-24

    Stearoyl-CoA desaturase-1 (SCD1) catalyzes the synthesis of monounsaturated fatty acids and is an important regulator of whole body energy homeostasis. Severe cutaneous changes in mice globally deficient in SCD1 also indicate a role for SCD1 in maintaining skin lipids. We have generated mice with a skin-specific deletion of SCD1 (SKO) and report here that SKO mice display marked sebaceous gland hypoplasia and depletion of sebaceous lipids. In addition, SKO mice have significantly increased energy expenditure and are protected from high fat diet-induced obesity, thereby recapitulating the hypermetabolic phenotype of global SCD1 deficiency. Genes of fat oxidation, lipolysis, and thermogenesis, including uncoupling proteins and peroxisome proliferator-activated receptor-gamma co-activator-1alpha, are up-regulated in peripheral tissues of SKO mice. However, unlike mice globally deficient in SCD1, SKO mice have an intact hepatic lipogenic response to acute high carbohydrate feeding. Despite increased basal thermogenesis, SKO mice display severe cold intolerance because of rapid depletion of fuel substrates, including hepatic glycogen, to maintain core body temperature. These data collectively indicate that SKO mice have increased cold perception because of loss of insulating factors in the skin. This results in up-regulation of thermogenic processes for temperature maintenance at the expense of fuel economy, illustrating cross-talk between the skin and peripheral tissues in maintaining energy homeostasis.

  18. Deletion of AIF1 but not of YCA1/MCA1 protects Saccharomyces cerevisiae and Candida albicans cells from caspofungin-induced programmed cell death

    Directory of Open Access Journals (Sweden)

    Christopher Chin

    2014-01-01

    Full Text Available Caspofungin was the first member of a new class of antifungals called echinocandins to be approved by a drug regulatory authority. Like the other echinocandins, caspofungin blocks the synthesis of β(1,3-D-glucan of the fungal cell wall by inhibiting the enzyme, β(1,3-D-glucan synthase. Loss of β(1,3-D-glucan leads to osmotic instability and cell death. However, the precise mechanism of cell death associated with the cytotoxicity of caspofungin was unclear. We now provide evidence that Saccharomyces cerevisiae cells cultured in media containing caspofungin manifest the classical hallmarks of programmed cell death (PCD in yeast, including the generation of reactive oxygen species (ROS, the fragmentation of mitochondria, and the production of DNA strand breaks. Our data also suggests that deleting AIF1 but not YCA1/MCA1 protects S. cerevisiae and Candida albicans from caspofungin-induced cell death. This is not only the first time that AIF1 has been specifically tied to cell death in Candida but also the first time that caspofungin resistance has been linked to the cell death machinery in yeast.

  19. Genetic deletion and pharmacological inhibition of phosphodiesterase 10A protects mice from diet-induced obesity and insulin resistance.

    Science.gov (United States)

    Nawrocki, Andrea R; Rodriguez, Carlos G; Toolan, Dawn M; Price, Olga; Henry, Melanie; Forrest, Gail; Szeto, Daphne; Keohane, Carol Ann; Pan, Yie; Smith, Karen M; Raheem, Izzat T; Cox, Christopher D; Hwa, Joyce; Renger, John J; Smith, Sean M

    2014-01-01

    Phosphodiesterase 10A (PDE10A) is a novel therapeutic target for the treatment of schizophrenia. Here we report a novel role of PDE10A in the regulation of caloric intake and energy homeostasis. PDE10A-deficient mice are resistant to diet-induced obesity (DIO) and associated metabolic disturbances. Inhibition of weight gain is due to hypophagia after mice are fed a highly palatable diet rich in fats and sugar but not a standard diet. PDE10A deficiency produces a decrease in caloric intake without affecting meal frequency, daytime versus nighttime feeding behavior, or locomotor activity. We tested THPP-6, a small molecule PDE10A inhibitor, in DIO mice. THPP-6 treatment resulted in decreased food intake, body weight loss, and reduced adiposity at doses that produced antipsychotic efficacy in behavioral models. We show that PDE10A inhibition increased whole-body energy expenditure in DIO mice fed a Western-style diet, achieving weight loss and reducing adiposity beyond the extent seen with food restriction alone. Therefore, chronic THPP-6 treatment conferred improved insulin sensitivity and reversed hyperinsulinemia. These data demonstrate that PDE10A inhibition represents a novel antipsychotic target that may have additional metabolic benefits over current medications for schizophrenia by suppressing food intake, alleviating weight gain, and reducing the risk for the development of diabetes.

  20. Partial deletion of argininosuccinate synthase protects from pyrazole plus lipopolysaccharide-induced liver injury by decreasing nitrosative stress.

    Science.gov (United States)

    Lu, Yongke; Leung, Tung Ming; Ward, Stephen C; Nieto, Natalia

    2012-02-01

    Argininosuccinate synthase (ASS) is the rate-limiting enzyme in the urea cycle. Along with nitric oxide synthase (NOS)-2, ASS endows cells with the L-citrulline/nitric oxide (NO·) salvage pathway to continually supply L-arginine from L-citrulline for sustained NO· generation. Because of the relevant role of NOS in liver injury, we hypothesized that downregulation of ASS could decrease the availability of intracellular substrate for NO· synthesis by NOS-2 and, hence, decrease liver damage. Previous work demonstrated that pyrazole plus LPS caused significant liver injury involving NO· generation and formation of 3-nitrotyrosine protein adducts; thus, wild-type (WT) and Ass+/- mice (Ass+/+ mice are lethal) were treated with pyrazole plus LPS, and markers of nitrosative stress, as well as liver injury, were analyzed. Partial ablation of Ass protected from pyrazole plus LPS-induced liver injury by decreasing nitrosative stress and hepatic and circulating TNFα. Moreover, apoptosis was prevented, since pyrazole plus LPS-treated Ass+/- mice showed decreased phosphorylation of JNK; increased MAPK phosphatase-1, which is known to deactivate JNK signaling; and lower cleaved caspase-3 than treated WT mice, and this was accompanied by less TdT-mediated dUTP nick end labeling-positive staining. Lastly, hepatic neutrophil accumulation was almost absent in pyrazole plus LPS-treated Ass+/- compared with WT mice. Partial Ass ablation prevents pyrazole plus LPS-mediated liver injury by reducing nitrosative stress, TNFα, apoptosis, and neutrophil infiltration.

  1. Prostaglandin E2 EP2 Receptor Deletion Attenuates Intracerebral Hemorrhage-Induced Brain Injury and Improves Functional Recovery

    Directory of Open Access Journals (Sweden)

    Jenna L. Leclerc

    2015-04-01

    Full Text Available Intracerebral hemorrhage (ICH is a devastating type of stroke characterized by bleeding into the brain parenchyma and secondary brain injury resulting from strong neuroinflammatory responses to blood components. Production of prostaglandin E2 (PGE2 is significantly upregulated following ICH and contributes to this inflammatory response in part through its E prostanoid receptor subtype 2 (EP2. Signaling through the EP2 receptor has been shown to affect outcomes of many acute and chronic neurological disorders; although, not yet explored in the context of ICH. Wildtype (WT and EP2 receptor knockout (EP2−/− mice were subjected to ICH, and various anatomical and functional outcomes were assessed by histology and neurobehavioral testing, respectively. When compared with age-matched WT controls, EP2−/− mice had 41.9 ± 4.7% smaller ICH-induced brain lesions and displayed significantly less ipsilateral hemispheric enlargement and incidence of intraventricular hemorrhage. Anatomical outcomes correlated with improved functional recovery as identified by neurological deficit scoring. Histological staining was performed to begin investigating the mechanisms involved in EP2-mediated neurotoxicity after ICH. EP2−/− mice exhibited 45.5 ± 5.8% and 41.4 ± 8.1% less blood and ferric iron accumulation, respectively. Furthermore, significantly less striatal and cortical microgliosis, striatal and cortical astrogliosis, blood–brain barrier breakdown, and peripheral neutrophil infiltration were seen in EP2−/− mice. This study is the first to suggest a deleterious role for the PGE2-EP2 signaling axis in modulating brain injury, inflammation, and functional recovery following ICH. Targeting the EP2 G protein-coupled receptor may represent a new therapeutic avenue for the treatment of hemorrhagic stroke.

  2. Detection of mitochondrial DNA deletion by a modified PCR method

    Institute of Scientific and Technical Information of China (English)

    汪振诚; 王学敏; 缪明永; 章卫平; 焦炳华; 倪庆桂

    2003-01-01

    Objective: To develop a simple and efficient method for detecting small populations of mitochondrial DNA deletion. Methods: Peripheral blood cell DNA was obtained from a victim who was accidently exposed to a 60Co radiation source 11 years ago. Using the DNA as template, PCR was performed to generate multiple products including true deletions and artifacts. The full length product was recovered and used as template of secondary PCR. The suspicious deletion product of mtDNA could be confirmed if it was only yielded by first PCR. Using either original primers or their nested primers, the suspicious deletion product was amplified and authenticated as true deletion product. The template was recovered and determined to be a deletion by sequencing directly. Results: A new mtDNA deletion, spanning 889 bp from nt11688 to nt12576, was detected in the peripheral blood cells of the victim. Conclusion: The new PCR-based method is more efficient in detecting small populations of mtDNA deletion than other routine methods. MtDNA deletion is found in the victim, suggesting there is relationship between the deletion and phenotypes of the disease.

  3. Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis.

    Science.gov (United States)

    Habgood, Anthony N; Tatler, Amanda L; Porte, Joanne; Wahl, Sharon M; Laurent, Geoffrey J; John, Alison E; Johnson, Simon R; Jenkins, Gisli

    2016-06-01

    following lung injury. However, these changes do not prevent the development of lung fibrosis. Overall, these data suggest that the absence of Slpi does not markedly modify the development of lung fibrosis following bleomycin-induced lung injury.

  4. The mTORC1 effectors S6K1 and 4E-BP play different roles in CNS axon regeneration.

    Science.gov (United States)

    Yang, Liu; Miao, Linqing; Liang, Feisi; Huang, Haoliang; Teng, Xiuyin; Li, Shaohua; Nuriddinov, Jaloliddin; Selzer, Michael E; Hu, Yang

    2014-11-10

    Using mouse optic nerve (ON) crush as a CNS injury model, we and others have found that activation of the mammalian target of rapamycin complex 1 (mTORC1) in mature retinal ganglion cells by deletion of the negative regulators, phosphatase and tensin homologue (PTEN), and tuberous sclerosis 1 promotes ON regeneration. mTORC1 activation inhibits eukaryotic translation initiation factor 4E-binding protein (4E-BP) and activates ribosomal protein S6 kinase 1 (S6K1), both of which stimulate translation. We reasoned that mTORC1's regeneration-promoting effects might be separable from its deleterious effects by differential manipulation of its downstream effectors. Here we show that S6K1 activation, but not 4E-BP inhibition, is sufficient to promote axon regeneration. However, inhibition of 4E-BP is required for PTEN deletion-induced axon regeneration. Both activation and inhibition of S6K1 decrease the effect of PTEN deletion on axon regeneration, implicating a dual role of S6K1 in regulating axon growth.

  5. Myeloid derived suppressor cells enhance stemness of cancer cells by inducing microRNA101 and suppressing the corepressor CtBP2

    Science.gov (United States)

    Cui, Tracy X.; Kryczek, Ilona; Zhao, Lili; Zhao, Ende; Kuick, Rork; Roh, Michael H.; Vatan, Linda; Szeliga, Wojciech; Mao, Yujun; Thomas, Dafydd G.; Kotarski, Jan; Tarkowski, Rafał; Wicha, Max; Cho, Kathleen; Giordano, Thomas; Liu, Rebecca; Zou, Weiping

    2013-01-01

    SUMMARY Myeloid derived suppressor cells (MDSCs) and cancer stem cells (CSCs) are important cellular components in the cancer microenvironment, and may affect cancer phenotype and patient outcome. The nature of MDSCs and their interaction with CSCs in ovarian carcinoma are unclear. We examined the interaction between MDSCs and CSCs in patients with ovarian carcinoma and showed MDSCs inhibited T cell activation, enhanced CSC gene expression, sphere formation and cancer metastasis. MDSCs triggered miRNA101 expression in cancer cells. miRNA101 subsequently repressesed the co-repressor gene C-terminal binding protein-2 (CtBP2), and CtBP2 directly targeted stem cell core genes resulting in increased cancer cell stemness, and increasing metastatic and tumorigenic potential. Increased MDSC density and tumor microRNA101 expression, and decreased tumor CtBP2 expression independently predict poor survival. Collectively, the work identifies an immune associated cellular, molecular and clinical network involving MDSCs-microRNA101-CtBP2-stem cell core genes, which extrinsically controls cancer stemness and impacts patient outcome. PMID:24012420

  6. Partial deletion 11q

    DEFF Research Database (Denmark)

    Hertz, Jens Michael; Tommerup, N; Sørensen, F B;

    1995-01-01

    We describe the cytogenetic findings and the dysmorphic features in a stillborn girl with a large de novo terminal deletion of the long arm of chromosome 11. The karyotype was 46,XX,del(11)(q21qter). By reviewing previous reports of deletion 11q, we found that cleft lip and palate are most...

  7. Intestine-specific Mttp deletion decreases mortality and prevents sepsis-induced intestinal injury in a murine model of Pseudomonas aeruginosa pneumonia.

    Directory of Open Access Journals (Sweden)

    Jessica A Dominguez

    Full Text Available BACKGROUND: The small intestine plays a crucial role in the pathophysiology of sepsis and has been referred to as the "motor" of the systemic inflammatory response. One proposed mechanism is that toxic gut-derived lipid factors, transported in mesenteric lymph, induce systemic injury and distant organ failure. However, the pathways involved are yet to be defined and the role of intestinal chylomicron assembly and secretion in transporting these lipid factors is unknown. Here we studied the outcome of sepsis in mice with conditional, intestine-specific deletion of microsomal triglyceride transfer protein (Mttp-IKO, which exhibit a block in chylomicron assembly together with lipid malabsorption. METHODOLOGY/PRINCIPAL FINDINGS: Mttp-IKO mice and controls underwent intratracheal injection with either Pseudomonas aeruginosa or sterile saline. Mttp-IKO mice exhibited decreased seven-day mortality, with 0/20 (0% dying compared to 5/17 (29% control mice (p<0.05. This survival advantage in Mttp-IKO mice, however, was not associated with improvements in pulmonary bacterial clearance or neutrophil infiltration. Rather, Mttp-IKO mice exhibited protection against sepsis-associated decreases in villus length and intestinal proliferation and were also protected against increased intestinal apoptosis, both central features in control septic mice. Serum IL-6 levels, a major predictor of mortality in human and mouse models of sepsis, were elevated 8-fold in septic control mice but remained unaltered in septic Mttp-IKO mice. Serum high density lipoprotein (HDL levels were reduced in septic control mice but were increased in septic Mttp-IKO mice. The decreased levels of HDL were associated with decreased hepatic expression of apolipoprotein A1 in septic control mice. CONCLUSIONS/SIGNIFICANCE: These studies suggest that strategies directed at blocking intestinal chylomicron secretion may attenuate the progression and improve the outcome of sepsis through effects

  8. Quantum deletion is possible

    CERN Document Server

    Elizalde, E

    2000-01-01

    A deleting operation is introduced which differs from the commonly used {\\it controlled-not} (C-not) conditional logical operation $-$to flip the (classical or quantum) state of the last copy in a chain in a deletion process. It is completely reversible, in the classical case, possessing a most natural cloning operation counterpart. We call this deleting procedure R-deletion since, in a way, it can be viewed as a `randomization' of the standard C-not operator. It is a nonlinear operation and has the remarkable property of avoiding in a simple manner the `impossibility of deletion of a quantum state' principle, put forward by Pati and Braunstein recently \\cite{pbn1}.

  9. Schizophrenia and chromosomal deletions

    Energy Technology Data Exchange (ETDEWEB)

    Lindsay, E.A.; Baldini, A. [Baylor College of Medicine, Houston, TX (United States); Morris, M. A. [Univ. of Geneva School of Medicine, NY (United States)] [and others

    1995-06-01

    Recent genetic linkage analysis studies have suggested the presence of a schizophrenia locus on the chromosomal region 22q11-q13. Schizophrenia has also been frequently observed in patients affected with velo-cardio-facial syndrome (VCFS), a disorder frequently associated with deletions within 22q11.1. It has been hypothesized that psychosis in VCFS may be due to deletion of the catechol-o-methyl transferase gene. Prompted by these observations, we screened for 22q11 deletions in a population of 100 schizophrenics selected from the Maryland Epidemiological Sample. Our results show that there are schizophrenic patients carrying a deletion of 22q11.1 and a mild VCFS phenotype that might remain unrecognized. These findings should encourage a search for a schizophrenia-susceptibility gene within the deleted region and alert those in clinical practice to the possible presence of a mild VCFS phenotype associated with schizophrenia. 9 refs.

  10. Expanding the BP1-BP2 15q11.2 Microdeletion Phenotype: Tracheoesophageal Fistula and Congenital Cataracts

    Directory of Open Access Journals (Sweden)

    D. Wong

    2013-01-01

    Full Text Available The proximal q arm of chromosome 15 contains breakpoint regions BP1–BP5 with the classic deletion of BP1–BP3 best known to be associated with Prader-Willi and Angelman syndromes. The region is approximately 500 kb and microdeletions within the BP1-BP2 region have been reported in patients with developmental delay, behavioral abnormalities, and motor apraxia as well as dysmorphic features including hypertelorism, cleft or narrow palate, ear abnormalities, and recurrent upper airway infections. We report two patients with unique, never-before-reported 15q11.2 BP1-2 microdeletion syndrome findings, one with proximal esophageal atresia and distal tracheoesophageal fistula (type C and one with congenital cataracts. Cataracts have been described in Prader-Willi syndrome but we could not find any description of cataracts in Angelman syndrome. Esophageal atresia and tracheoesophageal fistula have not been reported to our knowledge in either syndrome. A chance exists that both cases are sporadic birth defects; however, the findings of the concomitant microdeletion cannot be overlooked as a possible cause. Based on our review of the literature and the presentation of our patients, we recommend that esophageal atresia and distal tracheoesophageal fistula as well as congenital cataracts be included in the phenotypic spectrum of 15q11.2 BP1-2 microdeletion syndrome.

  11. NFKBIA Deletion in Glioblastomas

    Science.gov (United States)

    Bredel, Markus; Scholtens, Denise M.; Yadav, Ajay K.; Alvarez, Angel A.; Renfrow, Jaclyn J.; Chandler, James P.; Yu, Irene L.Y.; Carro, Maria S.; Dai, Fangping; Tagge, Michael J.; Ferrarese, Roberto; Bredel, Claudia; Phillips, Heidi S.; Lukac, Paul J.; Robe, Pierre A.; Weyerbrock, Astrid; Vogel, Hannes; Dubner, Steven; Mobley, Bret; He, Xiaolin; Scheck, Adrienne C.; Sikic, Branimir I.; Aldape, Kenneth D.; Chakravarti, Arnab; Harsh, Griffith R.

    2013-01-01

    BACKGROUND Amplification and activating mutations of the epidermal growth factor receptor (EGFR) oncogene are molecular hallmarks of glioblastomas. We hypothesized that deletion of NFKBIA (encoding nuclear factor of κ-light polypeptide gene enhancer in B-cells inhibitor-α), an inhibitor of the EGFR-signaling pathway, promotes tumorigenesis in glioblastomas that do not have alterations of EGFR. METHODS We analyzed 790 human glioblastomas for deletions, mutations, or expression of NFKBIA and EGFR. We studied the tumor-suppressor activity of NFKBIA in tumor-cell culture. We compared the molecular results with the outcome of glioblastoma in 570 affected persons. RESULTS NFKBIA is often deleted but not mutated in glioblastomas; most deletions occur in nonclassical subtypes of the disease. Deletion of NFKBIA and amplification of EGFR show a pattern of mutual exclusivity. Restoration of the expression of NFKBIA attenuated the malignant phenotype and increased the vulnerability to chemotherapy of cells cultured from tumors with NFKBIA deletion; it also reduced the viability of cells with EGFR amplification but not of cells with normal gene dosages of both NFKBIA and EGFR. Deletion and low expression of NFKBIA were associated with unfavorable outcomes. Patients who had tumors with NFKBIA deletion had outcomes that were similar to those in patients with tumors harboring EGFR amplification. These outcomes were poor as compared with the outcomes in patients with tumors that had normal gene dosages of NFKBIA and EGFR. A two-gene model that was based on expression of NFKBIA and O6-methylguanine DNA methyltransferase was strongly associated with the clinical course of the disease. CONCLUSIONS Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. PMID:21175304

  12. Molecular characterization of microbial mutations induced by ion beam irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Ichida, Hiroyuki [Graduate School of Science and Technology, Chiba University, Matsudo, Chiba 271-8510 (Japan); Accelerator Applications Research Group, Nishina Center for Accelerator-Based Science, RIKEN, Wako, Saitama 351-0198 (Japan)], E-mail: ichida@riken.jp; Matsuyama, Tomoki [Cellular Biochemistry Laboratory, Discovery Research Institute, RIKEN, Wako, Saitama 351-0198 (Japan); Ryuto, Hiromichi [Accelerator Operation Group, Nishina Center for Accelerator-Based Science, RIKEN, Wako, Saitama 351-0198 (Japan); Hayashi, Yoriko [Accelerator Applications Research Group, Nishina Center for Accelerator-Based Science, RIKEN, Wako, Saitama 351-0198 (Japan); Fukunishi, Nobuhisa [Accelerator Operation Group, Nishina Center for Accelerator-Based Science, RIKEN, Wako, Saitama 351-0198 (Japan); Abe, Tomoko [Accelerator Applications Research Group, Nishina Center for Accelerator-Based Science, RIKEN, Wako, Saitama 351-0198 (Japan); Koba, Takato [Graduate School of Science and Technology, Chiba University, Matsudo, Chiba 271-8510 (Japan)

    2008-03-01

    A positive selection system for gene disruption using a sucrose-sensitive transgenic rhizobium was established and used for the molecular characterization of mutations induced by ion beam irradiations. Single nucleotide substitutions, insertions, and deletions were found to occur in the sucrose sensitivity gene, sacB, when the reporter line was irradiated with highly accelerated carbon and iron ion beams. In all of the insertion lines, fragments of essentially the same sequence and of approximately 1188 bp in size were identified in the sacB regions. In the deletion lines, iron ions showed a tendency to induce larger deletions than carbon ions, suggesting that higher LET beams cause larger deletions. We found also that ion beams, particularly 'heavier' ion beams, can produce single gene disruptions and may present an effective alternative to transgenic approaches.

  13. Deletion and deletion/insertion mutations in the juxtamembrane domain of the FLT3 gene in adult acute myeloid leukemia

    Directory of Open Access Journals (Sweden)

    Kristin K. Deeb

    2014-01-01

    Full Text Available In contrast to FLT3 ITD mutations, in-frame deletions in the FLT3 gene have rarely been described in adult acute leukemia. We report two cases of AML with uncommon in-frame mutations in the juxtamembrane domain of the FLT3 gene: a 3-bp (c.1770_1774delCTACGinsGT; p.F590_V592delinsLF deletion/insertion and a 12-bp (c.1780_1791delTTCAGAGAATAT; p.F594_Y597del deletion. We verified by sequencing that the reading frame of the FLT3 gene was preserved and by cDNA analysis that the mRNA of the mutant allele was expressed in both cases. Given the recent development of FLT3 inhibitors, our findings may be of therapeutic value for AML patients harboring similar FLT3 mutations.

  14. Inducible deletion of CD28 prior to secondary nippostrongylus brasiliensis infection impairs worm expulsion and recall of protective memory CD4⁺ T cell responses.

    Directory of Open Access Journals (Sweden)

    Hlumani Ndlovu

    2014-02-01

    Full Text Available IL-13 driven Th2 immunity is indispensable for host protection against infection with the gastrointestinal nematode Nippostronglus brasiliensis. Disruption of CD28 mediated costimulation impairs development of adequate Th2 immunity, showing an importance for CD28 during the initiation of an immune response against this pathogen. In this study, we used global CD28⁻/⁻ mice and a recently established mouse model that allows for inducible deletion of the cd28 gene by oral administration of tamoxifen (CD28(-/loxCre⁺/⁻+TM to resolve the controversy surrounding the requirement of CD28 costimulation for recall of protective memory responses against pathogenic infections. Following primary infection with N. brasiliensis, CD28⁻/⁻ mice had delayed expulsion of adult worms in the small intestine compared to wild-type C57BL/6 mice that cleared the infection by day 9 post-infection. Delayed expulsion was associated with reduced production of IL-13 and reduced serum levels of antigen specific IgG1 and total IgE. Interestingly, abrogation of CD28 costimulation in CD28(-/loxCre⁺/⁻ mice by oral administration of tamoxifen prior to secondary infection with N. brasiliensis resulted in impaired worm expulsion, similarly to infected CD28⁻/⁻ mice. This was associated with reduced production of the Th2 cytokines IL-13 and IL-4, diminished serum titres of antigen specific IgG1 and total IgE and a reduced CXCR5⁺ T(FH cell population. Furthermore, total number of CD4⁺ T cells and B220⁺ B cells secreting Th1 and Th2 cytokines were significantly reduced in CD28⁻/⁻ mice and tamoxifen treated CD28(-/loxCre⁺/⁻ mice compared to C57BL/6 mice. Importantly, interfering with CD28 costimulatory signalling before re-infection impaired the recruitment and/or expansion of central and effector memory CD4⁺ T cells and follicular B cells to the draining lymph node of tamoxifen treated CD28(-/loxCre⁺/⁻ mice. Therefore, it can be concluded that CD28

  15. In vitro and in silico studies of urea-induced denaturation of yeast iso-1-cytochrome c and its deletants at pH 6.0 and 25 °C.

    Science.gov (United States)

    Haque, Md Anzarul; Zaidi, Sobia; Ubaid-Ullah, Shah; Prakash, Amresh; Hassan, Md Imtaiyaz; Islam, Asimul; Batra, Janendra K; Ahmad, Faizan

    2015-01-01

    Yeast iso-1-cytochrome c (y-cyt-c) has five extra residues at N-terminus in comparison to the horse cytochrome c. These residues are numbered as -5 to -1. Here, these extra residues are sequentially removed from y-cyt-c to establish their role in folding and stability of the protein. We performed urea-induced denaturation of wild-type (WT) y-cyt-c and its deletants. Denaturation was followed by observing change in Δε405 (probe for measuring change in the heme environment within the protein), [θ]405 (probe for measuring the change in Phe82 and Met80 axial bonding), [θ]222 (probe for measuring change in secondary structure) and [θ]416 (probe for measuring change in the heme-methionine environment). The urea-induced reversible denaturation curves were used to estimate Δ[Formula: see text], the value of Gibbs free energy change (ΔGD) in the absence of urea; Cm, the midpoint of the denaturation curve, i.e. molar urea concentration ([urea]) at which ΔGD = 0; and m, the slope (=∂ΔGD/∂[urea]). Our in vitro results clearly show that except Δ(-5/-4) all deletants are less stable than WT protein. Coincidence of normalized transition curves of all physical properties suggests that unfolding/refolding of WT protein and its deletants is a two-state process. To confirm our in vitro observations, we performed 40 ns MD simulation of both WT y-cyt-c and its deletants. MD simulation results clearly show that extra N-terminal residues play a role in stability but not in folding of the protein.

  16. Deleted in breast cancer-1 regulates SIRT1 activity and contributes to high-fat diet-induced liver steatosis in mice.

    NARCIS (Netherlands)

    Escande, C.; Chini, C.C.; Nin, V.; Dykhouse, K.M.; Novak, C.M.; Levine, J.; Deursen, J.M.A. van; Gores, G.J.; Chen, J.; Lou, Z.; Chini, E.N.

    2010-01-01

    The enzyme sirtuin 1 (SIRT1) is a critical regulator of many cellular functions, including energy metabolism. However, the precise mechanisms that modulate SIRT1 activity remain unknown. As SIRT1 activity in vitro was recently found to be negatively regulated by interaction with the deleted in breas

  17. Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes.

    Science.gov (United States)

    Belyaev, Igor Y; Markovà, Eva; Hillert, Lena; Malmgren, Lars O G; Persson, Bertil R R

    2009-02-01

    We have recently described frequency-dependent effects of mobile phone microwaves (MWs) of global system for mobile communication (GSM) on human lymphocytes from persons reporting hypersensitivity to electromagnetic fields and healthy persons. Contrary to GSM, universal global telecommunications system (UMTS) mobile phones emit wide-band MW signals. Hypothetically, UMTS MWs may result in higher biological effects compared to GSM signal because of eventual "effective" frequencies within the wideband. Here, we report for the first time that UMTS MWs affect chromatin and inhibit formation of DNA double-strand breaks co-localizing 53BP1/gamma-H2AX DNA repair foci in human lymphocytes from hypersensitive and healthy persons and confirm that effects of GSM MWs depend on carrier frequency. Remarkably, the effects of MWs on 53BP1/gamma-H2AX foci persisted up to 72 h following exposure of cells, even longer than the stress response following heat shock. The data are in line with the hypothesis that the type of signal, UMTS MWs, may have higher biological efficiency and possibly larger health risk effects compared to GSM radiation emissions. No significant differences in effects between groups of healthy and hypersensitive subjects were observed, except for the effects of UMTS MWs and GSM-915 MHz MWs on the formation of the DNA repair foci, which were different for hypersensitive (P 0.05). The non-parametric statistics used here did not indicate specificity of the differences revealed between the effects of GSM and UMTS MWs on cells from hypersensitive subjects and more data are needed to study the nature of these differences.

  18. Deletion of fucose residues in plant N-glycans by repression of the GDP-mannose 4,6-dehydratase gene using virus-induced gene silencing and RNA interference.

    Science.gov (United States)

    Matsuo, Kouki; Matsumura, Takeshi

    2011-02-01

    Production of pharmaceutical glycoproteins in plants has many advantages in terms of safety and reduced costs. However, plant-produced glycoproteins have N-glycans with plant-specific sugar residues (core β-1,2-xylose and α-1,3-fucose) and a Lewis a (Le(a) ) epitope, i.e., Galβ(1-3)[Fucα(1-4)]GlcNAc. Because these sugar residues and glycan structures seemed to be immunogenic, several attempts have been made to delete them by repressing their respective glycosyltransferase genes. However, until date, such deletions have not been successful in completely eliminating the fucose residues. In this study, we simultaneously reduced the plant-specific core α-1,3-fucose and α-1,4-fucose residues in the Le(a) epitopes by repressing the Guanosine 5'-diphosphate (GDP)-D-mannose 4,6-dehydratase (GMD) gene, which is associated with GDP-L-fucose biosynthesis, in Nicotiana benthamiana plants. Repression of GMD was achieved using virus-induced gene silencing (VIGS) and RNA interference (RNAi). The proportion of fucose-free N-glycans found in total soluble protein from GMD gene-repressed plants increased by 80% and 95% following VIGS and RNAi, respectively, compared to wild-type plants. A small amount of putative galactose substitution in N-glycans from the NbGMD gene-repressed plants was observed, similar to what has been previously reported GMD-knockout Arabidopsis mutant. On the other hand, the recombinant mouse granulocyte-macrophage colony-stimulating factor (GM-CSF) with fucose-deleted N-glycans was successfully produced in NbGMD-RNAi transgenic N. benthamiana plants. Thus, repression of the GMD gene is thus very useful for deleting immunogenic total fucose residues and facilitating the production of pharmaceutical glycoproteins in plants.

  19. Male gametophytic sterility. 1 - Gametic sterilities and deletions in petunia

    Energy Technology Data Exchange (ETDEWEB)

    Cornu, A.; Maizonnier, D. (Station d' Amelioration des Plantes de l' I.N.R.A., Dijon (France))

    1982-01-01

    Terminal deletions induced by ionizing radiations in Petunia are not sexually transmitted. Cytogenetic study of plants with a heterozygous deletion and their progenies shows that this lack of transmission is accompanied by a gametic semi-sterility due to the fact that gametes carrying the deleted chromosome are not viable. The interest of such a male sterility with a gametophytic determinism for the study of sporophyte-gametophyte relationships is underlined.

  20. Deletion of BCY1 from the Saccharomyces cerevisiae Genome Is Semidominant and Induces Autolytic Phenotypes Suitable for Improvement of Sparkling Wines

    Science.gov (United States)

    Tabera, Laura; Muñoz, Rosario; Gonzalez, Ramon

    2006-01-01

    Autolysis of Saccharomyces cerevisiae is the main source of molecules that contribute to the quality of sparkling wines made by the traditional method. In this work the possibility of accelerating this slow process in order to improve the quality of sparkling wines by using genetically engineered wine yeast strains was explored. The effect of partial or total deletion of BCY1 (which encodes a regulatory subunit of cAMP-dependent protein kinase A) in haploid and diploid (heterozygous and homozygous) yeast strains was studied. We proved that heterozygous strains having partial or complete BCY1 deletions have a semidominant phenotype for several of the properties studied, including autolysis under simulated second-fermentation conditions, in contrast to previously published reports describing mutations in BCY1 as recessive. Considering the degree of autolysis, ethanol tolerance, and technical feasibility, we propose that deletion of the 3′ end of the open reading frame of a single copy of BCY1 is a way to improve the quality of sparkling wines. PMID:16597929

  1. NF-κBp50参与IL-4在THP-1细胞中诱导DC-SIGN的表达%NF-κBp50 is Associated With DC-SIGN Expression Induced by IL-4 in THP-1 Cells

    Institute of Scientific and Technical Information of China (English)

    许利军; 常秀春; 姚航平; 吴南屏

    2008-01-01

    DC-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) is specific receptor on Dendritic cells, and plays a pivotal role on antigens presentation. Uptodate, the clear regulation mechanisms for DC-SIGN expression are not available.IL-4 is one of the most important cytokines inducing DC-SIGN production, while, NF-κB is an important transcription factor controlling signaling transduction. Both IL-4 and NF-κB are closely related to DC-SIGN regulation. NF-κB and IL-4 actions on DC-SIGN promoter activity, DC-SIGN expression as well as interactions between IL-4 and NF-κB were investigated in THP-1 cell. It was found that the mutation of NF-κB binding site in DC-SIGN promoter results in DC-SIGN promoter activity decrease about 50%.NF-κBp50 stimulates DC-SIGN expression in THP-1 cells. IL-4 upregulates DC-SIGN expression on THP-1 cells as well as NF-κB production. These data reveal that NF-κB is associated with IL-4 induced DC-SIGN expression.%树突状细胞表面特异的胞间黏附分子3捕获非整合素(DC-specific intercellular adhesion molecule-3-grabbing nonintegrin,DC-SIGN)是树突状细胞表面特异的蛋白,在抗原呈递过程中起关键作用.这种特异性的表达和DC-SIGN的调节机制有关.到目前为止,DC-SIGN表达调控的机制还不是很清楚.IL-4是诱导DC-SIGN表达的最重要的细胞因子之一,而NF-κB是调控细胞信号转导的一个重要调控因子,两者都和DC-SIGN的表达调节相关.研究了IL-4和NF-κB对DC-SIGN启动子活性、对DC-SIGN表达的影响以及IL-4和NF-κB之间相互作用的关系.发现:DC-SIGN启动子中NF-κB位点缺失可以使DC-SIGN启动子活性下降大约50%,NF-κBp50可以促进DC-SIGN在THP-1细胞的表达,IL-在THP-1细胞诱导DC-SIGN表达的同时,也促进了NF-κBp50的表达.这些结果显示,在THP-1细胞中NF-κBp50参与IL-4诱导的DC-SIGN表达.

  2. The rates and patterns of deletions in the human factor IX gene

    Energy Technology Data Exchange (ETDEWEB)

    Ketterling, R.P.; Vielhaber, E.L.; Lind, T.J.; Thorland, E.C.; Sommer S.S. (Mayo Clinic/Foundation, Rochester, MN (United States))

    1994-02-01

    Deletions are commonly observed in genes with either segments of highly homologous sequences or excessive gene length. However, in the factor IX gene and in most genes, deletions (of [ge]21 bp) are uncommon. The authors have analyzed DNA from 290 families with hemophilia B (203 independent mutations) and have found 12 deletions >20 bp. Eleven of these are >2 kb (range >3-163 kb), and one is 1.1 kb. The junctions of the four deletions that are completely contained within the factor IX gene have been determined. A novel mutation occurred in patient HB128: the data suggest that a 26.8-kb deletion occurred between two segments of alternating purines and pyrimidines and that a 2.3-kb sense strand segment derived from the deleted region was inserted. For a sample of 203 independent mutations, the authors estimate the [open quotes]baseline[close quotes] rates of deletional mutation per base pair per generation as a function of size. The rate for large (>2 kb)I deletions is exceedingly low. For every mutational event in which a given base is at the junction of a large deletion, there are an estimated 58 microdeletions (<20 bp) and 985 single-base substitutions at that base. Analysis of the nine reported deletion junctions in the factor IX gene literature reveals that (i) five are associated with inversion, orphan sequences, or sense strand insertions; (ii) four are simple deletions that display an excess of short direct repeats at their junctions; (iii) there is no dramatic clustering of junctions within the gene; and (iv) with the exception of alternating purines and pyrimidines, deletion junctions are not preferentially associated with repetitive DNA. 58 refs., 5 figs., 5 tabs.

  3. Source to sink element geochemistry and clay mineralogy in Lake Towuti, Indonesia: understanding climate-induced controls on sediment composition during the past 60 kyr BP

    Science.gov (United States)

    Morlock, Marina; Vogel, Hendrik; Nigg, Valentin; Hasberg, Ascelina; Melles, Martin; Russell, James M.; Bijaksana, Satria

    2016-04-01

    Lake Towuti is a large (560 km2 surface area; 198 m max. water depth) ultraoligotrophic lake hosted in the East Sulawesi ophiolite, characterised by high iron and very low sulphur contents. The lake is surrounded by several 10s of metres thick deeply weathered laterite soils and closed-canopy rainforest. In May-July 2015, we recovered more than 1000 m of sediment core capturing the entire sediment infill to bedrock in the course of the ICDP Towuti Drilling Project. In the tropics very little is known about the influence of climatic changes on weathering and erosion on glacial-interglacial time-scales. It is expected that varying hydroclimatic conditions will lead to changes in the weathering and erosion rates and greatly influence terrestrial elemental cycling. The direction of change and more quantitative estimates of the rates of changes are, however, unknown. In order to characterise modern erosional processes and element cycling in the lake and its catchment, we collected catchment-characteristic bedrock samples and profiles of their overlying laterites, riverine sediments, and 85 samples of surface sediments from the lake. All samples were analysed for their geochemical and clay-mineralogical (changes in sediment composition, and assess the spatial variability in Lake Towuti. The relationships found in the modern system were then applied to two sediment cores, dating back 30,000 and 60,000 years BP, respectively. The laterite soils in the catchment show a characteristic zonation with high concentrations of Al, Ti, Fe, and Cr in the uppermost horizon, while Mg is enriched in the saprolite zone directly above bedrock. Weathering intensity increases from bedrock (least weathered) across river bedload of the 15 inlets to the sediments in the deepest basin of the lake (most weathered). The largest inlet to Lake Towuti, the Mahalona River, supplies sediments with low Al and high Mg concentrations and exerts a dominant control on the present-day sediment composition

  4. Skin-specific Deletion of Stearoyl-CoA Desaturase-1 Alters Skin Lipid Composition and Protects Mice from High Fat Diet-induced Obesity*

    OpenAIRE

    Sampath, Harini; Flowers, Matthew T; Liu, Xueqing; Chad M Paton; Sullivan, Ruth; Chu, Kiki; Zhao, Minghui; Ntambi, James M.

    2009-01-01

    Stearoyl-CoA desaturase-1 (SCD1) catalyzes the synthesis of monounsaturated fatty acids and is an important regulator of whole body energy homeostasis. Severe cutaneous changes in mice globally deficient in SCD1 also indicate a role for SCD1 in maintaining skin lipids. We have generated mice with a skin-specific deletion of SCD1 (SKO) and report here that SKO mice display marked sebaceous gland hypoplasia and depletion of sebaceous lipids. In addition, SKO mice have significantly increased en...

  5. Do mtDNA Deletions Play a Role in the Development of Nasal Polyposis?

    Directory of Open Access Journals (Sweden)

    Arzu Tatar

    2014-04-01

    Full Text Available Objective:Nasal polyposis (NP is an inflammatory disease of the nasal mucosa and paranasal sinuses. Mitochondria are the cellular organelles which produce cellular energy by Oxidative Phosphorylation (OXPHOS, and they have own inheritance material, mtDNA. mtDNA is affected by reactive oxygen samples (ROS which are produced by both OXPHOS and the inflammatory process. The aim of this study was to investigate the 4977 bp and 7400 bp deletions of mtDNA in nasal polyposis tissue, and to indicate the possible association of mtDNA deletions with NP. Methods:Thirty-three patients, aged 15 to 65 years, with nasal polyposis were selected to be assessed for mitochondrial DNA deletions. The patients with possible mtDNA mutations due to mitochondrial disease, being treated with radiotherapy, of advanced age, with a familiar history, aspirin hypersensitivity, or a history of asthma, were excluded. Polyp excision surgery was applied to the treatment of the NP, and after histopathological diagnosis 1x1 cm of polyp tissue samples were used to isolate mtDNA. The 4977 bp and 7400 bp deletion regions, and two control regions of mtDNA were assessed by using four pairs of primers. DNA extractions from the NP tissues and peripheral blood samples of the patients were made, and then Polymerase Chain Reactions (PCR were made. PCR products were separated in 2% agarose gel.Results:No patient had either the 4977 bp deletion or the 7400 bp deletion in their NP tissue, and neither were these deletions evident in their peripheral blood. Two control sequences, one of them from a non-deleted region, and the other from a possible deletion region, were detected in the NP tissues and peripheral blood of all the patients.Conclusions:We had anticipated that some mtDNA deletion might have occurred in NP tissue due to the increased ROS levels caused by chronic inflammation, but we did not detect any deletion. Probably, the duration of inflammation in NP is insufficient to form mt

  6. Deletion (2)(q37)

    Energy Technology Data Exchange (ETDEWEB)

    Stratton, R.F.; Tolworthy, J.A.; Young, R.S. [South Texas Genetics Center, San Antonio, TX (United States)

    1994-06-01

    We report on a 5-month-old girl with widely spaced nipples, redundant nuchal skin, coarctation of the aorta, anal atresia with distal fistula, postnatal growth retardation, hypotonia, and sparse scalp hair. Initial clinical assessment suggested the diagnosis of Ullrich-Turner syndrome. Chromosome analysis showed a 46,XX,del(2)(q37) karyotype in peripheral lymphocytes. We compare her findings to those of other reported patients with terminal deletions of 2q. 8 refs., 2 figs., 1 tab.

  7. A 200 bp region of the pea ENOD12 promoter is sufficient for nodule-specific and nod factor induced expression

    DEFF Research Database (Denmark)

    Vijn, I; Christiansen, H; Lauridsen, P

    1995-01-01

    ENOD12 is one of the first nodulin genes expressed upon inoculation with Rhizobium and also purified Nod factors are able to induce ENOD12 expression. The ENOD12 gene family in pea (Pisum sativum) has two members. A cDNA clone representing PsENOD12A [26] and a PsENOD12B genomic clone [7] have been...

  8. Vasopressin Type 1A Receptor Deletion Enhances Cardiac Contractility, β-Adrenergic Receptor Sensitivity and Acute Cardiac Injury-induced Dysfunction.

    Science.gov (United States)

    Wasilewski, Melissa A; Grisanti, Laurel A; Song, Jianliang; Carter, Rhonda L; Repas, Ashley A; Myers, Valerie D; Gao, Erhe; Koch, Walter J; Cheung, Joseph Y; Feldman, Arthur M; Tilley, Douglas

    2016-09-02

    V1AR expression is elevated in chronic human heart failure and contributes to cardiac dysfunction in animal models, in part via reduced βAR responsiveness.  While cardiac V1AR overexpression and V1AR stimulation are each sufficient to decrease βAR activity, it is unknown whether V1AR inhibition conversely augments βAR responsiveness.  Further, although V1AR has been shown to contribute to chronic progression of heart failure, its impact on cardiac function following acute ischemic injury has not been reported.  Using V1AR KO mice we assessed the impact of V1AR deletion on cardiac contractility at baseline and following ischemic injury, βAR sensitivity and cardiomyocyte responsiveness to βAR stimulation.  Strikingly, baseline cardiac contractility was enhanced in V1AR KO mice and they experienced a greater loss in contractile function than control mice following acute ischemic injury, although the absolute levels of cardiac dysfunction and survival rates did not differ.  Enhanced cardiac contractility in V1AR KO mice was associated with augmented β-blocker sensitivity, suggesting increased basal βAR activity, and indeed levels of left ventricular cAMP, as well as phospholamban and cardiac troponin I phosphorylation were elevated versus control mice.  At the cellular level, myocytes isolated from V1AR KO mice demonstrated increased responsiveness to βAR stimulation consistent with the finding that acute pharmacological V1AR inhibition enhanced βAR-mediated contractility in control myocytes.  Therefore, while V1AR deletion does not protect the heart from the rapid development of cardiac dysfunction following acute ischemic injury, its effects on βAR activity suggest that acute V1AR inhibition could be utilized to promote myocyte contractile performance.

  9. The effect of overexpression of PGC-1α on the mtDNA4834 common deletion in a rat cochlear marginal cell senescence model.

    Science.gov (United States)

    Zhao, Xue-Yan; Sun, Jin-Li; Hu, Yu-Juan; Yang, Yang; Zhang, Wen-Juan; Hu, Yuan; Li, Jun; Sun, Yu; Zhong, Yi; Peng, Wei; Zhang, Hong-Lian; Kong, Wei-Jia

    2013-02-01

    Aging is a natural process usually defined as a progressive loss of function with an accumulation of senescent cells. The clinical manifestations of this process include age-related hearing loss (AHL)/presbycusis. Several investigations indicated the association between a mitochondrial common deletion (CD) (mtDNA 4977-bp deletion in humans, corresponding to 4834-bp deletion in rats) and presbycusis. Previous researches have shown that peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) is a key regulator of mitochondrial biogenesis and energy metabolism. However, the expression of PGC-1α in the inner ear and the possible effect of PGC-1α on presbycusis are not clear. Our data demonstrated the distribution of PGC-1α and its downstream transcription factors nuclear respiratory factor-1 (NRF-1), mitochondrial transcription factor A (Tfam) and nuclear factor κB (NF-κB) in marginal cells (MCs) for the first time. To explore the role of PGC-1α in cellular senescence, we established a model of marginal cell senescence harboring the mtDNA4834 common deletion induced by d-galactose. We also found that PGC-1α and its downstream transcription factors compensatorily increased in our cell senescence model. Furthermore, the overexpression of PGC-1α induced by transfection largely increased the expression levels of NRF-1 and TFAM and significantly decreased the expression level of NF-κB in the cell senescence model. And the levels of CD, senescent cells and apoptotic cells in the cell model decreased after PGC-1α overexpression. These results suggested that PGC-1α might protect MCs in this cell model from senescence through a nuclear-mitochondrial interaction and against apoptosis. Our study may shed light on the pathogenesis of presbycusis and provide a new therapeutic target for presbycusis.

  10. Dystrophin expression in a Duchenne muscular dystrophy patient with a frame shift deletion.

    Science.gov (United States)

    Prior, T W; Bartolo, C; Papp, A C; Snyder, P J; Sedra, M S; Burghes, A H; Kissel, J T; Luquette, M H; Tsao, C Y; Mendell, J R

    1997-02-01

    The exon 45 deletion is a common dystrophin gene deletion. Although this is an out-of-frame deletion, which should not allow for protein synthesis, it has been observed in mildly affected patients. We describe a patient with an exon 45 deletion who produced protein, but still had a severe Duchenne muscular dystrophy phenotype. RT-PCR analysis and cDNA sequencing from the muscle biopsy sample revealed that the exon 45 deletion induced exon skipping of exon 44, which resulted in an in-frame deletion and the production of dystrophin. A conformational change in dystrophin induced by the deletion is proposed as being responsible for the severe phenotype in the patient. We feel that the variable clinical phenotype observed in patients with the exon 45 deletion is not due to exon splicing but may be the result of other environmental or genetic factors, or both.

  11. The Cell Death Inhibitor ARC Is Induced in a Tissue-Specific Manner by Deletion of the Tumor Suppressor Gene Men1, but Not Required for Tumor Development and Growth.

    Directory of Open Access Journals (Sweden)

    Wendy M McKimpson

    Full Text Available Multiple endocrine neoplasia type 1 (MEN1 is a genetic disorder characterized by tissue-specific tumors in the endocrine pancreas, parathyroid, and pituitary glands. Although tumor development in these tissues is dependent upon genetic inactivation of the tumor suppressor Men1, loss of both alleles of this gene is not sufficient to induce these cancers. Men1 encodes menin, a nuclear protein that influences transcription. A previous ChIP on chip analysis suggested that menin binds promoter sequences of nol3, encoding ARC, which is a cell death inhibitor that has been implicated in cancer pathogenesis. We hypothesized that ARC functions as a co-factor with Men1 loss to induce the tissue-restricted distribution of tumors seen in MEN1. Using mouse models that recapitulate this syndrome, we found that biallelic deletion of Men1 results in selective induction of ARC expression in tissues that develop tumors. Specifically, loss of Men1 in all cells of the pancreas resulted in marked increases in ARC mRNA and protein in the endocrine, but not exocrine, pancreas. Similarly, ARC expression increased in the parathyroid with inactivation of Men1 in that tissue. To test if ARC contributes to MEN1 tumor development in the endocrine pancreas, we generated mice that lacked none, one, or both copies of ARC in the context of Men1 deletion. Studies in a cohort of 126 mice demonstrated that, although mice lacking Men1 developed insulinomas as expected, elimination of ARC in this context did not significantly alter tumor load. Cellular rates of proliferation and death in these tumors were also not perturbed in the absence of ARC. These results indicate that ARC is upregulated by loss Men1 in the tissue-restricted distribution of MEN1 tumors, but that ARC is not required for tumor development in this syndrome.

  12. The Cell Death Inhibitor ARC Is Induced in a Tissue-Specific Manner by Deletion of the Tumor Suppressor Gene Men1, but Not Required for Tumor Development and Growth.

    Science.gov (United States)

    McKimpson, Wendy M; Yuan, Ziqiang; Zheng, Min; Crabtree, Judy S; Libutti, Steven K; Kitsis, Richard N

    2015-01-01

    Multiple endocrine neoplasia type 1 (MEN1) is a genetic disorder characterized by tissue-specific tumors in the endocrine pancreas, parathyroid, and pituitary glands. Although tumor development in these tissues is dependent upon genetic inactivation of the tumor suppressor Men1, loss of both alleles of this gene is not sufficient to induce these cancers. Men1 encodes menin, a nuclear protein that influences transcription. A previous ChIP on chip analysis suggested that menin binds promoter sequences of nol3, encoding ARC, which is a cell death inhibitor that has been implicated in cancer pathogenesis. We hypothesized that ARC functions as a co-factor with Men1 loss to induce the tissue-restricted distribution of tumors seen in MEN1. Using mouse models that recapitulate this syndrome, we found that biallelic deletion of Men1 results in selective induction of ARC expression in tissues that develop tumors. Specifically, loss of Men1 in all cells of the pancreas resulted in marked increases in ARC mRNA and protein in the endocrine, but not exocrine, pancreas. Similarly, ARC expression increased in the parathyroid with inactivation of Men1 in that tissue. To test if ARC contributes to MEN1 tumor development in the endocrine pancreas, we generated mice that lacked none, one, or both copies of ARC in the context of Men1 deletion. Studies in a cohort of 126 mice demonstrated that, although mice lacking Men1 developed insulinomas as expected, elimination of ARC in this context did not significantly alter tumor load. Cellular rates of proliferation and death in these tumors were also not perturbed in the absence of ARC. These results indicate that ARC is upregulated by loss Men1 in the tissue-restricted distribution of MEN1 tumors, but that ARC is not required for tumor development in this syndrome.

  13. Robust inducible Cre recombinase activity in the human malaria parasite Plasmodium falciparum enables efficient gene deletion within a single asexual erythrocytic growth cycle.

    Science.gov (United States)

    Collins, Christine R; Das, Sujaan; Wong, Eleanor H; Andenmatten, Nicole; Stallmach, Robert; Hackett, Fiona; Herman, Jean-Paul; Müller, Sylke; Meissner, Markus; Blackman, Michael J

    2013-05-01

    Asexual blood stages of the malaria parasite, which cause all the pathology associated with malaria, can readily be genetically modified by homologous recombination, enabling the functional study of parasite genes that are not essential in this part of the life cycle. However, no widely applicable method for conditional mutagenesis of essential asexual blood-stage malarial genes is available, hindering their functional analysis. We report the application of the DiCre conditional recombinase system to Plasmodium falciparum, the causative agent of the most dangerous form of malaria. We show that DiCre can be used to obtain rapid, highly regulated site-specific recombination in P. falciparum, capable of excising loxP-flanked sequences from a genomic locus with close to 100% efficiency within the time-span of a single erythrocytic growth cycle. DiCre-mediated deletion of the SERA5 3' UTR failed to reduce expression of the gene due to the existence of alternative cryptic polyadenylation sites within the modified locus. However, we successfully used the system to recycle the most widely used drug resistance marker for P. falciparum, human dihydrofolate reductase, in the process producing constitutively DiCre-expressing P. falciparum clones that have broad utility for the functional analysis of essential asexual blood-stage parasite genes.

  14. Assessment of the Immune Responses Induced in Cattle after Inoculation of a Mycobacterium bovis Strain Deleted in Two mce2 Genes

    Directory of Open Access Journals (Sweden)

    Federico Carlos Blanco

    2012-01-01

    Full Text Available The generation of efficient candidate vaccines against bovine tuberculosis will contribute to the control of this zoonotic disease. Rationally attenuated Mycobacterium bovis strains generated by knockout of virulence genes are promising candidate vaccines. However, to be effective, these candidate vaccines should at least maintain the immunological properties of their virulent parental M. bovis strains. Therefore, the aim of this study was to obtain an M. bovis strain deleted in the mce2 genes and evaluate the effect of the mutation on the immunological profile elicited by the bacteria in cattle. We showed that the activation of CD4+ T cells in cattle inoculated with the mutant strain was equivalent to that in animals inoculated with the parental strain. Moreover, after in vitro stimulation, peripheral blood mononuclear cells from animals inoculated with the mutant produced higher levels of mRNA Th-1 cytokines than the parental strain. Therefore, these results indicate that the mce2 mutant is a promising candidate vaccine against bovine tuberculosis.

  15. Deletion of the β-acetoacetyl synthase FabY in Pseudomonas aeruginosa induces hypoacylation of lipopolysaccharide and increases antimicrobial susceptibility.

    Science.gov (United States)

    Six, David A; Yuan, Yanqiu; Leeds, Jennifer A; Meredith, Timothy C

    2014-01-01

    The β-acetoacetyl-acyl carrier protein synthase FabY is a key enzyme in the initiation of fatty acid biosynthesis in Pseudomonas aeruginosa. Deletion of fabY results in an increased susceptibility of P. aeruginosa in vitro to a number of antibiotics, including vancomycin and cephalosporins. Because antibiotic susceptibility can be influenced by changes in membrane lipid composition, we determined the total fatty acid profile of the ΔfabY mutant, which suggested alterations in the lipid A region of the lipopolysaccharide. The majority of lipid A species in the ΔfabY mutant lacked a single secondary lauroyl group, resulting in hypoacylated lipid A. Adding exogenous fatty acids to the growth media restored the wild-type antibiotic susceptibility profile and the wild-type lipid A fatty acid profile. We suggest that incorporation of hypoacylated lipid A species into the outer membrane contributes to the shift in the antibiotic susceptibility profile of the ΔfabY mutant.

  16. Myocardial infarction-induced N-terminal fragment of cardiac myosin-binding protein C (cMyBP-C) impairs myofilament function in human myocardium.

    Science.gov (United States)

    Witayavanitkul, Namthip; Ait Mou, Younss; Kuster, Diederik W D; Khairallah, Ramzi J; Sarkey, Jason; Govindan, Suresh; Chen, Xin; Ge, Ying; Rajan, Sudarsan; Wieczorek, David F; Irving, Thomas; Westfall, Margaret V; de Tombe, Pieter P; Sadayappan, Sakthivel

    2014-03-28

    Myocardial infarction (MI) is associated with depressed cardiac contractile function and progression to heart failure. Cardiac myosin-binding protein C, a cardiac-specific myofilament protein, is proteolyzed post-MI in humans, which results in an N-terminal fragment, C0-C1f. The presence of C0-C1f in cultured cardiomyocytes results in decreased Ca(2+) transients and cell shortening, abnormalities sufficient for the induction of heart failure in a mouse model. However, the underlying mechanisms remain unclear. Here, we investigate the association between C0-C1f and altered contractility in human cardiac myofilaments in vitro. To accomplish this, we generated recombinant human C0-C1f (hC0C1f) and incorporated it into permeabilized human left ventricular myocardium. Mechanical properties were studied at short (2 μm) and long (2.3 μm) sarcomere length (SL). Our data demonstrate that the presence of hC0C1f in the sarcomere had the greatest effect at short, but not long, SL, decreasing maximal force and myofilament Ca(2+) sensitivity. Moreover, hC0C1f led to increased cooperative activation, cross-bridge cycling kinetics, and tension cost, with greater effects at short SL. We further established that the effects of hC0C1f occur through direct interaction with actin and α-tropomyosin. Our data demonstrate that the presence of hC0C1f in the sarcomere is sufficient to induce depressed myofilament function and Ca(2+) sensitivity in otherwise healthy human donor myocardium. Decreased cardiac function post-MI may result, in part, from the ability of hC0C1f to bind actin and α-tropomyosin, suggesting that cleaved C0-C1f could act as a poison polypeptide and disrupt the interaction of native cardiac myosin-binding protein C with the thin filament.

  17. Bovine spongiform encephalopathy associated insertion/deletion polymorphisms of the prion protein gene in the four beef cattle breeds from North China.

    Science.gov (United States)

    Zhu, Xiang-Yuan; Feng, Fu-Ying; Xue, Su-Yuan; Hou, Ting; Liu, Hui-Rong

    2011-10-01

    Two insertion/deletion (indel) polymorphisms of the prion protein gene (PRNP), a 23-bp indel in the putative promoter region and a 12-bp indel within intron I, are associated with the susceptibility to bovine spongiform encephalopathy (BSE) in cattle. In the present study, the polymorphism frequencies of the two indels in four main beef cattle breeds (Hereford, Simmental, Black Angus, and Mongolian) from North China were studied. The results showed that the frequencies of deletion genotypes and alleles of 23- and 12-bp indels were lower, whereas the frequencies of insertion genotypes and alleles of the two indels were higher in Mongolian cattle than in the other three cattle breeds. In Mongolian cattle, the 23-bp insertion / 12-bp insertion was the major haplotype, whereas in Hereford, Simmental, and Black Angus cattle, the 23-bp deletion / 12-bp deletion was the major haplotype. These results demonstrated that Mongolian cattle could be more resistant to BSE, compared with the other three cattle breeds, because of its relatively low frequencies of deletion genotypes and alleles of 23- and 12-bp indel polymorphisms. Thus, this race could be important for selective breeding to improve resistance against BSE in this area.

  18. Genetic deletion of laminin isoforms β2 and γ3 induces a reduction in Kir4.1 and aquaporin-4 expression and function in the retina.

    Directory of Open Access Journals (Sweden)

    Petra G Hirrlinger

    Full Text Available Glial cells such as retinal Müller glial cells are involved in potassium ion and water homeostasis of the neural tissue. In these cells, inwardly rectifying potassium (Kir channels and aquaporin-4 water channels play an important role in the process of spatial potassium buffering and water drainage. Moreover, Kir4.1 channels are involved in the maintenance of the negative Müller cell membrane potential. The subcellular distribution of Kir4.1 and aquaporin-4 channels appears to be maintained by interactions with extracellular and intracellular molecules. Laminins in the extracellular matrix, dystroglycan in the membrane, and dystrophins in the cytomatrix form a complex mediating the polarized expression of Kir4.1 and aquaporin-4 in Müller cells.The aim of the present study was to test the function of the β2 and γ3 containing laminins in murine Müller cells. We used knockout mice with genetic deletion of both β2 and γ3 laminin genes to assay the effects on Kir4.1 and aquaporin-4. We studied protein and mRNA expression by immunohistochemistry, Western Blot, and quantitative RT-PCR, respectively, and membrane currents of isolated cells by patch-clamp experiments. We found a down-regulation of mRNA and protein of Kir4.1 as well as of aquaporin-4 protein in laminin knockout mice. Moreover, Müller cells from laminin β2 and γ3 knockout mice had reduced Kir-mediated inward currents and their membrane potentials were more positive than those in age-matched wild-type mice.These findings demonstrate a strong impact of laminin β2 and γ3 subunits on the expression and function of both aquaporin-4 and Kir4.1, two important membrane proteins in Müller cells.

  19. Deletion of CDKAL1 affects high-fat diet-induced fat accumulation and glucose-stimulated insulin secretion in mice, indicating relevance to diabetes.

    Directory of Open Access Journals (Sweden)

    Tadashi Okamura

    Full Text Available BACKGROUND/OBJECTIVE: The CDKAL1 gene is among the best-replicated susceptibility loci for type 2 diabetes, originally identified by genome-wide association studies in humans. To clarify a physiological importance of CDKAL1, we examined effects of a global Cdkal1-null mutation in mice and also evaluated the influence of a CDKAL1 risk allele on body mass index (BMI in Japanese subjects. METHODS: In Cdkal1-deficient (Cdkal1⁻/⁻ mice, we performed oral glucose tolerance test, insulin tolerance test, and perfusion experiments with and without high-fat feeding. Based on the findings in mice, we tested genetic association of CDKAL1 variants with BMI, as a measure of adiposity, and type 2 diabetes in Japanese. PRINCIPAL FINDINGS: On a standard diet, Cdkal1⁻/⁻ mice were modestly lighter in weight than wild-type littermates without major alterations in glucose metabolism. On a high fat diet, Cdkal1⁻/⁻ mice showed significant reduction in fat accumulation (17% reduction in %intraabdominal fat, P = 0.023 vs. wild-type littermates with less impaired insulin sensitivity at an early stage. High fat feeding did not potentiate insulin secretion in Cdkal1⁻/⁻ mice (1.0-fold, contrary to the results in wild-type littermates (1.6-fold, P<0.01. Inversely, at a later stage, Cdkal1⁻/⁻ mice showed more prominent impairment of insulin sensitivity and glucose tolerance. mRNA expression analysis indicated that Scd1 might function as a critical mediator of the altered metabolism in Cdkal1⁻/⁻ mice. In accordance with the findings in mice, a nominally significant (P<0.05 association between CDKAL1 rs4712523 and BMI was replicated in 2 Japanese general populations comprising 5,695 and 12,569 samples; the risk allele for type 2 diabetes was also associated with decreased BMI. CONCLUSIONS: Cdkal1 gene deletion is accompanied by modestly impaired insulin secretion and longitudinal fluctuations in insulin sensitivity during high-fat feeding in mice

  20. The single N-glycan deletion mutant of soluble ErbB3 protein attenuates heregulin β1-induced tumor progression by blocking of the HIF-1 and Nrf2 pathway

    Energy Technology Data Exchange (ETDEWEB)

    Takamiya, Rina, E-mail: rinataka0429@gmail.com; Takahashi, Motoko; Uehara, Yasuaki; Ariki, Shigeru; Hashimoto, Jiro; Hasegawa, Yoshihiro; Kuroki, Yoshio

    2014-11-21

    Highlights: • The sErbB3 N418Q mutant blocks heregulin β1 induced nuclear accumulation of HIF-1α. • The sErbB3 N418Q mutant attenuates cancer cell migration induced by heregulin β1. • The sErbB3 N418Q mutant blocks heregulin β1 induced nuclear accumulation of Nrf2. • The sErbB3 N418Q mutant may be a potential therapeutic application for tumor. - Abstract: It has been well documented that activation of the ErbB3–PI3K–Akt pathway is implicated in tumor survival and progression. We previously demonstrated that the single N-glycan deletion mutant of soluble ErbB3 protein (sErbB3 N418Q) attenuates heregulin β1-induced ErbB3 signaling. The active PI3K–Akt pathway augments the nuclear accumulation of hypoxia inducible factor (HIF)-1α, which activates the transcription of many target genes and drives cancer progression. In this study, we focused on the effects of sErbB3 N418Q mutant on nuclear accumulation of HIF-1α. Pretreatment with the sErbB3 N418Q mutant suppressed heregulin β1-induced HIF-1α activation in MCF7 cells. Similar results were also obtained in other breast cancer cell lines, T47D and BT474. Interestingly, these suppressive effects were not observed with the sErbB3 wild type. In addition, pretreatment with the sErbB3 N418Q mutant suppressed the cell migration of MCF7 cells induced by heregulin β1. Furthermore, incubation with heregulin β1 also induced the nuclear accumulation of Nrf2, and this effect was also reduced by the sErbB3 N418Q mutant, but not the sErbB3 wild type. These findings indicated that the sErbB3 N418Q mutant suppressed malignant formation of cancer cells by blocking of the HIF-1α and Nrf2 pathways.

  1. The low-temperature- and salt-induced RCI2A gene of Arabidopsis complements the sodium sensitivity caused by a deletion of the homologous yeast gene SNA1.

    Science.gov (United States)

    Nylander, M; Heino, P; Helenius, E; Palva, E T; Ronne, H; Welin, B V

    2001-02-01

    Two closely related, tandemly arranged, low-temperature- and salt-induced Arabidopsis genes, corresponding to the previously isolated cDNAs RCI2A and RCI2B, were isolated and characterized. The RCI2A transcript accumulated primarily in response to low temperature or high salinity, and to a lesser extent in response to ABA treatment or water deficit stress. The RCI2B transcript was present at much lower levels than RCI2A, and could only be detected by reverse transcription-PCR amplification. The predicted 6 kDa RCI2 proteins are highly hydrophobic and contain two putative membrane-spanning regions. The polypeptides exhibit extensive similarity to deduced low-temperature- and/or salt-induced proteins from barley, wheat grass and strawberry, and to predicted proteins from bacteria, fungi, nematodes and yeast. Interestingly, we found that a deletion of the RCI2 homologous gene, SNA1 (YRD276c), in yeast causes a salt-sensitive phenotype. This effect is specific for sodium, since no growth defect was observed for the sna1 mutant on 1.7 M sorbitol, 1 M KCl or 0.6 M LiCl. Finally, we found that the Arabidopsis RCI2A cDNA can complement the sna1 mutant when expressed in yeast, indicating that the plant and yeast proteins have similar functions during high salt stress.

  2. Voltage-programming-based capillary gel electrophoresis for the fast detection of angiotensin-converting enzyme insertion/deletion polymorphism with high sensitivity.

    Science.gov (United States)

    Woo, Nain; Kim, Su-Kang; Kang, Seong Ho

    2016-08-01

    A voltage-programming-based capillary gel electrophoresis method with a laser-induced fluorescence detector was developed for the fast and highly sensitive detection of DNA molecules related to angiotensin-converting enzyme insertion/deletion polymorphism, which has been reported to influence predisposition to various diseases such as cardiovascular disease, high blood pressure, myocardial infarction, and Alzheimer's disease. Various voltage programs were investigated for fast detection of specific DNA molecules of angiotensin-converting enzyme insertion/deletion polymorphism as a function of migration time and separation efficiency to establish the effect of voltage strength to resolution. Finally, the amplified products of the angiotensin-converting enzyme insertion/deletion polymorphism (190 and 490 bp DNA) were analyzed in 3.2 min without losing resolution under optimum voltage programming conditions, which were at least 75 times faster than conventional slab gel electrophoresis. In addition, the capillary gel electrophoresis method also successfully applied to the analysis of real human blood samples, although no polymorphism genes were detected by slab gel electrophoresis. Consequently, the developed voltage-programming capillary gel electrophoresis method with laser-induced fluorescence detection is an effective, rapid analysis technique for highly sensitive detection of disease-related specific DNA molecules.

  3. Ku80-deleted cells are defective at base excision repair

    Energy Technology Data Exchange (ETDEWEB)

    Li, Han [The University of Texas Health Science Center at San Antonio, The Institute of Biotechnology, The Department of Molecular Medicine, 15355 Lambda Drive, San Antonio, TX 78245-3207 (United States); Tumor Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid 28029 (Spain); Marple, Teresa [The University of Texas Health Science Center at San Antonio, The Institute of Biotechnology, The Department of Molecular Medicine, 15355 Lambda Drive, San Antonio, TX 78245-3207 (United States); Hasty, Paul, E-mail: hastye@uthscsa.edu [The University of Texas Health Science Center at San Antonio, The Institute of Biotechnology, The Department of Molecular Medicine, 15355 Lambda Drive, San Antonio, TX 78245-3207 (United States); Tumor Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid 28029 (Spain)

    2013-05-15

    Graphical abstract: - Highlights: • Ku80-deleted cells are hypersensitive to ROS and alkylating agents. • Cells deleted for Ku80, but not Ku70 or Lig4, have reduced BER capacity. • OGG1 rescues hypersensitivity to H{sub 2}O{sub 2} and paraquat in Ku80-mutant cells. • Cells deleted for Ku80, but not Lig4, are defective at repairing AP sites. • Cells deleted for Ku80, but not Lig4 or Brca2 exon 27, exhibit increased PAR. - Abstract: Ku80 forms a heterodimer with Ku70, called Ku, that repairs DNA double-strand breaks (DSBs) via the nonhomologous end joining (NHEJ) pathway. As a consequence of deleting NHEJ, Ku80-mutant cells are hypersensitive to agents that cause DNA DSBs like ionizing radiation. Here we show that Ku80 deletion also decreased resistance to ROS and alkylating agents that typically cause base lesions and single-strand breaks (SSBs). This is unusual since base excision repair (BER), not NHEJ, typically repairs these types of lesions. However, we show that deletion of another NHEJ protein, DNA ligase IV (Lig4), did not cause hypersensitivity to these agents. In addition, the ROS and alkylating agents did not induce γ-H2AX foci that are diagnostic of DSBs. Furthermore, deletion of Ku80, but not Lig4 or Ku70, reduced BER capacity. Ku80 deletion also impaired BER at the initial lesion recognition/strand scission step; thus, involvement of a DSB is unlikely. Therefore, our data suggests that Ku80 deletion impairs BER via a mechanism that does not repair DSBs.

  4. An environment-mediated quantum deleter

    CERN Document Server

    Srikanth, R; Banerjee, Subhashish

    2006-01-01

    Environment-induced decoherence presents a great challenge to realizing a quantum computer. We point out the somewhat surprising fact that decoherence can be useful, indeed necessary, for practical quantum computation, in particular, for the effective erasure of quantum memory in order to initialize the state of the quantum computer. The essential point behind the deleter is that the environment, by means of a dissipative interaction, furnishes a contractive map towards a pure state. We present a specific example of an amplitude damping channel provided by a two-level system's interaction with its environment in the weak Born-Markov approximation. This is contrasted with a purely dephasing, non-dissipative channel provided by a two-level system's interaction with its environment by means of a quantum nondemolition interaction. We point out that currently used state preparation techniques, for example using optical pumping, essentially perform as quantum deleters.

  5. Deletion of Marek's disease virus large subunit of ribonucleotide reductase impairs virus growth in vitro and in vivo.

    Science.gov (United States)

    Sun, Aijun; Lee, Lucy F; Khan, Owais A; Heidari, Mohammad; Zhang, Huanmin; Lupiani, Blanca; Reddy, Sanjay M

    2013-06-01

    Marek's disease virus (MDV), a highly cell-associated lymphotropic alphaherpesvirus, is the causative agent of a neoplastic disease in domestic chickens called Marek's disease (MD). In the unique long (UL) region of the MDV genome, open reading frames UL39 and UL40 encode the large and small subunits of the ribonucleotide reductase (RR) enzyme, named RR1 and RR2, respectively. MDV RR is distinguishable from that present in chicken and duck cells by monoclonal antibody T81. Using recombinant DNA technology we have generated a mutant MDV (Md5deltaRR1) in which RR1 was deleted. PCR amplification of the RR gene in Md5deltaRR1-infected duck embryo fibroblasts (DEF) confirmed the deletion of the 2.4 kb RR1 gene with a resultant amplicon of a 640-bp fragment. Restriction enzyme digests with SalI confirmed a UL39 deletion and the absence of gross rearrangement. The biologic characteristics of Md5deltaRR1 virus were studied in vitro and in vivo. The Md5deltaRR1 replicated in DEF, but significantly slower than parental Md5-BAC, suggesting that RR is important but not essential for replication in fibroblasts. In vivo studies, however, showed that the RR1 deletion virus was impaired for its ability to replicate in chickens. Inoculation of specific-pathogen-free (SPF) chickens with Md5deltaRR1 showed the mutant virus is nonpathogenic and does not induce MD in birds. A revertant virus, Md5deltaRR1/R, was generated with the restored phenotype of the parental Md5-BAC in vivo, indicating that RR is essential for replication of the virus in chickens. Protection studies in SPF chickens indicated that the Md5deltaRR1 virus is not a candidate vaccine against MD.

  6. A New Intergenic α-Globin Deletion (α-αΔ125) Found in a Kabyle Population.

    Science.gov (United States)

    Singh, Amrathlal Rabbind; Lacan, Philippe; Cadet, Estelle; Bignet, Patricia; Dumesnil, Cécile; Vannier, Jean-Pierre; Joly, Philippe; Rochette, Jacques

    2016-01-01

    We have identified a deletion of 125 bp (α-α(Δ125)) (NG_000006.1: g.37040_37164del) in the α-globin gene cluster in a Kabyle population. A combination of singlex and multiplex polymerase chain reaction (PCR)-based assays have been used to identify the molecular defect. Sequencing of the abnormal PCR amplification product revealed a novel α1-globin promoter deletion. The endpoints of the deletion were characterized by sequencing the deletion junctions of the mutated allele. The observed deletion was located 378 bp upstream of the α1-globin gene transcription initiation site and leaves the α2 gene intact. In some patients, the α-α(Δ125) deletion was shown to segregate with Hb S (HBB: c.20A>T) and/or Hb C (HBB: c.19G>A) or a β-thalassemic allele. The α-α(Δ125) deletion has no discernible effect on red cell indices when inherited with no other abnormal globin genes. The family study demonstrated that the deletion is heritable. This is the only example of an intergenic α2-α1 non coding DNA deletion, leaving the α2-globin gene and the α1 coding part intact.

  7. Intestine-specific deletion of acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 protects mice from diet-induced obesity and glucose intolerance.

    Science.gov (United States)

    Nelson, David W; Gao, Yu; Yen, Mei-I; Yen, Chi-Liang Eric

    2014-06-20

    The absorption of dietary fat involves the re-esterification of digested triacylglycerol in the enterocytes, a process catalyzed by acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2. Mice without a functional gene encoding MGAT2 (Mogat2(-/-)) are protected from diet-induced obesity. Surprisingly, these mice absorb normal amounts of dietary fat but increase their energy expenditure. MGAT2 is expressed in tissues besides intestine, including adipose tissue in both mice and humans. To test the hypothesis that intestinal MGAT2 regulates systemic energy balance, we generated and characterized mice deficient in MGAT2 specifically in the small intestine (Mogat2(IKO)). We found that, like Mogat2(-/-) mice, Mogat2(IKO) mice also showed a delay in fat absorption, a decrease in food intake, and a propensity to use fatty acids as fuel when first exposed to a high fat diet. Mogat2(IKO) mice increased energy expenditure although to a lesser degree than Mogat2(-/-) mice and were protected against diet-induced weight gain and associated comorbidities, including hepatic steatosis, hypercholesterolemia, and glucose intolerance. These findings illustrate that intestinal lipid metabolism plays a crucial role in the regulation of systemic energy balance and may be a feasible intervention target. In addition, they suggest that MGAT activity in extraintestinal tissues may also modulate energy metabolism.

  8. Antigen S1, encoded by the MIC1 gene, is characterized as an epitope of human CD59, enabling measurement of mutagen-induced intragenic deletions in the AL cell system

    Science.gov (United States)

    Wilson, A. B.; Seilly, D.; Willers, C.; Vannais, D. B.; McGraw, M.; Waldren, C. A.; Hei, T. K.; Davies, A.; Chatterjee, A. (Principal Investigator)

    1999-01-01

    S1 cell membrane antigen is encoded by the MIC1 gene on human chromosome 11. This antigen has been widely used as a marker for studies in gene mapping or in analysis of mutagen-induced gene deletions/mutations, which utilized the human-hamster hybrid cell-line, AL-J1, carrying human chromosome 11. Evidence is presented here which identifies S1 as an epitope of CD59, a cell membrane complement inhibiting protein. E7.1 monoclonal antibody, specific for the S1 determinant, was found to react strongly with membrane CD59 in Western blotting, and to bind to purified, urinary form of CD59 in ELISAs. Cell membrane expression of S1 on various cell lines always correlated with that of CD59 when examined by immunofluorescent staining. In addition, E7.1 antibody inhibited the complement regulatory function of CD59. Identification of S1 protein as CD59 has increased the scope of the AL cell system by enabling analysis of intragenic mutations, and multiplex PCR analysis of mutated cells is described, showing variable loss of CD59 exons.

  9. Targeted deletion of growth hormone (GH) receptor in macrophage reveals novel osteopontin-mediated effects of GH on glucose homeostasis and insulin sensitivity in diet-induced obesity.

    Science.gov (United States)

    Lu, Chunxia; Kumar, P Anil; Sun, Jinhong; Aggarwal, Anjali; Fan, Yong; Sperling, Mark A; Lumeng, Carey N; Menon, Ram K

    2013-05-31

    We investigated GH action on macrophage (MΦ) by creating a MΦ-specific GH receptor-null mouse model (MacGHR KO). On a normal diet (10% fat), MacGHR KO and littermate controls exhibited similar growth profiles and glucose excursions on intraperitoneal glucose (ipGTT) and insulin tolerance (ITT) tests. However, when challenged with high fat diet (HFD, 45% fat) for 18 weeks, MacGHR KO mice exhibited impaired ipGTT and ITT compared with controls. In MacGHR KO, adipose-tissue (AT) MΦ abundance was increased with skewing toward M1 polarization. Expression of pro-inflammatory cytokines (IL1β, TNF-α, IL6, and osteopontin (OPN)) were increased in MacGHR KO AT stromal vascular fraction (SVF). In MacGHR KO AT, crown-like-structures were increased with decreased insulin-dependent Akt phosphorylation. The abundance of phosphorylated NF-κB and of OPN was increased in SVF and bone-marrow-derived MΦ in MacGHR KO. GH, acting via an NF-κB site in the distal OPN promoter, inhibited the OPN promoter. Thus in diet-induced obesity (DIO), lack of GH action on the MΦ exerts an unexpected deleterious effect on glucose homeostasis by accentuating AT inflammation and NF-κB-dependent activation of OPN expression. These novel results in mice support the possibility that administration of GH could have salutary effects on DIO-associated chronic inflammation and insulin resistance in humans.

  10. Mitochondrial Myopathy with DNA Deletions

    OpenAIRE

    J Gordon Millichap

    1992-01-01

    Deletions of mitochondrial DNA (mtDNA) are reported in 19 of 56 patients with mitochondrial myopathy examined in the Department of Neurology and Neuromuscular Research Laboratory, Mayo Clinic, Rochester, MN.

  11. The effect of deletion of cyclooxygenase-2, prostaglandin receptor EP2, or EP4 in bone marrow cells on osteoclasts induced by mouse mammary cancer cell lines.

    Science.gov (United States)

    Ono, Katsuhiro; Akatsu, Takuhiko; Kugai, Nobuo; Pilbeam, Carol C; Raisz, Lawrence G

    2003-11-01

    The inducible prostaglandin (PG) synthesis enzyme, cyclooxygenase-2 (COX-2), is involved in osteoclast (OC) formation in cocultures of mouse mammary cancer cell lines (MMT060562 or BALB/c-MC) and bone marrow cells through production of PGE(2). There are four PGE(2) receptors but only the EP2 and EP4 receptors are reported to be important for OC formation. We have investigated the role of COX-2, EP2 receptor, and EP4 receptor in marrow cells for osteoclastogenesis in cocultures of cancer cells and bone marrow cells. We cocultured cancer cell lines with bone marrow cells from COX-2 knockout (-/-), EP2 -/- or EP4 -/- mice compared to wild-type mice. In addition, an EP4 receptor antagonist (EP4 RA) was added in some cocultures. Disruption of COX-2 gene in bone marrow cells had no effect on PGE(2) production and OC formation in cocultures with MMT060562, while it abrogated PGE(2) production and OC formation in cocultures with BALB/c-MC. Disruption of the EP2 gene in bone marrow cells had no effect on OC formation in the cocultures, while disruption of the EP4 gene in bone marrow cells abrogated OC formation in the cocultures. Furthermore, EP4 RA suppressed OC formation and prevented the increase in receptor activator of nuclear factor kappaB ligand (RANKL) mRNA levels in the cocultures. We conclude that COX-2 in cancer cells is responsible for PGE(2) and OC production in cocultures with MMT060562, while COX-2 in bone marrow cells, not cancer cells, is responsible for PGE(2) and OC production in cocultures with BALB/c-MC, and EP4 receptors are essential for OC formation in both cocultures.

  12. Defining the ends of Parkin exon 4 deletions in two different families with Parkinson's disease.

    Science.gov (United States)

    Clarimon, Jordi; Johnson, Janel; Dogu, Okan; Horta, Wagner; Khan, Naheed; Lees, Andrew J; Hardy, John; Singleton, Andrew

    2005-02-05

    Autosomal recessive juvenile parkinsonism (AR-JP, PARK2) is characterized by an early onset parkinsonism, often presenting with dystonia as an early feature. Mutations in Parkin are a relatively common cause of AR-JP and are estimated to be present in approximately 30% of familial young onset Parkinson disease (PD) [Abbas et al. (1999); Hum Mol Genet 8:567-574]. These mutations include exon rearrangements (deletions and duplications), point mutations, and small deletions. Similar genomic mutations have been described in unrelated patients, thereby indicating independent mutational events or ancient founder effects. We have identified homozygous deletion mutations of exon 4 in Parkin in two unrelated families, one from Brazil and the other from Turkey [Dogu et al. (2004); Mov Dis 9:812-816; Khan et al., Mov Dis, in press]. We have performed molecular analysis of the deletion breakpoints and this data indicates these mutations originated independently. We present here data demonstrating that the mutation responsible for disease in the Brazilian kindred consists of two separate deletions (1,069 and 1,750 bp) surrounding and including exon 4. The deletion removing parkin exon 4 identified in the Turkish family extended 156,203 bp. In addition to demonstrating that disease in these families is not caused by a single founder mutation, these data show that there is no common fragile site between these mutational events.

  13. Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication.

    Science.gov (United States)

    Xu, Yongpeng; Wang, Shuo; Jiang, Lulu; Wang, Hui; Yang, Yilin; Li, Ming; Wang, Xujing; Zhao, Xiulan; Xie, Keqin

    2016-01-01

    1-Bromopropane (1-BP) has been used as an alternative for fluoride compounds and 1-BP intoxication may involve lung, liver, and central neural system (CNS). Our previous studies showed that 1-BP impaired memory ability by compromising antioxidant cellular defenses. Melatonin is a powerful endogenousantioxidant, and the objective of this study was to explore the therapeutic role of melatonin in the treatment of 1-BP intoxication. Rats were intragastrically treated with 1-BP with or without melatonin, and then sacrificed on 27th day after 1-BP administration. The Morris water maze (MWM) test was used to evaluate the spatial learning and memory ability of the experimental animals, and NeuN staining was performed to assess neuron loss in hippocampus. We found that rats treated with 1-BP spent more time and swam longer distance before landing on the hidden platform with a comparable swimming speed, which was markedly mitigated by the pretreatment with melatonin in a concentration-dependent manner. In addition, 1-BP-induced notable decrease in neuron population in hippocampus by promoting apoptosis, and melatonin pretreatment attenuated those changes in brain. The GSH/GSSG ratio was proportionately decreased and heme oxygenase 1 was increased in the rats exposed to 1-BP (Figure 6), and administration of melatonin restored them. Meanwhile, MDA, the level of lipid peroxidation product, was significantly increased upon exposed to 1-BP, which was significantly attenuated by melatonin pretreatment, indicating that administration of 1-BP could interfere with redox homeostasis of brain in rat, and such 1-BP-induced biomedical changes were reversed by treatment with melatonin.We conclude that treatment with melatonin attenuates 1-BP-induced CNS toxicity through its ROS scavenging effect.

  14. Alu-Alu Recombination Underlying the First Large Genomic Deletion in GlcNAc-Phosphotransferase Alpha/Beta (GNPTAB) Gene in a MLII Alpha/Beta Patient

    DEFF Research Database (Denmark)

    Coutinho, F; da Silva Santos, L; Lacerda, L

    2012-01-01

    to the identification of a 21 bp repetitive motif in introns 18 and 19. Further analysis revealed that both the 5' and 3' breakpoints were located within highly homologous Alu elements (Alu-Sz in intron 18 and Alu-Sq2, in intron 19), suggesting that this deletion has probably resulted from Alu-Alu unequal homologous......), and a third in which exon 19 was substituted by a pseudoexon inclusion consisting of a 62 bp fragment from intron 18 (p.Arg1145Serfs*16). Interestingly, this 62 bp fragment corresponds to the Alu-Sz element integrated in intron 18.This represents the first description of a large deletion identified...

  15. EST Table: BP178736 [KAIKOcDNA[Archive

    Lifescience Database Archive (English)

    Full Text Available BP178736 maV31588 10/09/28 41 %/146 aa ref|XP_001648294.1| Juvenile hormone-inducib...le protein, putative [Aedes aegypti] gb|EAT44634.1| Juvenile hormone-inducible protein, putative [Aedes aegy... 10/09/10 34 %/143 aa gi|91080979|ref|XP_974925.1| PREDICTED: similar to Juvenile hormone-inducible protein, putative [Tribolium castaneum] FS808716 maV3 ...

  16. EST Table: BP122410 [KAIKOcDNA[Archive

    Lifescience Database Archive (English)

    Full Text Available BP122410 ceN-6197 10/09/28 43 %/182 aa ref|XP_001648294.1| Juvenile hormone-inducib...le protein, putative [Aedes aegypti] gb|EAT44634.1| Juvenile hormone-inducible protein, putative [Aedes aegy... 10/09/10 37 %/179 aa gi|91080979|ref|XP_974925.1| PREDICTED: similar to Juvenile hormone-inducible protein, putative [Tribolium castaneum] FS808716 ceN- ...

  17. EST Table: BP120634 [KAIKOcDNA[Archive

    Lifescience Database Archive (English)

    Full Text Available BP120634 ceN-3457 10/09/28 41 %/153 aa ref|XP_001648294.1| Juvenile hormone-inducib...le protein, putative [Aedes aegypti] gb|EAT44634.1| Juvenile hormone-inducible protein, putative [Aedes aegy... 10/09/10 34 %/148 aa gi|91080979|ref|XP_974925.1| PREDICTED: similar to Juvenile hormone-inducible protein, putative [Tribolium castaneum] FS808716 ceN- ...

  18. EST Table: BP118870 [KAIKOcDNA[Archive

    Lifescience Database Archive (English)

    Full Text Available BP118870 ceN-0128 10/09/28 42 %/138 aa ref|XP_001648294.1| Juvenile hormone-inducib...le protein, putative [Aedes aegypti] gb|EAT44634.1| Juvenile hormone-inducible protein, putative [Aedes aegy... 10/09/10 34 %/135 aa gi|91080979|ref|XP_974925.1| PREDICTED: similar to Juvenile hormone-inducible protein, putative [Tribolium castaneum] FS808716 ceN- ...

  19. Large scale deletions of the mitochondrial DNA in astheno, asthenoterato and oligoasthenoterato-spermic men.

    Science.gov (United States)

    Hosseinzadeh Colagar, Abasalt; Karimi, Fatemeh

    2014-08-01

    The purpose of this study was to investigate the association of large-scale deletions of mtDNA between idiopathic astheno, asthenoterato and oligoasthenoterato-spermic as patient group and normospermic as control group. Forty semen samples including: 10 asthenospermic (A), 10 asthenoteratospermic (AT), 10 oligoasthenoteratospermic (OAT) and 10 normospermic samples as control group, were collected from IVF center. Our analysis of long-range polymerase chain reaction were shown multiple deletions; 4977-bp, 7599-bp and 7491-bp of mtDNA in spermatozoa of patients (A, AT and OAT) and control groups. However, the frequency of multiple mtDNA deletions in astheno (60%), asthenoterato (60%), oligoasthenoterato (70%) spermic groups were significantly higher than normal (40%) group. These results suggest that mtDNA mutations cause infertility through an effect on sperm motility. Therefore, identification of mtDNA mutations and large scale deletions in the pathophysiology of human spermatozoa dysfunction is considered to be important to better understanding of the etiology of idiopathic infertility.

  20. Isolation of Persicaria minor sesquiterpene synthase promoter and its deletions for transgenic Arabidopsis thaliana

    Science.gov (United States)

    Omar, Aimi Farehah; Ismail, Ismanizan

    2016-11-01

    Sesquiterpene synthase (SS) catalyzes the formation of sesquiterpenes from farnesyl diphosphate (FDP) via carbocation intermediates. In this study, the promoter region of sesquiterpene synthase was isolated from Persicaria minor to identify possible cis-acting elements in the promoter. The full-length PmSS promoter of P. minor is 1824-bp sequences. The sequence was analyzed and several putative cis-acting regulatory elements were identified. Three cis-acting regulatory elements were selected for deletion analysis which are cis-acting element involved in wound responsiveness (WUN), cis - acting element involved in defense and stress responsiveness (TC) and cis-acting element involved in ABA responsiveness (ABRE). Series of deletions were conducted to assess the promoter activity producing three truncated fragments promoter; Prom 2 1606-bp, Prom 3 1144- bp, and Prom 4 921-bp. The full-length promoter and its deletion series were cloned into the pBGWFS7 vector which contain β-glucuronidase (GUS) gene and green fluorescent protein (GFP) as the reporter gene. All constructs were successfully transformed into Arabidopsis thaliana based on PCR of positive BASTA resistance plants.

  1. Application of genetic BP network to discriminating earthquakes and explosions

    Institute of Scientific and Technical Information of China (English)

    边银菊

    2002-01-01

    In this paper, we develop GA-BP algorithm by combining genetic algorithm (GA) with back propagation (BP) algorithm and establish genetic BP neural network. We also applied BP neural network based on BP algorithm and genetic BP neural network based on GA-BP algorithm to discriminate earthquakes and explosions. The obtained result shows that the discriminating performance of genetic BP network is slightly better than that of BP network.

  2. Deletion of protein tyrosine phosphatase 1b in proopiomelanocortin neurons reduces neurogenic control of blood pressure and protects mice from leptin- and sympatho-mediated hypertension.

    Science.gov (United States)

    Bruder-Nascimento, Thiago; Butler, Benjamin R; Herren, David J; Brands, Michael W; Bence, Kendra K; Belin de Chantemèle, Eric J

    2015-12-01

    Protein tyrosine phosphatase 1b (Ptp1b), which represses leptin signaling, is a promising therapeutic target for obesity. Genome wide deletion of Ptp1b, increases leptin sensitivity, protects mice from obesity and diabetes, but alters cardiovascular function by increasing blood pressure (BP). Leptin-control of metabolism is centrally mediated and involves proopiomelanocortin (POMC) neurons. Whether these neurons contribute to leptin-mediated increases in BP remain unclear. We hypothesized that increasing leptin signaling in POMC neurons with Ptp1b deletion will sensitize the cardiovascular system to leptin and enhance neurogenic control of BP. We analyzed the cardiovascular phenotype of Ptp1b+/+ and POMC-Ptp1b-/- mice, at baseline and after 7 days of leptin infusion or sympatho-activation with phenylephrine. POMCPtp1b deletion did not alter baseline cardiovascular hemodynamics (BP, heart rate) but reduced BP response to ganglionic blockade and plasma catecholamine levels that suggests a decreased neurogenic control of BP. In contrast, POMC-Ptp1b deletion increased vascular adrenergic reactivity and aortic α-adrenergic receptors expression. Chronic leptin treatment reduced vascular adrenergic reactivity and blunted diastolic and mean BP increases in POMC-Ptp1b-/- mice only. Similarly POMC-Ptp1b-/- mice exhibited a blunted increased in diastolic and mean BP accompanied by a gradual reduction in adrenergic reactivity in response to chronic vascular sympatho-activation with phenylephrine. Together these data rule out our hypothesis but suggest that deletion of Ptp1b in POMC neurons protects from leptin- and sympatho-mediated increases in BP. Vascular adrenergic desensitization appears as a protective mechanism against hypertension, and POMC-Ptp1b as a key therapeutic target for the treatment of metabolic and cardiovascular dysfunctions associated with obesity.

  3. Molecular investigations of mitochondrial deletions: evaluating the usefulness of different genetic tests.

    Science.gov (United States)

    Tońska, Katarzyna; Piekutowska-Abramczuk, Dorota; Kaliszewska, Magdalena; Kowalski, Paweł; Tańska, Anna; Bartnik, Ewa; Pronicka, Ewa; Krajewska-Walasek, Małgorzata

    2012-09-10

    Deletions in mitochondrial DNA are a common cause of mitochondrial disorders. The molecular diagnosis of mtDNA deletions for years was based on Southern hybridization later replaced by PCR methods such as PCR with primers specific for a particular deletion (mainly the so-called common deletion of 4977 bp) and long PCR. In order to evaluate the usefulness of MLPA (Multiplex Ligation-dependent Probe Amplification) in molecular diagnosis of large scale mtDNA deletions we compare four diagnostic methods: Southern hybridization, PCR, long-PCR and MLPA in a group of 16 patients with suspected deletions. Analysis was performed on blood, muscle and in one case hepatic tissue DNA. The MLPA was not able to confirm all the deletions detected by PCR methods, but due to its relative ease of processing, minimal equipment, low costs and the additional possibility to detect frequent point mtDNA mutations in one assay it is worth considering as a screening method. We recommend to always confirm MLPA results by PCR methods.

  4. Abnormal auditory and language pathways in children with 16p11.2 deletion

    Directory of Open Access Journals (Sweden)

    Jeffrey I. Berman

    2015-01-01

    Full Text Available Copy number variations at chromosome 16p11.2 contribute to neurodevelopmental disorders, including autism spectrum disorder (ASD. This study seeks to improve our understanding of the biological basis of behavioral phenotypes common in ASD, in particular the prominent and prevalent disruption of spoken language seen in children with the 16p11.2 BP4–BP5 deletion. We examined the auditory and language white matter pathways with diffusion MRI in a cohort of 36 pediatric deletion carriers and 45 age-matched controls. Diffusion MR tractography of the auditory radiations and the arcuate fasciculus was performed to generate tract specific measures of white matter microstructure. In both tracts, deletion carriers exhibited significantly higher diffusivity than that of controls. Cross-sectional diffusion parameters in these tracts changed with age with no group difference in the rate of maturation. Within deletion carriers, the left-hemisphere arcuate fasciculus mean and radial diffusivities were significantly negatively correlated with clinical language ability, but not non-verbal cognitive ability. Diffusion metrics in the right-hemisphere arcuate fasciculus were not predictive of language ability. These results provide insight into the link between the 16p11.2 deletion, abnormal auditory and language pathway structures, and the specific behavioral deficits that may contribute to neurodevelopmental disorders such as ASD.

  5. TopBP1 is required at mitosis to reduce transmission of DNA damage to G1 daughter cells

    DEFF Research Database (Denmark)

    Pedersen, Rune Troelsgaard; Kruse, Thomas; Nilsson, Jakob

    2015-01-01

    mitotic entry. In early mitosis, TopBP1 marks sites of and promotes unscheduled DNA synthesis. Moreover, TopBP1 is required for focus formation of the structure-selective nuclease and scaffold protein SLX4 in mitosis. Persistent TopBP1 foci transition into 53BP1 nuclear bodies (NBs) in G1 and precise...... temporal depletion of TopBP1 just before mitotic entry induced formation of 53BP1 NBs in the next cell cycle, showing that TopBP1 acts to reduce transmission of DNA damage to G1 daughter cells. Based on these results, we propose that TopBP1 maintains genome integrity in mitosis by controlling chromatin...

  6. Cytogenetic and molecular characterization of A2BP1/FOX1 as a candidate gene for autism.

    Science.gov (United States)

    Martin, Christa Lese; Duvall, Jacqueline A; Ilkin, Yesim; Simon, Jason S; Arreaza, M Gladys; Wilkes, Kristin; Alvarez-Retuerto, Ana; Whichello, Amy; Powell, Cynthia M; Rao, Kathleen; Cook, Edwin; Geschwind, Daniel H

    2007-10-05

    Cytogenetic imbalances are increasingly being realized as causes of autism. Here, we report a de novo translocation between the short arms of chromosomes 15 and 16 in a female with autism, epilepsy, and global developmental delay. FISH analysis identified a cryptic deletion of approximately 160 kb at the boundary of the first exon and first intron of the 1.7 Mb ataxin-2 binding protein-1 (A2BP1) gene, also called FOX1. Quantitative real time PCR (Q-PCR) analysis verified a deletion of exon 1 in the 5' promoter region of the A2BP1 gene. Reverse transcription PCR (qRT-PCR) showed reduced mRNA expression in the individual's lymphocytes, demonstrating the functional consequence of the deletion. A2BP1 codes for a brain-expressed RNA binding or splicing factor. Because of emerging evidence in the role of RNA processing and gene regulation in pervasive developmental disorders, we performed further screening of A2BP1 in additional individuals with autism from the Autism Genetics Resource Exchange (AGRE) collection. Twenty-seven SNPs were genotyped across A2BP1 in 206 parent-child trios and two regions showed association at P level. No additional deletions or clear mutations were identified in 88 probands by re-sequencing of all exons and surrounding intronic regions or quantitative PCR (Q-PCR) of exon 1. Although only nominal association was observed, and no obvious causal mutations were identified, these results suggest that A2BP1 may affect susceptibility or cause autism in a subset of patients. Further investigations in a larger sample may provide additional information regarding the involvement of this gene in the autistic phenotype.

  7. The mutation rate of the human mtDNA deletion mtDNA4977.

    Science.gov (United States)

    Shenkar, R; Navidi, W; Tavaré, S; Dang, M H; Chomyn, A; Attardi, G; Cortopassi, G; Arnheim, N

    1996-10-01

    The human mitochondrial mutation mtDNA4977 is a 4,977-bp deletion that originates between two 13-bp direct repeats. We grew 220 colonies of cells, each from a single human cell. For each colony, we counted the number of cells and amplified the DNA by PCR to test for the presence of a deletion. To estimate the mutation fate, we used a model that describes the relationship between the mutation rate and the probability that a colony of a given size will contain no mutants, taking into account such factors as possible mitochondrial turnover and mistyping due to PCR error. We estimate that the mutation rate for mtDNA4977 in cultured human cells is 5.95 x 10(-8) per mitochondrial genome replication. This method can be applied to specific chromosomal, as well as mitochondrial, mutations.

  8. The mutation rate of the human mtDNA deletion mtDNA{sup 4977}

    Energy Technology Data Exchange (ETDEWEB)

    Shenkar, R. [Univ. of Colorado Health Science Center, Denver, CO (United States); Navidi, W. [Colorado School of Mines, Golden, CO (United States); Tavare, S. [Univ. of California, Los Angeles, CA (United States)] [and others

    1996-10-01

    The human mitochondrial mutation mtDNA{sup 4977} is a 4,977-bp deletion that originates between two 13-bp direct repeats. We grew 220 colonies of cells, each from a single human cell. For each colony, we counted the number of cells and amplified the DNA by PCR to test for the presence of a deletion. To estimate the mutation rate, we used a model that describes the relationship between the mutation rate and the probability that a colony of a given size will contain no mutants, taking into account such factors as possible mitochondrial turnover and mistyping due to PCR error. We estimate that the mutation rate for mtDNA{sup 4977} in cultured human cells is 5.95 x 10{sup {minus}8} per mitochondrial genome replication. This method can be applied to specific chromosomal, as well as mitochondrial, mutations. 17 refs., 1 fig., 1 tab.

  9. The smt-0 mutation which abolishes mating-type switching in fission yeast is a deletion

    DEFF Research Database (Denmark)

    Styrkársdóttir, U; Egel, R; Nielsen, O;

    1993-01-01

    Mating-type switching in the fission yeast, S. pombe, is initiated by a DNA double-strand break (DSB) between the mat1 cassette and the H1 homology box. The mat1-cis-acting mutant, smt-0, abolishes mating-type switching and is shown here to be a 263-bp deletion. This deletion starts in the middle...... of the H1 homology box, 31 bp from the site of the DSB, and extends into the flanking region distal to mat1. The sequence of the region distal to H1 in the wild-type is also presented. In this region we observe a bias in the distribution of purine residues between the two DNA strands....

  10. 76 FR 9555 - Procurement List; Proposed Deletions

    Science.gov (United States)

    2011-02-18

    ... PEOPLE WHO ARE BLIND OR SEVERELY DISABLED Procurement List; Proposed Deletions AGENCY: Committee for Purchase From People Who Are Blind or Severely Disabled. ACTION: Proposed deletions from the Procurement...'Day Act (41 U.S.C. 46- 48c) in connection with the products proposed for deletion from the...

  11. Distinct profile of the mitochondrial DNA common deletion in benign skin lesions.

    Science.gov (United States)

    Hafner, Christian; Kamenisch, York; Landthaler, Michael; Berneburg, Mark

    2011-02-01

    Mutations of mitochondrial (mt) DNA, particularly the 4977 bp long common deletion, are increased in aging tissues and preferentially found in chronologically and photoaged skin. Mutations of human mitochondrial DNA (mtDNA) have also been identified in malignant tumors of the skin and of other organs. However, benign skin lesions have not yet been investigated. We analyzed the frequency of the common deletion in 27 benign skin lesions [8 seborrheic keratoses (SK), 5 epidermal nevi (EN), 14 solar lentigos (SL)] by quantitative real-time PCR, because SK and especially SL have been related to (photo)aged skin. All SK and four of five EN displayed reduced common deletion levels compared with adjacent normal skin. In contrast, 50% of SL revealed a higher percentage of the common deletion than the adjacent normal skin, and some SL showed very high absolute common deletion levels up to 14% of total mtDNA. Our results show that the amount of the common deletion is significantly different in benign skin lesions and raise further questions regarding the pathogenesis of SL and its possible role as a precursor lesion of SK.

  12. A novel contiguous gene deletion of AVPR2 and ARHGAP4 genes in male dizygotic twins with nephrogenic diabetes insipidus and intellectual disability.

    Science.gov (United States)

    Huang, Lingli; Poke, Gemma; Gecz, Jozef; Gibson, Kate

    2012-10-01

    The clinical features of loss of ARHGAP4 function remain unclear despite several reports of different patterns of deletions inactivating different functional regions of the protein. The protein encoded by ARHGAP4 is thought to function as a Rho GTPase activating protein. Characterization of the genetic defect causing X-linked nephrogenic diabetes insipidus (NDI) and intellectual disability in two dizygotic twin brothers revealed a novel contiguous deletion of 17,905 bp encompassing the entire AVPR2 gene and extending into intron 7 of the ARHGAP4 gene. Examination of their mother showed that she was a carrier of this deletion. An attempt was made to distinguish the putative clinical signs of an ARHGAP4 deletion from the well-defined phenotype of X-linked NDI caused by an AVPR2 gene deletion. By reviewing all characterized deletions encompassing ARHGAP4, we reconsider the potential role of ARHGAP4 in cognition.

  13. Exonal deletion of SLC24A4 causes hypomaturation amelogenesis imperfecta.

    Science.gov (United States)

    Seymen, F; Lee, K-E; Tran Le, C G; Yildirim, M; Gencay, K; Lee, Z H; Kim, J-W

    2014-04-01

    Amelogenesis imperfecta is a heterogeneous group of genetic conditions affecting enamel formation. Recently, mutations in solute carrier family 24 member 4 (SLC24A4) have been identified to cause autosomal recessive hypomaturation amelogenesis imperfecta. We recruited a consanguineous family with hypomaturation amelogenesis imperfecta with generalized brown discoloration. Sequencing of the candidate genes identified a 10-kb deletion, including exons 15, 16, and most of the last exon of the SLC24A4 gene. Interestingly, this deletion was caused by homologous recombination between two 354-bp-long homologous sequences located in intron 14 and the 3' UTR. This is the first report of exonal deletion in SLC24A4 providing confirmatory evidence that the function of SLC24A4 in calcium transport has a crucial role in the maturation stage of amelogenesis.

  14. Mitochondrial DNA deletion in a patient with combined features of Leigh and Pearson syndromes

    Energy Technology Data Exchange (ETDEWEB)

    Blok, R.B.; Thorburn, D.R.; Danks, D.M. [Royal Children`s Hospital, Melbourne (Australia)] [and others

    1994-09-01

    We describe a heteroplasmic 4237 bp mitochondrial DNA (mtDNA) deletion in an 11 year old girl who has suffered from progressive illness since birth. She has some features of Leigh syndrome (global developmental delay with regression, brainstem dysfunction and lactic acidosis), together with other features suggestive of Pearson syndrome (history of pancytopenia and failure to thrive). The deletion was present at a level greater than 50% in skeletal muscle, but barely detectable in skin fibroblasts following Southern blot analysis, and only observed in blood following PCR analysis. The deletion spanned nt 9498 to nt 13734, and was flanked by a 12 bp direct repeat. Genes for cytochrome c oxidase subunit III, NADH dehydrogenase subunits 3, 4L, 4 and 5, and tRNAs for glycine, arginine, histidine, serine({sup AGY}) and leucine({sup CUN}) were deleted. Southern blotting also revealed an altered Apa I restriction site which was shown by sequence analysis to be caused by G{r_arrow}A nucleotide substitution at nt 1462 in the 12S rRNA gene. This was presumed to be a polymorphism. No abnormalities of mitochondrial ultrastructure, distribution or of respiratory chain enzyme complexes I-IV in skeletal muscle were observed. Mitochondrial disorders with clinical features overlapping more than one syndrome have been reported previously. This case further demonstrates the difficulty in correlating observed clinical features with a specific mitochondrial DNA mutation.

  15. cMyBP-C was decreased via KLHL3-mediated proteasomal degradation in congenital heart diseases.

    Science.gov (United States)

    Wang, Leitong; Lai, Guangrui; Chu, Guoming; Liang, Xiaoyan; Zhao, Yanyan

    2017-03-15

    Cardiac myosin binding protein C (cMyBP-C) is a cardiac structural and regulatory protein; mutations of cMyBP-C are frequently associated with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Cardiac special transcription factors may regulate the expression of cMyBP-C. However, the role of cMyBP-C in congenital heart diseases (CHD) remains poorly understood. In the current study, western blotting and the MRM approach showed that cMyBP-C expression was significantly reduced in fetuses with CHD compared to those without. Furthermore, we found that cMyBP-C interacted with KLHL3 by immunoprecipitation and immunofluorescence, and the degradation of cMyBP-C was caused by KLHL3-mediated ubiquitination. In addition, homocysteine (Hcy, a risk factor of CHD) treatment caused a decrease in cMyBP-C and an increase in KLHL3 expression, and the proteasome inhibitor MG132 reversed the Hcy-induced reduction of cMyBP-C expression. Finally, we verified that reduced cMyBP-C by Hcy promoted apoptosis in cardiomyocytes. These results demonstrate that Hcy decreases the expression of cMyBP-C through a KLHL3-mediated ubiquitin-proteasome pathway, and thereby influences heart development.

  16. Interoperability of wearable cuffless BP measuring devices.

    Science.gov (United States)

    Liu, Jing; Zhang, Yuan-Ting

    2014-01-01

    While a traditional cuff-based Blood Pressure (BP) measuring device can only take a snap shot of BP, real-time and continuous measurement of BP without an occluding cuff is preferred which usually use the pulse transit time (PTT) in combination with other physiological parameters to estimate or track BP over a certain period of time after an initial calibration. This article discusses some perspectives of interoperability of wearable medical devices, based on IEEE P1708 draft standard that focuses on the objective performance evaluation of wearable cuffless BP measuring devices. The ISO/IEEE 11073 family of standards, supporting the plug-and play feature, is intended to enable medical devices to interconnect and interoperate with other medical devices and with computerized healthcare information systems in a manner suitable for the clinical environment. In this paper, the possible adoption of ISO/IEEE 11073 for the interoperability of wearable cuffless BP devices is proposed. In the consideration of the difference of the continuous and cuffless BP measuring methods from the conventional ones, the existing device specialization standards of ISO/IEEE 11073 cannot be directly followed when designing the cuffless BP device. Specifically, this paper discusses how the domain information model (DIM), in which vital sign information is abstracted as objects, is used to structure the information about the device and that generated from the device. Though attention should also be paid to adopt the communication standards for other parts for the communication system, applying communication standards that enable plug-and-play feature allows achieving the interoperability of different cuffless BP measuring devices with possible different configurations.

  17. CacyBP/SIP promotes the proliferation of colon cancer cells

    Science.gov (United States)

    Chen, Xiong; Wang, Jun; Lu, Yuanyuan; Zhang, Faming; Liu, Zhengxiong; Lei, Ting; Fan, Daiming

    2017-01-01

    CacyBP/SIP is a component of the ubiquitin pathway and is overexpressed in several transformed tumor tissues, including colon cancer, which is one of the most common cancers worldwide. It is unknown whether CacyBP/SIP promotes the proliferation of colon cancer cells. This study examined the expression level, subcellular localization, and binding activity of CacyBP/SIP in human colon cancer cells in the presence and absence of the hormone gastrin. We found that CacyBP/SIP was expressed in a high percentage of colon cancer cells, but not in normal colonic surface epithelium. CacyBP/SIP promoted the cell proliferation of colon cancer cells under both basal and gastrin stimulated conditions as shown by knockdown studies. Gastrin stimulation triggered the translocation of CacyBP/SIP to the nucleus, and enhanced interaction between CacyBP/SIP and SKP1, a key component of ubiquitination pathway which further mediated the proteasome-dependent degradation of p27kip1 protein. The gastrin induced reduction in p27kip1 was prevented when cells were treated with the proteasome inhibitor MG132. These results suggest that CacyBP/SIP may be promoting growth of colon cancer cells by enhancing ubiquitin-mediated degradation of p27kip1. PMID:28196083

  18. Improving the MVA vaccine potential by deleting the viral gene coding for the IL-18 binding protein.

    Directory of Open Access Journals (Sweden)

    Juliana Falivene

    Full Text Available BACKGROUND: Modified Vaccinia Ankara (MVA is an attenuated strain of Vaccinia virus (VACV currently employed in many clinical trials against HIV/AIDS and other diseases. MVA still retains genes involved in host immune response evasion, enabling its optimization by removing some of them. The aim of this study was to evaluate cellular immune responses (CIR induced by an IL-18 binding protein gene (C12L deleted vector (MVAΔC12L. METHODOLOGY/PRINCIPAL FINDINGS: BALB/c and C57BL/6 mice were immunized with different doses of MVAΔC12L or MVA wild type (MVAwt, then CIR to VACV epitopes in immunogenic proteins were evaluated in spleen and draining lymph nodes at acute and memory phases (7 and 40 days post-immunization respectively. Compared with parental MVAwt, MVAΔC12L immunization induced a significant increase of two to three-fold in CD8(+ and CD4(+ T-cell responses to different VACV epitopes, with increased percentage of anti-VACV cytotoxic CD8(+ T-cells (CD107a/b(+ during the acute phase of the response. Importantly, the immunogenicity enhancement was also observed after MVAΔC12L inoculation with different viral doses and by distinct routes (systemic and mucosal. Potentiation of MVA's CIR was also observed during the memory phase, in correlation with a higher protection against an intranasal challenge with VACV WR. Of note, we could also show a significant increase in the CIR against HIV antigens such as Env, Gag, Pol and Nef from different subtypes expressed from two recombinants of MVAΔC12L during heterologous DNA prime/MVA boost vaccination regimens. CONCLUSIONS/SIGNIFICANCE: This study demonstrates the relevance of IL-18 bp contribution in the immune response evasion during MVA infection. Our findings clearly show that the deletion of the viral IL-18 bp gene is an effective approach to increase MVA vaccine efficacy, as immunogenicity improvements were observed against vector antigens and more importantly to HIV antigens.

  19. Integration of BpMADS4 on various linkage groups improves the utilization of the rapid cycle breeding system in apple.

    Science.gov (United States)

    Weigl, Kathleen; Wenzel, Stephanie; Flachowsky, Henryk; Peil, Andreas; Hanke, Magda-Viola

    2015-02-01

    Rapid cycle breeding in apple is a new approach for the rapid introgression of agronomically relevant traits (e.g. disease resistances) from wild apple species into domestic apple cultivars (Malus × domestica Borkh.). This technique drastically shortens the long-lasting juvenile phase of apple. The utilization of early-flowering apple lines overexpressing the BpMADS4 gene of the European silver birch (Betula pendula Roth.) in hybridization resulted in one breeding cycle per year. Aiming for the selection of non-transgenic null segregants at the end of the breeding process, the flower-inducing transgene and the gene of interest (e.g. resistance gene) that will be introgressed by hybridization need to be located on different chromosomes. To improve the flexibility of the existing approach in apple, this study was focused on the development and characterization of eleven additional BpMADS4 overexpressing lines of four different apple cultivars. In nine lines, the flowering gene was mapped to different linkage groups. The differences in introgressed T-DNA sequences and plant genome deletions post-transformation highlighted the unique molecular character of each line. However, transgenic lines demonstrated no significant differences in flower organ development and pollen functionality compared with non-transgenic plants. Hybridization studies using pollen from the fire blight-resistant wild species accession Malus fusca MAL0045 and the apple scab-resistant cultivar 'Regia' indicated that BpMADS4 introgression had no significant effect on the breeding value of each transgenic line.

  20. Neuropsychological phenotype of a patient with a de novo 970 kb interstitial deletion in the distal 16p11.2 region

    Science.gov (United States)

    Egger, Jos I M; Verhoeven, Willem M A; Verbeeck, Wim; de Leeuw, Nicole

    2014-01-01

    The 16p11.2 microdeletion syndrome is characterized by a wide range of phenotypic expressions and is frequently associated with developmental delay, symptoms from the autism spectrum, epilepsy, congenital anomalies, and obesity. These phenotypes are often related to a proximal 16p11.2 deletion of approximately 600 kb (BP4–BP5) that includes the SH2B1 gene that is reported to be causative for morbid obesity. This more centromeric deletion is most strongly related to autism spectrum susceptibility and is functionally different from the more distal 16p12.2p11.2 region, which includes the so-called atypical 16p11.2 BP2–BP3 deletion (approximately 220 kb) presenting with developmental delay, behavioral problems and mild facial dysmorphisms. Here, an adult male with a long history of maladaptive behaviors is described who was referred for diagnostic assessment of his amotivational features. Extensive neuropsychological examination demonstrated rigid thinking, anxious beliefs, and ideas of reference in the presence of normal intelligence. Microarray analysis demonstrated a de novo 970 kb 16p11.2 BP1–BP4 microdeletion that can be regarded as explanatory for his behavioral profile. It is concluded that microdeletion syndromes are not exclusively related to intellectual disabilities and genetic testing is of putative relevance for the understanding of neuropsychiatric and neuropsychological phenomena. PMID:24707176

  1. The millimetre spectrum of BP Cru

    Science.gov (United States)

    Pestalozzi, Michele; Hobbs, George; Torkelsson, Ulf

    2010-04-01

    In this experiment we attempt to detect the millimetre emission from the high-mass X-ray binary BP Cru. This object is composed of a hypergiant (Wray 977) and a slow spinning X-ray pulsar (GX301-2). The recent ATCA observations of centimeter emission (Pestalozzi et al. 2009, this was the first detection of radio emission towards BP Cru) suggested that radio emission consists of two components, a transient non-thermal one and a persistent thermal one, probably arising from the large stellar wind of Wray 977. As stellar winds often show a positive spectral index, we ask to observe BP Cru at 13 and 7 mm, where we expect fluxes of around 1 mJy. Any detection will allow us to probe the inner parts of the wind and characterise the structure of the stellar wind of BP Cru. For this detection experiment we require 11 hours of observations with ATCA.

  2. BP Investment Exceeds $4 Bln in china

    Institute of Scientific and Technical Information of China (English)

    Wang Ping

    2008-01-01

    @@ British Petroleum (BP) recently signed a series of agreements with China including those in clean energy and wind power generation, during British Prime Minister Gordon Brown's visit to China in mid-January.

  3. The evolution of small insertions and deletions in the coding genes of Drosophila melanogaster.

    Science.gov (United States)

    Chong, Zechen; Zhai, Weiwei; Li, Chunyan; Gao, Min; Gong, Qiang; Ruan, Jue; Li, Juan; Jiang, Lan; Lv, Xuemei; Hungate, Eric; Wu, Chung-I

    2013-12-01

    Studies of protein evolution have focused on amino acid substitutions with much less systematic analysis on insertion and deletions (indels) in protein coding genes. We hence surveyed 7,500 genes between Drosophila melanogaster and D. simulans, using D. yakuba as an outgroup for this purpose. The evolutionary rate of coding indels is indeed low, at only 3% of that of nonsynonymous substitutions. As coding indels follow a geometric distribution in size and tend to fall in low-complexity regions of proteins, it is unclear whether selection or mutation underlies this low rate. To resolve the issue, we collected genomic sequences from an isogenic African line of D. melanogaster (ZS30) at a high coverage of 70× and analyzed indel polymorphism between ZS30 and the reference genome. In comparing polymorphism and divergence, we found that the divergence to polymorphism ratio (i.e., fixation index) for smaller indels (size ≤ 10 bp) is very similar to that for synonymous changes, suggesting that most of the within-species polymorphism and between-species divergence for indels are selectively neutral. Interestingly, deletions of larger sizes (size ≥ 11 bp and ≤ 30 bp) have a much higher fixation index than synonymous mutations and 44.4% of fixed middle-sized deletions are estimated to be adaptive. To our surprise, this pattern is not found for insertions. Protein indel evolution appear to be in a dynamic flux of neutrally driven expansion (insertions) together with adaptive-driven contraction (deletions), and these observations provide important insights for understanding the fitness of new mutations as well as the evolutionary driving forces for genomic evolution in Drosophila species.

  4. EXPRESSION AND DELETION ANALYSIS OF EcoRII ENDONUCLEASE AND METHYLASE GENE

    Institute of Scientific and Technical Information of China (English)

    刘金毅; 赵晓娟; 孟雁; 沈洁; 薛越强; 史顺娣; 蔡有余

    2001-01-01

    Objective. To clone complete EcoRII restriction endonuclease gene (ecoRllR) and methyltransferase gene(ecoRllM) in one ector and to analyze the coordinating expression of this whole R-M system.Methods. Unidirectional deletion subclones were constructed with ExolII. ecoRllR/M genes were preliminari-ly located in the cloned fragment according to the enzyme activities of subclones. Exact deletion sites were deter-mined by sequencing, and transcriptional start sites were determined by S1 mapping.Results. The DNA fragment which was cloned into pBluescript SK + contained intact ecoRIlR gene andecoRllM gene, anc two transcriptional start sites of ecoRllR gene were determined. 132bp to 458bp from 3' endof ecoRllR gene ar.e indispensable to enzyme activities and deletion of 202bp from 3' end of ecoRllM gene madeenzyme lose the capability in DNA protection to resist specific cut with EcoRII endonuclease (EcoRII. R). Dele-tion of the coding ar d flanking sequences of one gene did not affect the expression of the other gene, and the recombi-nants only containing ecoRllR gene appeared to be lethal to dcm+ host.Conclusion. scoRllM gene linking closely to ecoRIIR gene is very important for the existence of the R-M sys-tem in process of evolution, but the key to control EcoRlI R-M order may not exist in transcriptional level .``Liu Jmy,Corresponding author.

  5. Evidence that Mono-ADP-Ribosylation of CtBP1/BARS Regulates Lipid Storage

    OpenAIRE

    Bartz, René; Seemann, Joachim; Zehmer, John K.; Serrero, Ginette; Kent D. Chapman; Anderson, Richard G. W.; Liu, Pingsheng

    2007-01-01

    Mono-ADP-ribosylation is emerging as an important posttranslational modification that modulates a variety of cell signaling pathways. Here, we present evidence that mono-ADP-ribosylation of the transcriptional corepressor C terminal binding protein, brefeldin A (BFA)-induced ADP-ribosylated substrate (CtBP1/BARS) regulates neutral lipid storage in droplets that are surrounded by a monolayer of phospholipid and associated proteins. CtBP1/BARS is an NAD-binding protein that becomes ribosylated ...

  6. Germinal mosaicism for a deletion of the FMR1 gene leading to fragile X syndrome.

    Science.gov (United States)

    Jiraanont, P; Hagerman, R J; Neri, G; Zollino, M; Murdolo, M; Tassone, F

    2016-09-01

    Aberrant CGG trinucleotide amplification within the FMR1 gene, which spans approximately 38 Kb of genomic DNA is almost always what leads to fragile X syndrome (FXS). However, deletions of part or the entire FMR1 gene can also cause FXS. Both CGG amplification-induced silencing and deletions result in the absence of the FMR1 gene product, FMRP. Here, we report a rare case of germinal mosaicism of a deletion encompassing approximately 300 Kb of DNA, which by removing the entire FMR1 gene led to FXS. The male proband, carrying the deletion, presented in clinic with the typical features of FXS. His mother was analyzed by FISH on metaphase chromosomes with cosmid probe c22.3 spanning the FMR1 locus, and she was found not to carry the deletion on 30 analyzed cells from peripheral blood lymphocytes. Prenatal examination of the mother's third pregnancy showed that the male fetus also had the same deletion as the proband. Following this prenatal diagnosis, FISH analysis in the mother was expanded to 400 metaphases from peripheral lymphocytes, and a heterozygous FMR1 deletion was found in three. Although this result could be considered questionable from a diagnostic point of view, it indicates that the deletion is in the ovary's germinal cells.

  7. Mitochondrial myopathy associated with high levels of mitochondrial DNA harboring a 260 bp tandem duplication in the D-loop region

    Energy Technology Data Exchange (ETDEWEB)

    Manfredi, G.; Shanske, S.; Schon, E.A. [Columbia Univ., NY (United States)] [and others

    1994-09-01

    Low levels of a 260 bp duplication in the D-loop of the mitochondrial DNA (mtDNA) were reported in some patients with mitochondrial disorders harboring large-scale mtDNA deletions. Because the same duplication was observed in unaffected mothers of these patients, it was suggested that the 260 bp duplication predispose mtDNA to deletion. More recently, PCR-levels of this duplication were also observed in a subgroup of normal Caucasions. To test the hypothesis that this genetic abnormality may be prevalent in patients with large-scale deletions of the mitochondrial genome, we used a semi-quantitative PCR protocol to search for the 260 by duplication in 34 patients with, and 35 without mtDNA deletions. Our results do not support the hypothesis that the 260 bp duplication precedes large-scale deletions of mtDNA. They suggest, however, that the duplication may be pathogenic per se, if its level reaches a specific threshold. We are presently trying to test this hypothesis, as well as the stability of the duplication, in a cell culture system.

  8. R3-R4 deletion in the PRNP gene is associated with Creutzfeldt-Jakob disease (CJD)

    Energy Technology Data Exchange (ETDEWEB)

    Cervenakova, L.; Brown, P.; Nagle, J. [and others

    1994-09-01

    There are conflicting reports on the association of deletions in the PRNP gene on chromosome 20 with CJD, a rapidly progressive fatal spongiform encephalopathy. We accumulated data suggesting that a deletion of R3-R4 type (parts of the third and fourth repeats are deleted from the area of four repeating 24 bp sequences in the 5{prime} region of the gene) is causing CJD. Screening of 129 unaffected control individuals demonstrated presence of a deletion of R2 type in four (1.55% of the studied chromosomes), but none of them had the R3-R4 type. Of 181 screened patients with spongiform encephalopathies, two had a deletion of R3-R4 type with no other mutations in the coding sequence. Both patients had a classical rapidly progressive dementing disease and diffuse spongiform degeneration, and both cases were apparently sporadic. The same R3-R4 type of deletion was detected in three additional neuropathologically confirmed spongiform encephalopathy patients, of which two had other known pathogenic mutations in the PRNP gene: at codon 178 on the methionine allele exhibiting the phenotype of fatal familial insomnia, and codon 200 causing CJD with severe dementia; the third was a patient with iatrogenic CJD who developed the disease after treatment with growth hormone extracted from cadaveric human pituitary glands. In all cases the deletion coincided with a variant sequence at position 129 coding for methionine.

  9. A Japanese boy with myalgia and cramps has a novel in-frame deletion of the dystrophin gene.

    Science.gov (United States)

    Ishigaki, C; Patria, S Y; Nishio, H; Yabe, M; Matsuo, M

    1996-05-01

    We report a Japanese Becker muscular dystrophy (BMD) patient with occasional myalgia and cramps during normal activity that developed at the age of 28 months. His family history was negative for neuromuscular diseases. Muscle biopsy analyses, including dystrophin immunostaining, disclosed no clinically relevant findings. The diagnosis of BMD was initially made at the age of 10 years, when indications of persistent high serum levels of CK prompted us to screen deletions in the dystrophin gene by amplification of 19 deletion-prone exons from the genomic DNA by the polymerase chain reaction (PCR). Among the exons examined, exons 13 and 17 were deleted. To clarify the size of the deletion, the dystrophin transcript was analyzed by reverse transcription PCR. The determined nucleotide sequence of the amplified product encompassing exons 10 to 20 disclosed that the entire segment corresponding to exons 13 to 18 (810 bp) was absent, a deletion that would be expected to cause the production of a dystrophin protein lacking 270 amino acids from the rod domain. This result indicates that occasional myalgia and cramps could be early clinical manifestations of mild BMD, especially in patients who have a deletion in the rod domain, and that deletion screening of the dystrophin gene might be the only reliable method to diagnose such cases.

  10. A novel break point of the BMPR2 gene exonic deletion in a patient with pulmonary arterial hypertension.

    Science.gov (United States)

    Aimi, Yuki; Hirayama, Tomomi; Kataoka, Masaharu; Momose, Yuichi; Nishimaki, Saiko; Matsushita, Kenichi; Yoshino, Hideaki; Satoh, Toru; Gamou, Shinobu

    2013-12-01

    The presence of genetic rearrangements of bone morphogenetic protein type 2 receptor (BMPR2) was identified in pulmonary arterial hypertension (PAH) patients as the deletion or duplication of one or more exons of the gene. We recently investigated the deletion break points in exonic deletions of BMPR2 in two Japanese familial cases with PAH, and found that these were Alu-mediated via either non-allelic homologous recombination or non-homologous recombination. We herein report the third case of exonic deletion, which was in a 25-year-old female PAH patient with a deletion of BMPR2 exon 3. The break point in this case was not located in an Alu sequence. The 5'- and 3'-break point maps between the inverted Alu sequences in intron 2 and in exon 3, respectively, resulted in a 759-bp deletion. This novel exonic deletion in this PAH case may be a unique and non-recurrent rearrangement, and appears to be of a different size from that in other patients.

  11. 1p36 deletion syndrome: an update

    Directory of Open Access Journals (Sweden)

    Jordan VK

    2015-08-01

    Full Text Available Valerie K Jordan,1 Hitisha P Zaveri,2 Daryl A Scott1,2 1Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX, USA; 2Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA Abstract: Deletions of chromosome 1p36 affect approximately 1 in 5,000 newborns and are the most common terminal deletions in humans. Medical problems commonly caused by terminal deletions of 1p36 include developmental delay, intellectual disability, seizures, vision problems, hearing loss, short stature, distinctive facial features, brain anomalies, orofacial clefting, congenital heart defects, cardiomyopathy, and renal anomalies. Although 1p36 deletion syndrome is considered clinically recognizable, there is significant phenotypic variation among affected individuals. This variation is due, at least in part, to the genetic heterogeneity seen in 1p36 deletions which include terminal and interstitial deletions of varying lengths located throughout the 30 Mb of DNA that comprise chromosome 1p36. Array-based copy number variant analysis can easily identify genomic regions of 1p36 that are deleted in an affected individual. However, predicting the phenotype of an individual based solely on the location and extent of their 1p36 deletion remains a challenge since most of the genes that contribute to 1p36-related phenotypes have yet to be identified. In addition, haploinsufficiency of more than one gene may contribute to some phenotypes. In this article, we review recent successes in the effort to map and identify the genes and genomic regions that contribute to specific 1p36-related phenotypes. In particular, we highlight evidence implicating MMP23B, GABRD, SKI, PRDM16, KCNAB2, RERE, UBE4B, CASZ1, PDPN, SPEN, ECE1, HSPG2, and LUZP1 in various 1p36 deletion phenotypes. Keywords: chromosome 1p36, chromosome deletion, 1p36 deletion syndrome, monosomy 1p36

  12. A novel deletion/insertion caused by a replication error in the β-globin gene locus control region.

    Science.gov (United States)

    Joly, Philippe; Lacan, Philippe; Garcia, Caroline; Meley, Roland; Pondarré, Corinne; Francina, Alain

    2011-01-01

    Deletions in the β-globin locus control region (β-LCR) lead to (εγδβ)(0)-thalassemia [(εγδβ)(0)-thal]. In patients suffering from these rare deletions, a normal hemoglobin (Hb), phenotype is found, contrasting with a hematological thalassemic phenotype. Multiplex-ligation probe amplification (MLPA) is an efficient tool to detect β-LCR deletions combined with long-range polymerase chain reaction (PCR) and DNA sequencing to pinpoint deletion breakpoints. We present here a novel 11,155 bp β-LCR deletion found in a French Caucasian patient which removes DNase I hypersensitive site 2 (HS2) to HS4 of the β-LCR. Interestingly, a 197 bp insertion of two inverted sequences issued from the HS2-HS3 inter-region is present and suggests a complex rearrangement during replication. Carriers of this type of thalassemia can be misdiagnosed as an α-thal trait. Consequently, a complete α- and β-globin gene cluster analysis is required to prevent a potentially damaging misdiagnosis in genetic counselling.

  13. The first Dutch SDHB founder deletion in paraganglioma – pheochromocytoma patients

    Directory of Open Access Journals (Sweden)

    Devilee Peter

    2009-04-01

    Full Text Available Abstract Background Germline mutations of the tumor suppressor genes SDHB, SDHC and SDHD play a major role in hereditary paraganglioma and pheochromocytoma. These three genes encode subunits of succinate dehydrogenase (SDH, the mitochondrial tricarboxylic acid cycle enzyme and complex II component of the electron transport chain. The majority of variants of the SDH genes are missense and nonsense mutations. To date few large deletions of the SDH genes have been described. Methods We carried out gene deletion scanning using MLPA in 126 patients negative for point mutations in the SDH genes. We then proceeded to the molecular characterization of deletions, mapping breakpoints in each patient and used haplotype analysis to determine whether the deletions are due to a mutation hotspot or if a common haplotype indicated a single founder mutation. Results A novel deletion of exon 3 of the SDHB gene was identified in nine apparently unrelated Dutch patients. An identical 7905 bp deletion, c.201-4429_287-933del, was found in all patients, resulting in a frameshift and a predicted truncated protein, p.Cys68HisfsX21. Haplotype analysis demonstrated a common haplotype at the SDHB locus. Index patients presented with pheochromocytoma, extra-adrenal PGL and HN-PGL. A lack of family history was seen in seven of the nine cases. Conclusion The identical exon 3 deletions and common haplotype in nine patients indicates that this mutation is the first Dutch SDHB founder mutation. The predominantly non-familial presentation of these patients strongly suggests reduced penetrance. In this small series HN-PGL occurs as frequently as pheochromocytoma and extra-adrenal PGL.

  14. Becker muscular dystrophy in Indian patients: Analysis of dystrophin gene deletion patterns

    Directory of Open Access Journals (Sweden)

    Dastur Rashna

    2008-01-01

    Full Text Available Background: Becker muscular dystrophy (BMD is caused by mutations in the dystrophin gene with variable phenotypes. Becker muscular dystrophy patients have low levels of nearly full-length dystrophin and carry in-frame mutations, which allow partial functioning of the protein. Aim: To study the deletion patterns of BMD and to correlate the same with reading frame rule and different phenotypes. Setting: A tertiary care teaching hospital. Design: This is a prospective hospital-based study. Materials and Methods: Thirty-two exons spanning different "hot spot" regions using Multiplex PCR techniques were studied in 347 patients. Two hundred and twenty-two showed deletions in one or more of the 32 exons. Out of these, 46 diagnosed as BMD patients were analyzed. Results: Forty-six BMD patients showed deletions in both regions of the dystrophin gene. Out of these 89.1% (41/46 were in-frame deletions. Deletions starting with Exon 45 were found in 76.1% (35/46 of the cases. Mutations in the majority of cases i.e. 39/46 (84.8% were seen in 3′ downstream region (Exon 45-55, distal rod domain. Few, i.e. 5/46 (10.8% showed deletions in 5′ upstream region (Exons 3-20, N-terminus and proximal rod domain of the gene, while in 2/46 (4.4% large mutations (>40 bp spanning both regions (Exons 3-55 were detected. Conclusion: This significant gene deletion analysis has been carried out for BMD patients particularly from Western India using 32 exons.

  15. An atypical case of fragile X syndrome caused by a deletion that includes FMRI gene

    Energy Technology Data Exchange (ETDEWEB)

    Quan, F.; Zonana, J.; Gunter, K.; Peterson, K.L.; Magenis, R.E., Popovich, B.W. [Shriners Hospital for Crippled Children, Portland, OR (United States)

    1995-05-01

    Fragile X syndrome is the most common form of inherited mental retardation and results from the transcriptional inactivation of the FMR1 gene. In the vast majority of cases, this is caused by the expansion of an unstable CGG repeat in the first exon of the FMR1 gene. We describe here a phenotypically atypical case of fragile X syndrome, caused by a deletion that includes the entire FMR1 gene and {ge}9.0 Mb of flanking DNA. The proband, RK, was a 6-year-old mentally retarded male with obesity and anal atresia. A diagnosis of fragile X syndrome was established by the failure of RK`s DNA to hybridize to a 558-bp PstI-XhoI fragment (pfxa3) specific for the 5{prime}-end of the FMR1 gene. The analysis of flanking markers in the interval from Xq26.3-q28 indicated a deletion extending from between 160-500 kb distal and 9.0 Mb proximal to the FMR1 gene. High-resolution chromosome banding confirmed a deletion with breakpoints in Xq26.3 and Xq27.3. This deletion was maternally transmitted and arose as a new mutation on the grandpaternal X chromosome. The maternal transmission of the deletion was confirmed by FISH using a 34-kb cosmid (c31.4) containing most of the FMR1 gene. These results indicated that RK carried a deletion of the FMR1 region with the most proximal breakpoint described to date. This patient`s unusual clinical presentation may indicate the presence of genes located in the deleted interval proximal to the FMR1 locus that are able to modify the fragile X syndrome phenotype. 36 refs., 7 figs.

  16. Factor IX[sub Madrid 2]: A deletion/insertion in Facotr IX gene which abolishes the sequence of the donor junction at the exon IV-intron d splice site

    Energy Technology Data Exchange (ETDEWEB)

    Solera, J. (Unidades de Genetica Molecular, Madrid (Spain)); Magallon, M.; Martin-Villar, J. (Hemofilia Hospital, Madrid (Spain)); Coloma, A. (Departamento deBioquimica de la Facultad de Medicina de la Universidad Autonoma, Madrid (Spain))

    1992-02-01

    DNA from a patient with severe hemophilia B was evaluated by RFLP analysis, producing results which suggested the existence of a partial deletion within the factor IX gene. The deletion was further localized and characterized by PCR amplification and sequencing. The altered allele has a 4,442-bp deletion which removes both the donor splice site located at the 5[prime] end of intron d and the two last coding nucleotides located at the 3[prime] end of exon IV in the normal factor IX gene; this fragment has been inserted in inverted orientation. Two homologous sequences have been discovered at the ends of the deleted DNA fragment.

  17. Hereditary vitamin D resistant rickets due to deletion of exon 3 of the vitamin D receptor

    Energy Technology Data Exchange (ETDEWEB)

    Rut, A.R.; O`Riordan, J.L.H.; Hughes, M.R. [Baylor College of Medicine, Houston, TX (United States)

    1994-09-01

    Hereditary vitamin D resistant rickets is an autosomal recessive disorder characterized by severe rickets, hypolcalcaemia, secondary hyperparathyroidism and occasionally, the absence of body hair. The pathological process involves resistance of target tissues to the actions of calcitriol [1,25(OH{sub 2}D{sub 3})], the hormonal form of vitamin D. Calcitriol mediates its actions through a nuclear receptor (VDR) which has been cloned and shown to be a member of the superfamily of steriod/thyroid/retinoic acid receptors. Skin fibroblasts were obtained from a Greek child with characteristic features of the condition. Total RNA was extracted from rapidly dividing cells and reverse transcribed. The coding region was amplified by PCR with primers 31a in the 5{prime} untranslated region and 31b in the 3{prime} untranslated region of the VDR cDNA sequence. The 5{prime} and 3{prime} halves of VDR were further amplified using primers tagged with M13 forward and reverse primer sequences. The whole process was carried out in duplicate starting with RNA. Sequence data was obtained using Taq dye primer cycle sequencing (ABI). Agarose gel electrophoresis revealed that the 5{prime} product was approximately 100 bp shorter than control. This was confirmed by sequencing which demonstrated a 131 bp deletion of the C-terminal part of the DNA binding domain (bases 147-277). Bases 147-277 are coded for by exon 3 and this deletion is bounded by the splice junctions. This is the first report of a deletion in VDR in any patient with vitamin D-resistant rickets. Such a deletion not only removes the second zinc finger but also results in a frameshift that corrupts the remainder of the receptor. Such a deletion may have arisen as a result of a microdeletion of genomic DNA or, more likely, as a result of defective splicing.

  18. Amelogenesis imperfecta in two families with defined AMELX deletions in ARHGAP6.

    Directory of Open Access Journals (Sweden)

    Jan C-C Hu

    Full Text Available Amelogenesis imperfecta (AI is a group of inherited conditions featuring isolated enamel malformations. About 5% of AI cases show an X-linked pattern of inheritance, which are caused by mutations in AMELX. In humans there are two, non-allelic amelogenin genes: AMELX (Xp22.3 and AMELY (Yp11.2. About 90% of amelogenin expression is from AMELX, which is nested within intron 1 of the gene encoding Rho GTPase activating protein 6 (ARHGAP6. We recruited two AI families and determined that their disease-causing mutations were partial deletions in ARHGAP6 that completely deleted AMELX. Affected males in both families had a distinctive enamel phenotype resembling "snow-capped" teeth. The 96,240 bp deletion in family 1 was confined to intron 1 of ARHGAP6 (g.302534_398773del96240, but removed alternative ARHGAP6 promoters 1c and 1d. Analyses of developing teeth in mice showed that ARHGAP6 is not expressed from these promoters in ameloblasts. The 52,654 bp deletion in family 2 (g.363924_416577del52654insA removed ARHGAP6 promoter 1d and exon 2, precluding normal expression of ARHGAP6. The male proband of family 2 had slightly thinner enamel with greater surface roughness, but exhibited the same pattern of enamel malformations characteristic of males in family 1, which themselves showed minor variations in their enamel phenotypes. We conclude that the enamel defects in both families were caused by amelogenin insufficiency, that deletion of AMELX results in males with a characteristic snow-capped enamel phenotype, and failed ARHGAP6 expression did not appreciably alter the severity of enamel defects when AMELX was absent.

  19. Equipment Design for Oxidation of 1BP/2BP Using NO_x

    Institute of Scientific and Technical Information of China (English)

    ZHOU; Xian-ming; CHANG; Shang-wen; LI; Gao-liang; LAN; Tian; LIU; Jin-ping; TANG; Hong-bin; HE; Hui

    2013-01-01

    NOx can Oxidize the reductants in 1BP and 2BP feed of Purex process,and can adjust the oxidation state of plutonium as Pu(Ⅳ)to meet the need of 2AF feed.Using NOx in Purex process can reduce the volumn of solid waste effectively,and attract more and more interest of researchers.In this work the oxidation of reductants in 1BP/2BP feed were investigated in glass column as the same-current mode,in

  20. Union-Find with Constant Time Deletions

    DEFF Research Database (Denmark)

    Alstrup, Stephen; Thorup, Mikkel; Gørtz, Inge Li;

    2014-01-01

    A union-find data structure maintains a collection of disjoint sets under the operations makeset, union, and find. Kaplan, Shafrir, and Tarjan [SODA 2002] designed data structures for an extension of the union-find problem in which items of the sets maintained may be deleted. The cost of a delete...

  1. The chromosome 9q subtelomere deletion syndrome

    NARCIS (Netherlands)

    Stewart, D.R.; Kleefstra, T.

    2007-01-01

    The chromosome 9q subtelomere deletion syndrome (9qSTDS) is among the first and most common clinically recognizable syndromes to arise from widespread testing by fluorescent in situ hybridization (FISH) of subtelomere deletions. There are about 50 reported cases worldwide. Affected individuals invar

  2. Seven gene deletions in seven days

    DEFF Research Database (Denmark)

    Ingemann Jensen, Sheila; Lennen, Rebecca; Herrgard, Markus;

    2015-01-01

    enables growth at 37 °C, thereby facilitating removal of integrated antibiotic cassettes and deletion of additional genes in the same day. Phosphorothioated primers were demonstrated to enable simultaneous deletions during one round of electroporation. Utilizing these methods, we constructed strains...

  3. Plk1-mediated stabilization of 53BP1 through USP7 regulates centrosome positioning to maintain bipolarity.

    Science.gov (United States)

    Yim, H; Shin, S-B; Woo, S U; Lee, P C-W; Erikson, R L

    2017-02-16

    Although 53BP1 has been established well as a mediator in DNA damage response, its function in mitosis is not clearly understood. We found that 53BP1 is a mitotic-binding partner of the kinases Plk1 and AuroraA, and that the binding with Plk1 increases the stability of 53BP1 by accelerating its interaction with the deubiquitinase USP7. Depletion of 53BP1 induces mitotic defects such as chromosomal missegregation, misorientation of spindle poles and the generation of extra centrosomes, which is similar phenotype to USP7-knockdown cells. In addition, 53BP1 depletion reduces the levels of p53 and centromere protein F (CENPF), interacting proteins of 53BP1. These phenotypes induced by 53BP1 depletion were rescued by expression of wild-type or phosphomimic mutant 53BP1 but not by expression of a dephosphomimic mutant. We propose that phosphorylation of 53BP1 at S380 accelerates complex formation with USP7 and CENPF to regulate their stability, thus having a crucial role in proper centrosome positioning, chromosomal alignment, and centrosome number.

  4. IGF2BP3 Modulates the Interaction of Invasion-Associated Transcripts with RISC

    Directory of Open Access Journals (Sweden)

    Hanane Ennajdaoui

    2016-05-01

    Full Text Available Insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3 expression correlates with malignancy, but its role(s in pathogenesis remains enigmatic. We interrogated the IGF2BP3-RNA interaction network in pancreatic ductal adenocarcinoma (PDAC cells. Using a combination of genome-wide approaches, we have identified 164 direct mRNA targets of IGF2BP3. These transcripts encode proteins enriched for functions such as cell migration, proliferation, and adhesion. Loss of IGF2BP3 reduced PDAC cell invasiveness and remodeled focal adhesion junctions. Individual nucleotide resolution crosslinking immunoprecipitation (iCLIP revealed significant overlap of IGF2BP3 and microRNA (miRNA binding sites. IGF2BP3 promotes association of the RNA-induced silencing complex (RISC with specific transcripts. Our results show that IGF2BP3 influences a malignancy-associated RNA regulon by modulating miRNA-mRNA interactions.

  5. Parental somatic and germ-line mosaicism for a multiexon deletion with unusual endpoints in a type III collagen (COL3Al) allele produces ehlers-danlos syndrome type IV in the heterozygous offspring

    Energy Technology Data Exchange (ETDEWEB)

    McGookey Milewicz, D.; Witz, A.M.; Byers, P.H. (Univ of Washington, Seattle (United States)); Smith, A.C.M.; Manchester, D.K.; Waldstein, G. (Children' s Hospital, Denver, CO (United States))

    1993-07-01

    Ehlers-Danlos syndrome (EDS) type IV is a dominantly inherited disorder that results from mutation in the type III collagen gene (COL3A1). The authors studied the structure of the COL3A1 gene of an individual with EDS type IV and that of her phenotypically normal parents. The proband was heterozygous for a 2-kb deletion in COL3A1, while her father was mosaic for the same deletion in somatic and germ cells. In fibroblasts from the father, approximately two-fifths of the COL3A1 alleles carried the deletion, but only 10% of the COL3A1 alleles in white blood cells were of the mutant species. The deletion in the mutant allele extended from intron 7 into intron 11. There was a 12-bp direct repeat in intron 7 and intron 11, the latter about 60 bp 5' to the junction. At the breakpoint there was a duplication of 10 bp from intron 11 separated by an insertion of 4 bp contained within the duplicated sequence. The father was mosaic for the deletion so that the gene rearrangement occurred during his early embryonic development prior to lineage allocation. These findings suggest that at least some of the deletions seen in human genes may occur during replication, rather than as a consequence of meiotic crossing-over, and that they thus have a risk for recurrence when observed de novo. 71 refs., 4 figs., 2 tabs.

  6. Parental somatic and germ-line mosaicism for a multiexon deletion with unusual endpoints in a type III collagen (COL3A1) allele produces Ehlers-Danlos syndrome type IV in the heterozygous offspring.

    Science.gov (United States)

    Milewicz, D M; Witz, A M; Smith, A C; Manchester, D K; Waldstein, G; Byers, P H

    1993-01-01

    Ehlers-Danlos syndrome (EDS) type IV is a dominantly inherited disorder that results from mutations in the type III collagen gene (COL3A1). We studied the structure of the COL3A1 gene of an individual with EDS type IV and that of her phenotypically normal parents. The proband was heterozygous for a 2-kb deletion in COL3A1, while her father was mosaic for the same deletion in somatic and germ cells. In fibroblasts from the father, approximately two-fifths of the COL3A1 alleles carried the deletion, but only 10% of the COL3A1 alleles in white blood cells were of the mutant species. The deletion in the mutant allele extended from intron 7 into intron 11. There was a 12-bp direct repeat in intron 7 and intron 11, the latter about 60 bp 5' to the junction. At the breakpoint there was a duplication of 10 bp from intron 11 separated by an insertion of 4 bp contained within the duplicated sequence. The father was mosaic for the deletion so that the gene rearrangement occurred during his early embryonic development prior to lineage allocation. These findings suggest that at least some of the deletions seen in human genes may occur during replication, rather than as a consequence of meiotic crossing-over, and that they thus have a risk for recurrence when observed de novo. Images Figure 1 Figure 2 Figure 3 PMID:8317500

  7. Telithromycin resistance in Streptococcus pneumoniae is conferred by a deletion in the leader sequence of erm(B) that increases rRNA methylation

    DEFF Research Database (Denmark)

    Wolter, Nicole; Smith, Anthony M; Farrell, David J

    2008-01-01

    A telithromycin-resistant clinical isolate of Streptococcus pneumoniae (strain P1501016) has been found to contain a version of erm(B) that is altered by a 136-bp deletion in the leader sequence. By allele replacement mutagenesis, a second strain of S. pneumoniae (PC13) with a wild-type erm(B) gene...

  8. BP to Increase Production Capacity of PTA at BP Zhuhai Chemical

    Institute of Scientific and Technical Information of China (English)

    2011-01-01

    BP has announced a strategic plan for its substantial development in China. It is actively proceeding with its project to increase its production capacity of purified terephthalic acid, or PTA, at the BP Zhuhai Chemical Company Limited facility i n Guangdong, China.

  9. 53BP1 regulates DSB repair using Rif1 to control 5' end resection.

    Science.gov (United States)

    Zimmermann, Michal; Lottersberger, Francisca; Buonomo, Sara B; Sfeir, Agnel; de Lange, Titia

    2013-02-08

    The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.

  10. Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days.

    Science.gov (United States)

    John, Kaarthik; Pratt, M Margaret; Beland, Frederick A; Churchwell, Mona I; McMullen, Gail; Olivero, Ofelia A; Pogribny, Igor P; Poirier, Miriam C

    2012-11-01

    We have evaluated DNA damage (DNA adduct formation) after feeding benzo[a]pyrene (BP) to wild-type (WT) and cancer-susceptible Xpa(-/-)p53(+/-) mice deficient in nucleotide excision repair and haploinsufficient for the tumor suppressor p53. DNA damage was evaluated by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC/ES-MS/MS), which measures r7,t8,t9-trihydroxy-c-10-(N (2)-deoxyguanosyl)-7,8,9,10-tetrahydrobenzo[a]pyrene (BPdG), and a chemiluminescence immunoassay (CIA), using anti-r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE)-DNA antiserum, which measures both BPdG and the other stable BP-DNA adducts. When mice were fed 100 ppm BP for 28 days, BP-induced DNA damage measured in esophagus, liver and lung was typically higher in Xpa(-/-)p53(+/-) mice, compared with WT mice. This result is consistent with the previously observed tumor susceptibility of Xpa(-/-)p53(+/-) mice. BPdG, the major DNA adduct associated with tumorigenicity, was the primary DNA adduct formed in esophagus (a target tissue in the mouse), whereas total BP-DNA adducts predominated in higher levels in the liver (a non-target tissue in the mouse). In an attempt to lower BP-induced DNA damage, we fed the WT and Xpa(-/-)p53(+/-) mice 0.3% chlorophyllin (CHL) in the BP-containing diet for 28 days. The addition of CHL resulted in an increase of BP-DNA adducts in esophagus, liver and lung of WT mice, a lowering of BPdG in esophagi of WT mice and livers of Xpa(-/-)p53(+/-) mice and an increase of BPdG in livers of WT mice. Therefore, the addition of CHL to a BP-containing diet showed a lack of consistent chemoprotective effect, indicating that oral CHL administration may not reduce PAH-DNA adduct levels consistently in human organs.

  11. TopBP1 is required at mitosis to reduce transmission of DNA damage to G1 daughter cells.

    Science.gov (United States)

    Pedersen, Rune Troelsgaard; Kruse, Thomas; Nilsson, Jakob; Oestergaard, Vibe H; Lisby, Michael

    2015-08-17

    Genome integrity is critically dependent on timely DNA replication and accurate chromosome segregation. Replication stress delays replication into G2/M, which in turn impairs proper chromosome segregation and inflicts DNA damage on the daughter cells. Here we show that TopBP1 forms foci upon mitotic entry. In early mitosis, TopBP1 marks sites of and promotes unscheduled DNA synthesis. Moreover, TopBP1 is required for focus formation of the structure-selective nuclease and scaffold protein SLX4 in mitosis. Persistent TopBP1 foci transition into 53BP1 nuclear bodies (NBs) in G1 and precise temporal depletion of TopBP1 just before mitotic entry induced formation of 53BP1 NBs in the next cell cycle, showing that TopBP1 acts to reduce transmission of DNA damage to G1 daughter cells. Based on these results, we propose that TopBP1 maintains genome integrity in mitosis by controlling chromatin recruitment of SLX4 and by facilitating unscheduled DNA synthesis.

  12. AcEST: BP919856 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_A02 514 Adiantum capillus-veneris mRNA. clone: YMU001_000130_A02. BP919856 - Show BP91985...is mRNA. clone: YMU001_000130_A02. Accession BP919856 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91985... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919856|Adiantum c

  13. AcEST: BP920173 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H07 454 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H07. BP920173 - Show BP92017...is mRNA. clone: YMU001_000133_H07. Accession BP920173 Tissue type prothallium Developmental stage - Contig I...Res. 25:3389-3402. Query= BP920173|Adiantum capillus-veneris mRNA, clone: YMU001_...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP920173|Adiantum capillus

  14. AcEST: BP921101 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000145_F04 489 Adiantum capillus-veneris mRNA. clone: YMU001_000145_F04. BP921101 - Show BP921101...is mRNA. clone: YMU001_000145_F04. Accession BP921101 Tissue type prothallium Developmental stage - Contig I...se search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921101|Adiantum cap... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921101

  15. AcEST: BP919841 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_G06 496 Adiantum capillus-veneris mRNA. clone: YMU001_000129_G06. BP919841 - Show BP91984...is mRNA. clone: YMU001_000129_G06. Accession BP919841 Tissue type prothallium Developmental stage - Contig I...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919841|Adiantum ca...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919841|Adiantum capi

  16. AcEST: BP920154 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_F09 487 Adiantum capillus-veneris mRNA. clone: YMU001_000133_F09. BP920154 - Show BP92015...is mRNA. clone: YMU001_000133_F09. Accession BP920154 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920154|Adia...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920154|Adiantum

  17. AcEST: BP919887 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C10 511 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C10. BP919887 - Show BP91988...is mRNA. clone: YMU001_000130_C10. Accession BP919887 Tissue type prothallium Developmental stage - Contig I...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91988...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91988

  18. AcEST: BP914001 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000038_G04 493 Adiantum capillus-veneris mRNA. clone: YMU001_000038_G04. BP914001 - Show BP91400...is mRNA. clone: YMU001_000038_G04. Accession BP914001 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914001|...ic Acids Res. 25:3389-3402. Query= BP914001|Adiantum capillus-veneris mRNA, clone

  19. AcEST: BP919212 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E05 508 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E05. BP919212 - Show BP91921...is mRNA. clone: YMU001_000122_E05. Accession BP919212 Tissue type prothallium Developmental stage - Contig I... programs, Nucleic Acids Res. 25:3389-3402. Query= BP919212|Adiantum capillus-ven...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919212|Adiantum capillus-

  20. 2000 Johnston Site 1B-P

    Data.gov (United States)

    US Fish and Wildlife Service, Department of the Interior — Underwater Site 1B-P was established at Johnston Atoll by Dr. James Maragos, U.S. Fish & Wildlife Service, on June 29, 2000. With a start point (meter 0) at...

  1. 2000 Johnston Site 2B-P

    Data.gov (United States)

    US Fish and Wildlife Service, Department of the Interior — Underwater Site 2B-P was established at Johnston Atoll by Dr. James Maragos, U.S. Fish & Wildlife Service, on June 30, 2000. With a start point (meter 0) at...

  2. 2000 Johnston Site 3B-P

    Data.gov (United States)

    US Fish and Wildlife Service, Department of the Interior — Underwater Site 3B-P was established at Johnston Atoll by Dr. James Maragos, U.S. Fish & Wildlife Service, on July 3, 2000. With a start point (meter 0) at...

  3. SCYL1-BP1 affects cell cycle arrest in human hepatocellular carcinoma cells via Cyclin F and RRM2.

    Science.gov (United States)

    Wang, Yang; Zhi, Qiaoming; Ye, Qin; Zhou, Chengyuan; Zhang, Lei; Yan, Wei; Wu, Qun; Zhang, Di; Li, Pu; Huo, Keke

    2016-01-01

    The cell cycle is regulated via important biological mechanisms. Controlled expression of cell cycle regulatory proteins is crucial to maintain cell cycle progression. However, unbalanced protein expression leads to many diseases, such as cancer. Previous research suggests that SCYL1-BP1 function might be related to cell cycle progression and SCYL1-BP1 dysfunction to diseases through undefined mechanisms. In this research, an unbiased yeast two-hybrid screen was used to find protein(s) with potential biological relevance to SCYL1-BP1 function, and a novel interaction was recognized between SCYL1-BP1 and Cyclin F. This interaction was chosen as a paradigm to study SCYL1-BP1 function in cell cycle progression and its possible role in tumorigenesis. We found that SCYL1-BP1 binds to Cyclin F both in vivo and in vitro. SCYL1-BP1 overexpression promoted expression of the CCNF gene and simultaneously delayed Cyclin F protein degradation. SCYL1-BP1 knockdown reduced the expression of endogenous Cyclin F. It was also demonstrated in functional assays that SCYL1-BP1 overexpression induces G2/M arrest in cultured liver cells. Furthermore, SCYL1-BP1 sustained RRM2 protein expression by reducing its ubiquitination. Thus, we propose that SCYL1- BP1 affects the cell cycle through increasing steady state levels of Cyclin F and RRM2 proteins, thus constituting a dual regulatory circuit. This study provides a possible mechanism for SCYL1-BP1-mediated cell cycle regulation and related diseases.

  4. Comparative genome analysis of deleted genes in Shigella flexneri 2a strain 301

    Institute of Scientific and Technical Information of China (English)

    2003-01-01

    Comparative genome analysis is performed between Shigella flexneri 2a strain 301 and its close relatives, the nonpathogenic E. Coli K-12 strain MG1655. Result shows that there are 136 DNA segments whose size is larger than 1000 bp absent from Shigella flexneri 2a strain 301, which is up to 717253 bp in total length. These deleted segments altogether contain 670 open reading frames (ORFs). Prediction of these ORFs indicates that there are 40% genes of unknown function. The other genes of definite functions encode metabolic enzymes, structure proteins, transcription regulatory factors and some elements correlated with horizontal transfer. Here we compare the complete genomic sequences of the two closely related species, which differ in pathogenic phenotype. To our knowledge, this not only reveals the difference of genomic sequence between the two important enteric pathogens for the first time, but also provides valuable clues to further researches in its process of physiological activity, pathogenesis and the evolution of enteric bacteria.

  5. Molecular cytogenetic characterization of an interstitial deletion of chromosome 21 (21q22.13q22.3) in a patient with dysmorphic features, intellectual disability and severe generalized epilepsy.

    Science.gov (United States)

    Valetto, Angelo; Orsini, Alessandro; Bertini, Veronica; Toschi, Benedetta; Bonuccelli, Alice; Simi, Francesca; Sammartino, Irene; Taddeucci, Grazia; Simi, Paolo; Saggese, Giuseppe

    2012-05-01

    We report on a de novo interstitial deletion of chromosome 21q in a patient presenting with characteristic facial features, intellectual disability, and epilepsy. The deletion extent was about 4.9 Mb from position 37713441 bp (21q22.13) to position 42665162 bp (21q22.3) (NCBI36/hg18 map). Patients with partial monosomy 21 are quite rare; this anomaly has been associated with a wide spectrum of clinical signs, ranging from very mild to quite severe phenotypes. This variability results from variability in the deleted regions, thus accurate molecular definition of the chromosomal breakpoints is necessary to make better genotype-phenotype correlations. We compared our patient's phenotype with the few other patients reported in the literature and found to have similar deletion when analyzed by array CGH. The minimal overlapping region contains only two genes, DYRK1A and KCNJ6, which may play a major role in these patients' phenotype.

  6. Heme oxygenase-1 deletion affects stress erythropoiesis.

    Directory of Open Access Journals (Sweden)

    Yu-An Cao

    Full Text Available BACKGROUND: Homeostatic erythropoiesis leads to the formation of mature red blood cells under non-stress conditions, and the production of new erythrocytes occurs as the need arises. In response to environmental stimuli, such as bone marrow transplantation, myelosuppression, or anemia, erythroid progenitors proliferate rapidly in a process referred to as stress erythropoiesis. We have previously demonstrated that heme oxygenase-1 (HO-1 deficiency leads to disrupted stress hematopoiesis. Here, we describe the specific effects of HO-1 deficiency on stress erythropoiesis. METHODOLOGY/PRINCIPAL FINDINGS: We used a transplant model to induce stress conditions. In irradiated recipients that received hmox(+/- or hmox(+/+ bone marrow cells, we evaluated (i the erythrocyte parameters in the peripheral blood; (ii the staining intensity of CD71-, Ter119-, and CD49d-specific surface markers during erythroblast differentiation; (iii the patterns of histological iron staining; and (iv the number of Mac-1(+-cells expressing TNF-α. In the spleens of mice that received hmox(+/- cells, we show (i decreases in the proerythroblast, basophilic, and polychromatophilic erythroblast populations; (ii increases in the insoluble iron levels and decreases in the soluble iron levels; (iii increased numbers of Mac-1(+-cells expressing TNF-α; and (iv decreased levels of CD49d expression in the basophilic and polychromatophilic erythroblast populations. CONCLUSIONS/SIGNIFICANCE: As reflected by effects on secreted and cell surface proteins, HO-1 deletion likely affects stress erythropoiesis through the retention of erythroblasts in the erythroblastic islands of the spleen. Thus, HO-1 may serve as a therapeutic target for controlling erythropoiesis, and the dysregulation of HO-1 may be a predisposing condition for hematologic diseases.

  7. The closure of Pak1-dependent macropinosomes requires the phosphorylation of CtBP1/BARS.

    Science.gov (United States)

    Liberali, Prisca; Kakkonen, Elina; Turacchio, Gabriele; Valente, Carmen; Spaar, Alexander; Perinetti, Giuseppe; Böckmann, Rainer A; Corda, Daniela; Colanzi, Antonino; Marjomaki, Varpu; Luini, Alberto

    2008-04-09

    Membrane fission is an essential process in membrane trafficking and other cellular functions. While many fissioning and trafficking steps are mediated by the large GTPase dynamin, some fission events are dynamin independent and involve C-terminal-binding protein-1/brefeldinA-ADP ribosylated substrate (CtBP1/BARS). To gain an insight into the molecular mechanisms of CtBP1/BARS in fission, we have studied the role of this protein in macropinocytosis, a dynamin-independent endocytic pathway that can be synchronously activated by growth factors. Here, we show that upon activation of the epidermal growth factor receptor, CtBP1/BARS is (a) translocated to the macropinocytic cup and its surrounding membrane, (b) required for the fission of the macropinocytic cup and (c) phosphorylated on a specific serine that is a substrate for p21-activated kinase, with this phosphorylation being essential for the fission of the macropinocytic cup. Importantly, we also show that CtBP1/BARS is required for macropinocytic internalization and infection of echovirus 1. These results provide an insight into the molecular mechanisms of CtBP1/BARS activation in membrane fissioning, and extend the relevance of CtBP1/BARS-induced fission to human viral infection.

  8. CtBP1 associates metabolic syndrome and breast carcinogenesis targeting multiple miRNAs

    Science.gov (United States)

    De Luca, Paola; Dalton, Guillermo N.; Scalise, Georgina D.; Moiola, Cristian P.; Porretti, Juliana; Massillo, Cintia; Kordon, Edith; Gardner, Kevin; Zalazar, Florencia; Flumian, Carolina; Todaro, Laura; Vazquez, Elba S.; Meiss, Roberto; De Siervi, Adriana

    2016-01-01

    Metabolic syndrome (MeS) has been identified as a risk factor for breast cancer. C-terminal binding protein 1 (CtBP1) is a co-repressor of tumor suppressor genes that is activated by low NAD+/NADH ratio. High fat diet (HFD) increases intracellular NADH. We investigated the effect of CtBP1 hyperactivation by HFD intake on mouse breast carcinogenesis. We generated a MeS-like disease in female mice by chronically feeding animals with HFD. MeS increased postnatal mammary gland development and generated prominent duct patterns with markedly increased CtBP1 and Cyclin D1 expression. CtBP1 induced breast cancer cells proliferation. Serum from animals with MeS enriched the stem-like/progenitor cell population from breast cancer cells. CtBP1 increased breast tumor growth in MeS mice modulating multiple genes and miRNA expression implicated in cell proliferation, progenitor cells phenotype, epithelial to mesenchymal transition, mammary development and cell communication in the xenografts. These results define a novel function for CtBP1 in breast carcinogenesis. PMID:26933806

  9. Tyrosine phosphorylation of 3BP2 is indispensable for the interaction with VAV3 in chicken DT40 cells

    Energy Technology Data Exchange (ETDEWEB)

    Chihara, Kazuyasu [Division of Genome Science and Microbiology, Department of Pathological Sciences, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Organization for Life Science Advancement Programs, University of Fukui, Fukui 910-1193 (Japan); Kimura, Yukihiro [Division of Genome Science and Microbiology, Department of Pathological Sciences, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Division of Otorhinolaryngology Head and Neck Surgery, Department of Sensory and Locomotor Medicine, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Honjoh, Chisato [Division of Genome Science and Microbiology, Department of Pathological Sciences, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Third Department of Internal Medicine, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Yamauchi, Shota; Takeuchi, Kenji [Division of Genome Science and Microbiology, Department of Pathological Sciences, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Organization for Life Science Advancement Programs, University of Fukui, Fukui 910-1193 (Japan); Sada, Kiyonao, E-mail: ksada@u-fukui.ac.jp [Division of Genome Science and Microbiology, Department of Pathological Sciences, Faculty of Medical Sciences, Fukui 910-1193 (Japan); Organization for Life Science Advancement Programs, University of Fukui, Fukui 910-1193 (Japan)

    2014-03-10

    Adaptor protein c-Abl SH3 domain-binding protein-2 (3BP2) is known to play regulatory roles in immunoreceptor-mediated signal transduction. We have previously demonstrated that Tyr{sup 174}, Tyr{sup 183} and Tyr{sup 446} in mouse 3BP2 are predominantly phosphorylated by Syk, and the phosphorylation of Tyr{sup 183} and the Src homology 2 (SH2) domain of mouse 3BP2 are critical for B cell receptor (BCR)-induced activation of nuclear factor of activated T cells (NFAT) in human B cells. In this report, we have shown that Syk, but not Abl family protein-tyrosine kinases, is critical for BCR-mediated tyrosine phosphorylation of 3BP2 in chicken DT40 cells. Mutational analysis showed that Tyr{sup 174}, Tyr{sup 183} and Tyr{sup 426} of chicken 3BP2 are the major phosphorylation sites by Syk and the SH2 domain of 3BP2 is critical for tyrosine phosphorylation. In addition, phosphorylation of Tyr{sup 426} is required for the inducible interaction with the SH2 domain of Vav3. Moreover, the expression of the mutant form of 3BP2 in which Tyr{sup 426} was substituted to Phe resulted in the reduction in BCR-mediated Rac1 activation, when compared with the case of wild-type. Altogether, these data suggest that 3BP2 is involved in the activation of Rac1 through the regulation of Vav3 by Syk-dependent phosphorylation of Tyr{sup 426} following BCR stimulation. - Highlights: • 3BP2 is phosphorylated by Syk, but not Abl family kinases in BCR signaling. • Tyr183 and Tyr426 in chicken 3BP2 are the major phosphorylation sites by Syk. • The SH2 domain of 3BP2 is critical for tyrosine phosphorylation of 3BP2. • Phosphorylation of Tyr426 in 3BP2 is required for the inducible binding with Vav3. • 3BP2 is involved in the regulation of BCR-mediated Rac1 activation.

  10. Characterization of large deletions occurring during a single round of retrovirus vector replication: novel deletion mechanism involving errors in strand transfer.

    Science.gov (United States)

    Pulsinelli, G A; Temin, H M

    1991-09-01

    Retroviruses mutate at a high rate during replication. We used a spleen necrosis virus-based vector system and helper cell line to characterize mutations occurring during a single round of retrovirus replication. The vector used, JD216HyNeo, codes for two drug resistance genes, hygromycin resistance (hygro) and neomycin resistance (neo). The downstream neo gene is expressed only when a mutation alleviates a block to splicing which is located in the upstream hygro gene. The mutations allowing splicing were large deletions, ranging in size from about 500 to about 2,000 bp. Most of the mutant proviruses lacked the encapsidation sequence, as shown by our inability to rescue the mutant proviruses with wild-type reticuloendotheliosis virus strain A and confirmed by Southern blotting and direct DNA sequence analysis. We therefore concluded that most of the deletions arose during reverse transcription in the target cell, rather than during transcription in the host cell. The sequence data also indicated that the deletions occurred by at least three different mechanisms: (i) misalignment of the growing point; (ii) incorrect synthesis and termination in the primer-binding sequence during synthesis of the plus-strand strong-stop DNA; and (iii) incorrect synthesis and termination before the primer-binding sequence during synthesis of the plus-strand strong-stop DNA. The second mechanism also led to the incorporation of cellular sequences into the proviral genome, pointing to a potential novel mechanism by which retroviruses can acquire cellular genes.

  11. Association Between the 313 bp Indel in Porcine POU1F1 Gene and Reproduction Traits

    Institute of Scientific and Technical Information of China (English)

    WU Han; SONG Chengyi; GAO Bo; TENG Shanghui; WANG Xiaoyang; LIU Ruoyu; CAI Huifen

    2009-01-01

    The study aims to analyze the distribution of the 313 bp indel (insertion/deletion termed as indel) in first intron of POUIF1 and it's association with reproduction traits in Sutai pigs by using the PCR-DSCP technique. The results showed that in this commercial pig population, the frequency of allele A was 0.6371, B was 0.3629; the genotype frequency of AA was 0.4516, AB was 0.3710, BB was 0.1774, and the X2 test showed that the allele frequencies were in Hardy-Weinberg equilibrium. The SPSS GLM procedure was used to identify the association of the 313 bp indel with reproductive traits. In Sutai pigs, the pigs with AA genotype represented higher value in all reproduction traits, except for higher survival rate of piglets at weaning. Higher weaning weight was significantly associated with AA genotype pigs and higher survival rate of piglets at weaning was significantly associated with BB genotype (P0.05); the P value of different traits affected by fixed factors were not significant as well (P>0.05). The result indicated that although this 313 bp indel was significantly associated with the weaning weight and survival rate at weaning, no any association with major reproduction traits was observed in Sutai pigs.

  12. UbcH7 regulates 53BP1 stability and DSB repair.

    Science.gov (United States)

    Han, Xiangzi; Zhang, Lei; Chung, Jinsil; Mayca Pozo, Franklin; Tran, Amanda; Seachrist, Darcie D; Jacobberger, James W; Keri, Ruth A; Gilmore, Hannah; Zhang, Youwei

    2014-12-09

    DNA double-strand break (DSB) repair is not only key to genome stability but is also an important anticancer target. Through an shRNA library-based screening, we identified ubiquitin-conjugating enzyme H7 (UbcH7, also known as Ube2L3), a ubiquitin E2 enzyme, as a critical player in DSB repair. UbcH7 regulates both the steady-state and replicative stress-induced ubiquitination and proteasome-dependent degradation of the tumor suppressor p53-binding protein 1 (53BP1). Phosphorylation of 53BP1 at the N terminus is involved in the replicative stress-induced 53BP1 degradation. Depletion of UbcH7 stabilizes 53BP1, leading to inhibition of DSB end resection. Therefore, UbcH7-depleted cells display increased nonhomologous end-joining and reduced homologous recombination for DSB repair. Accordingly, UbcH7-depleted cells are sensitive to DNA damage likely because they mainly used the error-prone nonhomologous end-joining pathway to repair DSBs. Our studies reveal a novel layer of regulation of the DSB repair choice and propose an innovative approach to enhance the effect of radiotherapy or chemotherapy through stabilizing 53BP1.

  13. Components of the CtBP1/BARS-dependent fission machinery.

    Science.gov (United States)

    Valente, Carmen; Luini, Alberto; Corda, Daniela

    2013-10-01

    The brefeldin A ADP-ribosylated substrate, a member of the C-terminal-binding protein family that is referred to as CtBP1/BARS, is a dual-function protein that acts as a transcriptional co-repressor in the nucleus and as an inducer of membrane fission in the cytoplasm. In this review, we first discuss the mechanisms that enable CtBP1/BARS to shift between the nuclear transcriptional co-repressor and the cytosolic fission-inducing activities. Then, we focus on the role of CtBP1/BARS in membrane fission. CtBP1/BARS controls several fission events including macropinocytosis, fluid-phase endocytosis, COPI-coated vesicle formation, basolaterally directed post-Golgi carrier formation, and Golgi partitioning in mitosis. We report on recent advances in our understanding of the CtBP1/BARS membrane fission machineries that operate at the trans-side and at the cis-side of the Golgi complex. Specifically, we discuss how these machineries are assembled and regulated, and how they operate in the formation of the basolaterally directed post-Golgi carriers.

  14. Characterization of the Tomato Prosystemin Promoter: Organ-specific Expression, Hormone Specificity and Methyl Jasmonate Responsiveness by Deletion Analysis in Transgenic Tobacco Plants(F)

    Institute of Scientific and Technical Information of China (English)

    Hamlet Avilés-Arnaut; John Paul Délano-Frier

    2012-01-01

    Tomato systemin is a bioactive peptide that regulates the systemic activation of wound-responsive genes.It is released from its 200 amino acid precursor called prosystemin.Initial tissue-localization and hormone-induced expression assays indicated that the tomato prosystemin gene (SIPS) accumulates mainly in floral tissues and in response to exogenous abscisic acid and methyl jasmonate (MeJA)treatments,respectively.Later,the promoter regions of the PS gene in tomato (Solanum lycopersicum L.cv.Castlemart),pepper (Capsicum annuum) and potato (Solanum tuberosum) were isolated and an in silico analysis of the SIPS promoter revealed an over-representation of stress- and MeJA-responsive motifs.A subsequent 5' deletion analysis of the SIPS promoter fused to theβ-glucuronidase reporter (GUS) gene showed that the -221 to +40 bp proximal SIPS promoter region was sufficient to direct the stigma,vascular bundle-specific and MeJA-responsive expression of GUS in transgenic tobacco plants.Important vascular-tissue-specific,light- and MeJA-responsive cis-elements were also present in this region.These findings provide relevant information regarding the transcriptional regulation mechanisms of the SIPS promoter operating in transgenic tobacco plants.They also suggest that its tissue-specificity and inducible nature could have wide applicability in plant biotechnology.

  15. The fragile X phenotype in a mosaic male with a deletion showing expression of the FMR1 protein in 28% of the cells

    Energy Technology Data Exchange (ETDEWEB)

    Graaf, E. de; Vries, B.B.A. de; Willemsen, R. [Erasmus Univ., Rotterdam (Netherlands)] [and others

    1996-08-09

    The instability of the CGG repeat region of FMR1 is not restricted to the CGG repeat but expands to flanking sequences as well. A mosaic fragile X male is reported with a deletion of part of the CGG repeat and 30 bp immediately 3{prime} of the repeat, thus confirming the presence of a hotspot for deletions in the CGG region of FMR1. The deletion, detected in 28% of his lymphocytes, did not impair the transcription and translation of FMR1, suggesting that regulatory elements are not present in the deleted region. The patient has the characteristic fragile X phenotype and assuming that the mosaic pattern detected in the lymphocytes reflects the mosaic pattern in brain, 28% expression of FMRP may not be sufficient for normal cognitive functioning. 43 refs., 3 figs.

  16. Catecholamine metabolism drives generation of mitochondrial DNA deletions in dopaminergic neurons.

    Science.gov (United States)

    Neuhaus, Johannes F G; Baris, Olivier R; Hess, Simon; Moser, Natasha; Schröder, Hannsjörg; Chinta, Shankar J; Andersen, Julie K; Kloppenburg, Peter; Wiesner, Rudolf J

    2014-02-01

    Accumulation of mitochondrial DNA deletions is observed especially in dopaminergic neurons of the substantia nigra during ageing and even more in Parkinson's disease. The resulting mitochondrial dysfunction is suspected to play an important role in neurodegeneration. However, the molecular mechanisms involved in the preferential generation of mitochondrial DNA deletions in dopaminergic neurons are still unknown. To study this phenomenon, we developed novel polymerase chain reaction strategies to detect distinct mitochondrial DNA deletions and monitor their accumulation patterns. Applying these approaches in in vitro and in vivo models, we show that catecholamine metabolism drives the generation and accumulation of these mitochondrial DNA mutations. As in humans, age-related accumulation of mitochondrial DNA deletions is most prominent in dopaminergic areas of mouse brain and even higher in the catecholaminergic adrenal medulla. Dopamine treatment of terminally differentiated neuroblastoma cells, as well as stimulation of dopamine turnover in mice over-expressing monoamine oxidase B both induce multiple mitochondrial DNA deletions. Our results thus identify catecholamine metabolism as the driving force behind mitochondrial DNA deletions, probably being an important factor in the ageing-associated degeneration of dopaminergic neurons.

  17. Detection of classical 17p11.2 deletions, an atypical deletion and RAI1 alterations in patients with features suggestive of Smith-Magenis syndrome.

    Science.gov (United States)

    Vieira, Gustavo H; Rodriguez, Jayson D; Carmona-Mora, Paulina; Cao, Lei; Gamba, Bruno F; Carvalho, Daniel R; de Rezende Duarte, Andréa; Santos, Suely R; de Souza, Deise H; DuPont, Barbara R; Walz, Katherina; Moretti-Ferreira, Danilo; Srivastava, Anand K

    2012-02-01

    Smith-Magenis syndrome (SMS) is a complex disorder whose clinical features include mild to severe intellectual disability with speech delay, growth failure, brachycephaly, flat midface, short broad hands, and behavioral problems. SMS is typically caused by a large deletion on 17p11.2 that encompasses multiple genes including the retinoic acid induced 1, RAI1, gene or a mutation in the RAI1 gene. Here we have evaluated 30 patients with suspected SMS and identified SMS-associated classical 17p11.2 deletions in six patients, an atypical deletion of ~139 kb that partially deletes the RAI1 gene in one patient, and RAI1 gene nonsynonymous alterations of unknown significance in two unrelated patients. The RAI1 mutant proteins showed no significant alterations in molecular weight, subcellular localization and transcriptional activity. Clinical features of patients with or without 17p11.2 deletions and mutations involving the RAI1 gene were compared to identify phenotypes that may be useful in diagnosing patients with SMS.

  18. Water Sampling Data for BP Spill/Deepwater Horizon

    Data.gov (United States)

    U.S. Environmental Protection Agency — The Deepwater Horizon oil spill (also referred to as the BP oil spill) began on 20 April 2010 in the Gulf of Mexico on the BP-operated Macondo Prospect. Following...

  19. Air Monitoring Data for BP Spill/Deepwater Horizon

    Data.gov (United States)

    U.S. Environmental Protection Agency — The Deepwater Horizon oil spill (also referred to as the BP oil spill) began on 20 April 2010 in the Gulf of Mexico on the BP-operated Macondo Prospect. Following...

  20. Waste Sampling Data for BP Spill/Deepwater Horizon

    Data.gov (United States)

    U.S. Environmental Protection Agency — The Deepwater Horizon oil spill (also referred to as the BP oil spill) began on 20 April 2010 in the Gulf of Mexico on the BP-operated Macondo Prospect. Following...

  1. Air Sampling Data for BP Spill/Deepwater Horizon

    Data.gov (United States)

    U.S. Environmental Protection Agency — The Deepwater Horizon oil spill (also referred to as the BP oil spill) began on 20 April 2010 in the Gulf of Mexico on the BP-operated Macondo Prospect. Following...

  2. Sediment Sampling Data for BP Spill/Deepwater Horizon

    Data.gov (United States)

    U.S. Environmental Protection Agency — The Deepwater Horizon oil spill (also referred to as the BP oil spill) began on 20 April 2010 in the Gulf of Mexico on the BP-operated Macondo Prospect. Following...

  3. A novel silent deletion, an insertion mutation and a nonsense mutation in the TCOF1 gene found in two Chinese cases of Treacher Collins syndrome.

    Science.gov (United States)

    Wang, Yan; Yin, Xiao-Juan; Han, Tao; Peng, Wei; Wu, Hong-Lin; Liu, Xin; Feng, Zhi-Chun

    2014-12-01

    Treacher Collins syndrome (TCS) is the most common and well-known craniofacial disorder caused by mutations in the genes involved in pre-rRNA transcription, which include the TCOF1 gene. This study explored the role of TCOF1 mutations in Chinese patients with TCS. Mutational analysis of the TCOF1 gene was performed in three patients using polymerase chain reaction and direct sequencing. Among these three patients, two additional TCOF1 variations, a novel 18 bp deletion and a novel 1 bp insertion mutation, were found in patient 1, together with a novel nonsense mutation (p.Ser476X) and a previously reported 4 bp deletion (c.1872_1875delTGAG) in other patients. Pedigree analysis allowed for prediction of the character of the mutation, which was either pathological or not. The 18 bp deletion of six amino acids, Ser-Asp-Ser-Glu-Glu-Glu (798*803), which was located in the CKII phosphorylation site of treacle, seemed relatively benign for TCS. By contrast, another novel mutation of c.1072_1073insC (p.Gln358ProfsX23) was a frameshift mutation and expected to result in a premature stop codon. This study provides insights into the functional domain of treacle and illustrates the importance of clinical and family TCS screening for the interpretation of novel sequence alterations.

  4. 9q22 Deletion - First Familial Case

    Directory of Open Access Journals (Sweden)

    Yamamoto Toshiyuki

    2011-06-01

    Full Text Available Abstract Background Only 29 cases of constitutional 9q22 deletions have been published and all have been sporadic. Most associate with Gorlin syndrome or nevoid basal cell carcinoma syndrome (NBCCS, MIM #109400 due to haploinsufficiency of the PTCH1 gene (MIM *601309. Methods and Results We report two mentally retarded female siblings and their cognitively normal father, all carrying a similar 5.3 Mb microdeletion at 9q22.2q22.32, detected by array CGH (244 K. The deletion does not involve the PTCH1 gene, but instead 30 other gene,s including the ROR2 gene (MIM *602337 which causing both brachydactyly type 1 (MIM #113000 and Robinow syndrome (MIM #268310, and the immunologically active SYK gene (MIM *600085. The deletion in the father was de novo and FISH analysis of blood lymphocytes did not suggest mosaicism. All three patients share similar mild dysmorphic features with downslanting palpebral fissures, narrow, high bridged nose with small nares, long, deeply grooved philtrum, ears with broad helix and uplifted lobuli, and small toenails. All have significant dysarthria and suffer from continuous middle ear and upper respiratory infections. The father also has a funnel chest and unilateral hypoplastic kidney but the daughters have no malformations. Conclusions This is the first report of a familial constitutional 9q22 deletion and the first deletion studied by array-CGH which does not involve the PTCH1 gene. The phenotype and penetrance are variable and the deletion found in the cognitively normal normal father poses a challenge in genetic counseling.

  5. Deletion 22q13.3 syndrome

    Directory of Open Access Journals (Sweden)

    Phelan Mary C

    2008-05-01

    Full Text Available Abstract The deletion 22q13.3 syndrome (deletion 22q13 syndrome or Phelan-McDermid syndrome is a chromosome microdeletion syndrome characterized by neonatal hypotonia, global developmental delay, normal to accelerated growth, absent to severely delayed speech, and minor dysmorphic features. The deletion occurs with equal frequency in males and females and has been reported in mosaic and non-mosaic forms. Due to lack of clinical recognition and often insufficient laboratory testing, the syndrome is under-diagnosed and its true incidence remains unknown. Common physical traits include long eye lashes, large or unusual ears, relatively large hands, dysplastic toenails, full brow, dolicocephaly, full cheeks, bulbous nose, and pointed chin. Behavior is autistic-like with decreased perception of pain and habitual chewing or mouthing. The loss of 22q13.3 can result from simple deletion, translocation, ring chromosome formation and less common structural changes affecting the long arm of chromosome 22, specifically the region containing the SHANK3 gene. The diagnosis of deletion 22q13 syndrome should be considered in all cases of hypotonia of unknown etiology and in individuals with absent speech. Although the deletion can sometimes be detected by high resolution chromosome analysis, fluorescence in situ hybridization (FISH or array comparative genomic hybridization (CGH is recommended for confirmation. Differential diagnosis includes syndromes associated with hypotonia, developmental delay, speech delay and/or autistic-like affect (Prader-Willi, Angelman, Williams, Smith-Magenis, Fragile X, Sotos, FG, trichorhinophalangeal and velocardiofacial syndromes, autism spectrum disorders, cerebral palsy. Genetic counseling is recommended and parental laboratory studies should be considered to identify cryptic rearrangements and detect parental mosaicism. Prenatal diagnosis should be offered for future pregnancies in those families with inherited rearrangements

  6. AcEST: BP920020 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_B05 91 Adiantum capillus-veneris mRNA. clone: YMU001_000132_B05. BP920020 - Show BP920020... mRNA. clone: YMU001_000132_B05. Accession BP920020 Tissue type prothallium Developmental stage - Contig ID

  7. AcEST: BP919848 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_H02 84 Adiantum capillus-veneris mRNA. clone: YMU001_000129_H02. BP919848 - Show BP91984... mRNA. clone: YMU001_000129_H02. Accession BP919848 Tissue type prothallium Developmental stage - Contig ID

  8. AcEST: BP916868 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000093_A02 72 Adiantum capillus-veneris mRNA. clone: YMU001_000093_A02. BP916868 - Show BP916868... mRNA. clone: YMU001_000093_A02. Accession BP916868 Tissue type prothallium Developmental stage - Contig ID

  9. AcEST: BP915006 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000065_D07 96 Adiantum capillus-veneris mRNA. clone: YMU001_000065_D07. BP915006 - Show BP91500... mRNA. clone: YMU001_000065_D07. Accession BP915006 Tissue type prothallium Developmental stage - Contig ID

  10. AcEST: BP911835 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_G02 27 Adiantum capillus-veneris mRNA. clone: YMU001_000009_G02. BP911835 - Show BP91183... mRNA. clone: YMU001_000009_G02. Accession BP911835 Tissue type prothallium Developmental stage - Contig ID

  11. AcEST: BP911839 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_G06 76 Adiantum capillus-veneris mRNA. clone: YMU001_000009_G06. BP911839 - Show BP91183... mRNA. clone: YMU001_000009_G06. Accession BP911839 Tissue type prothallium Developmental stage - Contig ID

  12. AcEST: BP912001 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_H05 68 Adiantum capillus-veneris mRNA. clone: YMU001_000011_H05. BP912001 - Show BP9120... mRNA. clone: YMU001_000011_H05. Accession BP912001 Tissue type prothallium Developmental stage - Contig ID

  13. AcEST: BP920096 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_H11 24 Adiantum capillus-veneris mRNA. clone: YMU001_000132_H11. BP920096 - Show BP9200... mRNA. clone: YMU001_000132_H11. Accession BP920096 Tissue type prothallium Developmental stage - Contig ID

  14. AcEST: BP917073 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000095_E10 67 Adiantum capillus-veneris mRNA. clone: YMU001_000095_E10. BP917073 - Show BP91707... mRNA. clone: YMU001_000095_E10. Accession BP917073 Tissue type prothallium Developmental stage - Contig ID

  15. AcEST: BP919947 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_A11 35 Adiantum capillus-veneris mRNA. clone: YMU001_000131_A11. BP919947 - Show BP91994... mRNA. clone: YMU001_000131_A11. Accession BP919947 Tissue type prothallium Developmental stage - Contig ID

  16. AcEST: BP915916 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D12 73 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D12. BP915916 - Show BP91591... mRNA. clone: YMU001_000079_D12. Accession BP915916 Tissue type prothallium Developmental stage - Contig ID

  17. Genetic deletion of mPGES-1 accelerates intestinal tumorigenesis in APC(Min/+) mice

    NARCIS (Netherlands)

    Elander, N.; Ungerback, J.; Olsson, H.; Uematsu, S.; Akira, S.; Soderkvist, P.

    2008-01-01

    The induced synthesis of bioactive prostanoids downstream of cyclooxygenase-2 (COX-2) and prostaglandin H(2) (PGH(2)) exerts a critical event in colorectal carcinogenesis. Here we demonstrate that APC(Min/+) mice with genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), which catalys

  18. Familial deletion 18p syndrome: case report

    Directory of Open Access Journals (Sweden)

    Lemyre Emmanuelle

    2006-07-01

    Full Text Available Abstract Background Deletion 18p is a frequent deletion syndrome characterized by dysmorphic features, growth deficiencies, and mental retardation with a poorer verbal performance. Until now, five families have been described with limited clinical description. We report transmission of deletion 18p from a mother to her two daughters and review the previous cases. Case presentation The proband is 12 years old and has short stature, dysmorphic features and moderate mental retardation. Her sister is 9 years old and also has short stature and similar dysmorphic features. Her cognitive performance is within the borderline to mild mental retardation range. The mother also presents short stature. Psychological evaluation showed moderate mental retardation. Chromosome analysis from the sisters and their mother revealed the same chromosomal deletion: 46, XX, del(18(p11.2. Previous familial cases were consistent regarding the transmission of mental retardation. Our family differs in this regard with variable cognitive impairment and does not display poorer verbal than non-verbal abilities. An exclusive maternal transmission is observed throughout those families. Women with del(18p are fertile and seem to have a normal miscarriage rate. Conclusion Genetic counseling for these patients should take into account a greater range of cognitive outcome than previously reported.

  19. AcEST: BP919858 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_A04 328 Adiantum capillus-veneris mRNA. clone: YMU001_000130_A04. BP919858 - Show BP91985...is mRNA. clone: YMU001_000130_A04. Accession BP919858 Tissue type prothallium Developmental stage - Contig I...AST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91985...ation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919858|Adiantum capillu

  20. AcEST: BP919857 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_A03 501 Adiantum capillus-veneris mRNA. clone: YMU001_000130_A03. BP91985...7 CL3173Contig1 Show BP919857 Clone id YMU001_000130_A03 Library YMU01 Length 501 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000130_A03. Accession BP919857 Tissue type prothallium Developmental stag...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91985...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919857|Ad

  1. AcEST: BP919852 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_H07 499 Adiantum capillus-veneris mRNA. clone: YMU001_000129_H07. BP919852 - Show BP91985...is mRNA. clone: YMU001_000129_H07. Accession BP919852 Tissue type prothallium Developmental stage - Contig I..., Nucleic Acids Res. 25:3389-3402. Query= BP919852|Adiantum capillus-veneris mRNA...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919852|Adiantum capillus-veneris mRNA, clo

  2. AcEST: BP911985 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_F08 421 Adiantum capillus-veneris mRNA. clone: YMU001_000011_F08. BP911985 - Show BP911985...is mRNA. clone: YMU001_000011_F08. Accession BP911985 Tissue type prothallium Developmental stage - Contig I...7), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91198...rams, Nucleic Acids Res. 25:3389-3402. Query= BP911985|Adiantum capillus-veneris

  3. AcEST: BP920171 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H05 509 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H05. BP920171 - Show BP92017...is mRNA. clone: YMU001_000133_H05. Accession BP920171 Tissue type prothallium Developmental stage - Contig I...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92017...s. 25:3389-3402. Query= BP920171|Adiantum capillus-veneris mRNA, clone: YMU001_000133_H05. (509 letters) Dat

  4. AcEST: BP912017 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_A11 578 Adiantum capillus-veneris mRNA. clone: YMU001_000012_A11. BP912017... CL1368Contig1 Show BP912017 Clone id YMU001_000012_A11 Library YMU01 Length 578 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000012_A11. Accession BP912017 Tissue type prothallium Developmental stag... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912017|Adiant...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912017|Adiantum capillus-veneris mRNA

  5. AcEST: BP920178 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000134_A02 473 Adiantum capillus-veneris mRNA. clone: YMU001_000134_A02. BP920178 - Show BP92017...is mRNA. clone: YMU001_000134_A02. Accession BP920178 Tissue type prothallium Developmental stage - Contig I...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92017... Res. 25:3389-3402. Query= BP920178|Adiantum capillus-veneris mRNA, clone: YMU001_000134_A02. (473 letters)

  6. AcEST: BP920175 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H09 490 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H09. BP920175 - Show BP92017...is mRNA. clone: YMU001_000133_H09. Accession BP920175 Tissue type prothallium Developmental stage - Contig I...ew generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92017...ew generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920175|Adiantum

  7. AcEST: BP920174 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H08 486 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H08. BP920174 - Show BP92017...is mRNA. clone: YMU001_000133_H08. Accession BP920174 Tissue type prothallium Developmental stage - Contig I... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92017...ped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92017

  8. AcEST: BP913036 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000025_F11 458 Adiantum capillus-veneris mRNA. clone: YMU001_000025_F11. BP913036 - Show BP91303...is mRNA. clone: YMU001_000025_F11. Accession BP913036 Tissue type prothallium Developmental stage - Contig I...25:3389-3402. Query= BP913036|Adiantum capillus-veneris mRNA, clone: YMU001_00002...ped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91303

  9. AcEST: BP913037 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000025_F12 436 Adiantum capillus-veneris mRNA. clone: YMU001_000025_F12. BP913037 - Show BP91303...is mRNA. clone: YMU001_000025_F12. Accession BP913037 Tissue type prothallium Developmental stage - Contig I...T and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91303...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913037|Adiantum capillus-veneris mR

  10. AcEST: BP912303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000017_E02 524 Adiantum capillus-veneris mRNA. clone: YMU001_000017_E02. BP912303 - Show BP912303...is mRNA. clone: YMU001_000017_E02. Accession BP912303 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP912303|Adiantum capillus-veneris mRNA, clone: YMU001_000017_E02. (524 l...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912303|Adiantum capillus-veneris mRNA, clon

  11. AcEST: BP921303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000148_B08 459 Adiantum capillus-veneris mRNA. clone: YMU001_000148_B08. BP921303 - Show BP921303...is mRNA. clone: YMU001_000148_B08. Accession BP921303 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP921303|Adiantum capillus-veneris mRNA, clone: YMU001_000148_B...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921303

  12. AcEST: BP913031 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000025_F06 302 Adiantum capillus-veneris mRNA. clone: YMU001_000025_F06. BP91303...1 CL1500Contig1 Show BP913031 Clone id YMU001_000025_F06 Library YMU01 Length 302 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000025_F06. Accession BP913031 Tissue type prothallium Developmental stag...apped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91303...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91303

  13. AcEST: BP913303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000028_G07 539 Adiantum capillus-veneris mRNA. clone: YMU001_000028_G07. BP913303 - Show BP913303...is mRNA. clone: YMU001_000028_G07. Accession BP913303 Tissue type prothallium Developmental stage - Contig I... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913303...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913303

  14. AcEST: BP914303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_D07 644 Adiantum capillus-veneris mRNA. clone: YMU001_000057_D07. BP914303... CL2270Contig1 Show BP914303 Clone id YMU001_000057_D07 Library YMU01 Length 644 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000057_D07. Accession BP914303 Tissue type prothallium Developmental stag... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914303|Adiantum capillus-veneri...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914303

  15. AcEST: BP913038 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000025_G01 564 Adiantum capillus-veneris mRNA. clone: YMU001_000025_G01. BP91303...8 CL793Contig1 Show BP913038 Clone id YMU001_000025_G01 Library YMU01 Length 564 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000025_G01. Accession BP913038 Tissue type prothallium Developmental stage...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913038|Adiant...Nucleic Acids Res. 25:3389-3402. Query= BP913038|Adiantum capillus-veneris mRNA, clone: YMU001_000025_G01. (

  16. AcEST: BP918303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000111_H04 288 Adiantum capillus-veneris mRNA. clone: YMU001_000111_H04. BP918303 - Show BP918303...is mRNA. clone: YMU001_000111_H04. Accession BP918303 Tissue type prothallium Developmental stage - Contig I... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918303|Adiantum capillus-veneris mRNA, clone: YM...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918303|

  17. AcEST: BP920303 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000135_E01 493 Adiantum capillus-veneris mRNA. clone: YMU001_000135_E01. BP920303 - Show BP920303...is mRNA. clone: YMU001_000135_E01. Accession BP920303 Tissue type prothallium Developmental stage - Contig I...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920303...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920303|Adiantum capillus-

  18. AcEST: BP918043 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A02 493 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A02. BP91804...3 CL3885Contig1 Show BP918043 Clone id YMU001_000109_A02 Library YMU01 Length 493 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000109_A02. Accession BP918043 Tissue type prothallium Developmental stag... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91804...-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91804

  19. AcEST: BP918040 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000108_H10 167 Adiantum capillus-veneris mRNA. clone: YMU001_000108_H10. BP918040 - Show BP91804...is mRNA. clone: YMU001_000108_H10. Accession BP918040 Tissue type prothallium Developmental stage - Contig I...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP918040|Adiantum capillus-veneris mRNA, clone: YMU001.... 25:3389-3402. Query= BP918040|Adiantum capillus-veneris mRNA, clone: YMU001_000108_H10. (167 letters) Data

  20. AcEST: BP911804 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_D03 453 Adiantum capillus-veneris mRNA. clone: YMU001_000009_D03. BP911804... CL245Contig1 Show BP911804 Clone id YMU001_000009_D03 Library YMU01 Length 453 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000009_D03. Accession BP911804 Tissue type prothallium Developmental stage...s Res. 25:3389-3402. Query= BP911804|Adiantum capillus-veneris mRNA, clone: YMU00... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911804|Adiantum capil

  1. AcEST: BP918044 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A03 150 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A03. BP918044 - Show BP91804...is mRNA. clone: YMU001_000109_A03. Accession BP918044 Tissue type prothallium Developmental stage - Contig I...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91804...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918044|Adiantum cap

  2. AcEST: BP918047 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A06 349 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A06. BP91804...7 CL1525Contig1 Show BP918047 Clone id YMU001_000109_A06 Library YMU01 Length 349 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000109_A06. Accession BP918047 Tissue type prothallium Developmental stag...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918047|Adiantum capillus-veneris mRNA...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918047|Adian

  3. AcEST: BP918045 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A04 467 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A04. BP91804...5 CL1689Contig1 Show BP918045 Clone id YMU001_000109_A04 Library YMU01 Length 467 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000109_A04. Accession BP918045 Tissue type prothallium Developmental stag... programs, Nucleic Acids Res. 25:3389-3402. Query= BP918045|Adiantum capillus-ven...grams, Nucleic Acids Res. 25:3389-3402. Query= BP918045|Adiantum capillus-veneris

  4. AcEST: BP918041 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000108_H11 404 Adiantum capillus-veneris mRNA. clone: YMU001_000108_H11. BP918041 - Show BP91804...is mRNA. clone: YMU001_000108_H11. Accession BP918041 Tissue type prothallium Developmental stage - Contig I... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918041|Adiantum c...eic Acids Res. 25:3389-3402. Query= BP918041|Adiantum capillus-veneris mRNA, clone: YMU001_000108_H11. (404

  5. AcEST: BP918048 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A07 409 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A07. BP918048 - Show BP91804...is mRNA. clone: YMU001_000109_A07. Accession BP918048 Tissue type prothallium Developmental stage - Contig I...SI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91804... Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91804

  6. AcEST: BP918046 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A05 481 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A05. BP91804...6 CL10Contig1 Show BP918046 Clone id YMU001_000109_A05 Library YMU01 Length 481 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000109_A05. Accession BP918046 Tissue type prothallium Developmental stage ...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918046|Adi...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918046|Adiantum capillus-v

  7. AcEST: BP918049 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_A08 458 Adiantum capillus-veneris mRNA. clone: YMU001_000109_A08. BP91804...9 CL2636Contig1 Show BP918049 Clone id YMU001_000109_A08 Library YMU01 Length 458 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000109_A08. Accession BP918049 Tissue type prothallium Developmental stag...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918049|Adiantum capill...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918049|Adiantum ca

  8. AcEST: BP921260 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_F02 609 Adiantum capillus-veneris mRNA. clone: YMU001_000147_F02. BP921260 - Show BP921260...is mRNA. clone: YMU001_000147_F02. Accession BP921260 Tissue type prothallium Developmental stage - Contig I...LAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921260...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP921260|Adiantum capillus-vener

  9. AcEST: BP913260 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000028_C08 256 Adiantum capillus-veneris mRNA. clone: YMU001_000028_C08. BP913260 - Show BP913260...is mRNA. clone: YMU001_000028_C08. Accession BP913260 Tissue type prothallium Developmental stage - Contig I...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP913260|Adiantum capillus-veneris mRNA, clone: YMU00...25:3389-3402. Query= BP913260|Adiantum capillus-veneris mRNA, clone: YMU001_000028_C08. (256 letters) Databa

  10. AcEST: BP912607 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_H02 459 Adiantum capillus-veneris mRNA. clone: YMU001_000020_H02. BP912607 - Show BP91260...is mRNA. clone: YMU001_000020_H02. Accession BP912607 Tissue type prothallium Developmental stage - Contig I...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912607|Adiantum capill...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91260

  11. AcEST: BP912604 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_G11 244 Adiantum capillus-veneris mRNA. clone: YMU001_000020_G11. BP912604 - Show BP91260...is mRNA. clone: YMU001_000020_G11. Accession BP912604 Tissue type prothallium Developmental stage - Contig I...s, Nucleic Acids Res. 25:3389-3402. Query= BP912604|Adiantum capillus-veneris mRNA, clone: YMU001_000020_G11...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91260

  12. AcEST: BP919260 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000123_A09 469 Adiantum capillus-veneris mRNA. clone: YMU001_000123_A09. BP919260 - Show BP919260...is mRNA. clone: YMU001_000123_A09. Accession BP919260 Tissue type prothallium Developmental stage - Contig I...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP919260|Adiantum capillu...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919260...ed signal transduction protein OS=Uncultured methanogenic archaeon RC-I GN=UNCMA_12260

  13. AcEST: BP918260 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000111_D07 541 Adiantum capillus-veneris mRNA. clone: YMU001_000111_D07. BP918260 - Show BP918260...is mRNA. clone: YMU001_000111_D07. Accession BP918260 Tissue type prothallium Developmental stage - Contig I...ds Res. 25:3389-3402. Query= BP918260|Adiantum capillus-veneris mRNA, clone: YMU001_000111_D07. (521 letters.... 25:3389-3402. Query= BP918260|Adiantum capillus-veneris mRNA, clone: YMU001_000111_D07. (521 letters) Data

  14. AcEST: BP912605 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_G12 437 Adiantum capillus-veneris mRNA. clone: YMU001_000020_G12. BP91260...5 CL1961Contig1 Show BP912605 Clone id YMU001_000020_G12 Library YMU01 Length 437 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000020_G12. Accession BP912605 Tissue type prothallium Developmental stag... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91260...ams, Nucleic Acids Res. 25:3389-3402. Query= BP912605|Adiantum capillus-veneris mRNA, clone: YMU001_000020_G

  15. AcEST: BP912608 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_H03 451 Adiantum capillus-veneris mRNA. clone: YMU001_000020_H03. BP912608 - Show BP91260...is mRNA. clone: YMU001_000020_H03. Accession BP912608 Tissue type prothallium Developmental stage - Contig I...Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91260...programs, Nucleic Acids Res. 25:3389-3402. Query= BP912608|Adiantum capillus-veneris mRNA, clone: YMU001_000

  16. AcEST: BP916260 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000085_C09 277 Adiantum capillus-veneris mRNA. clone: YMU001_000085_C09. BP916260 - Show BP916260...is mRNA. clone: YMU001_000085_C09. Accession BP916260 Tissue type prothallium Developmental stage - Contig I...of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916260|Adiantum capillus-vene...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916260

  17. AcEST: BP912600 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_G07 375 Adiantum capillus-veneris mRNA. clone: YMU001_000020_G07. BP91260...0 CL1497Contig1 Show BP912600 Clone id YMU001_000020_G07 Library YMU01 Length 375 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000020_G07. Accession BP912600 Tissue type prothallium Developmental stag...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912600|Adiantum capillus-vener...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912600|Adiantum capillus-vener

  18. AcEST: BP912601 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000020_G08 479 Adiantum capillus-veneris mRNA. clone: YMU001_000020_G08. BP912601 - Show BP91260...is mRNA. clone: YMU001_000020_G08. Accession BP912601 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP912601|Adiantum capillus-veneris m...ids Res. 25:3389-3402. Query= BP912601|Adiantum capillus-veneris mRNA, clone: YMU...SG-DTEDIHYQTITGLRKDLSGPSQEPSILTEQAIEDDSED 415 Query: 298 FLPVKANDQADDE 260 +++D +D E Sbjct: 416 SSSTESSDDSDT

  19. AcEST: BP919845 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_G11 376 Adiantum capillus-veneris mRNA. clone: YMU001_000129_G11. BP919845 - Show BP91984...is mRNA. clone: YMU001_000129_G11. Accession BP919845 Tissue type prothallium Developmental stage - Contig I...ms, Nucleic Acids Res. 25:3389-3402. Query= BP919845|Adiantum capillus-veneris mRNA, clone: YMU001_000129_G1...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919845|Adiantum capillus

  20. AcEST: BP919847 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_H01 512 Adiantum capillus-veneris mRNA. clone: YMU001_000129_H01. BP919847 - Show BP91984...is mRNA. clone: YMU001_000129_H01. Accession BP919847 Tissue type prothallium Developmental stage - Contig I... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91984...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP919847|Adiantum capillus-veneris mRNA, clone: YMU0

  1. AcEST: BP919849 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_H04 454 Adiantum capillus-veneris mRNA. clone: YMU001_000129_H04. BP919849 - Show BP91984...is mRNA. clone: YMU001_000129_H04. Accession BP919849 Tissue type prothallium Developmental stage - Contig I...s. 25:3389-3402. Query= BP919849|Adiantum capillus-veneris mRNA, clone: YMU001_00...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP919849|Adiantum capillus-veneris mRNA, clone: YMU001_0001

  2. AcEST: BP919842 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_G07 567 Adiantum capillus-veneris mRNA. clone: YMU001_000129_G07. BP919842 - Show BP91984...is mRNA. clone: YMU001_000129_G07. Accession BP919842 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919842|Adiantum capillus-veneris m...c Acids Res. 25:3389-3402. Query= BP919842|Adiantum capillus-veneris mRNA, clone: YMU001_000129_G07. (567 le

  3. AcEST: BP911984 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_F07 566 Adiantum capillus-veneris mRNA. clone: YMU001_000011_F07. BP911984... CL2332Contig1 Show BP911984 Clone id YMU001_000011_F07 Library YMU01 Length 566 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000011_F07. Accession BP911984 Tissue type prothallium Developmental stag...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911984|Adiantum capillus-veneris mR...I-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911984

  4. AcEST: BP919843 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_G09 473 Adiantum capillus-veneris mRNA. clone: YMU001_000129_G09. BP91984...3 CL2697Contig1 Show BP919843 Clone id YMU001_000129_G09 Library YMU01 Length 473 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000129_G09. Accession BP919843 Tissue type prothallium Developmental stag...ein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919843|Ad...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919843|Adiantum capillus-veneris

  5. AcEST: BP919840 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_G05 476 Adiantum capillus-veneris mRNA. clone: YMU001_000129_G05. BP919840 - Show BP91984...is mRNA. clone: YMU001_000129_G05. Accession BP919840 Tissue type prothallium Developmental stage - Contig I...Res. 25:3389-3402. Query= BP919840|Adiantum capillus-veneris mRNA, clone: YMU001_...es. 25:3389-3402. Query= BP919840|Adiantum capillus-veneris mRNA, clone: YMU001_0

  6. AcEST: BP921403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000149_D11 544 Adiantum capillus-veneris mRNA. clone: YMU001_000149_D11. BP921403... CL10Contig1 Show BP921403 Clone id YMU001_000149_D11 Library YMU01 Length 544 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000149_D11. Accession BP921403 Tissue type prothallium Developmental stage ...h programs, Nucleic Acids Res. 25:3389-3402. Query= BP921403|Adiantum capillus-veneris mRNA, clone: YMU001_0...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921403

  7. AcEST: BP914032 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_B03 607 Adiantum capillus-veneris mRNA. clone: YMU001_000039_B03. BP914032 - Show BP91403...is mRNA. clone: YMU001_000039_B03. Accession BP914032 Tissue type prothallium Developmental stage - Contig I...ew generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914032|Adiantum...programs, Nucleic Acids Res. 25:3389-3402. Query= BP914032|Adiantum capillus-veneris mRNA, clone: YMU001_000

  8. AcEST: BP914403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_E06 616 Adiantum capillus-veneris mRNA. clone: YMU001_000058_E06. BP914403 - Show BP914403...is mRNA. clone: YMU001_000058_E06. Accession BP914403 Tissue type prothallium Developmental stage - Contig I...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914403... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914403|Adiantum capillus-veneris mRNA, clone: YM...VEENATMHLPSLILILMKTCLD--PSISGKVTE 219 L D+ W + R +N TMHL ++ LM+ CLD P I+ V E Sbjct: 403

  9. AcEST: BP914034 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_B05 392 Adiantum capillus-veneris mRNA. clone: YMU001_000039_B05. BP91403...4 CL1150Contig1 Show BP914034 Clone id YMU001_000039_B05 Library YMU01 Length 392 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000039_B05. Accession BP914034 Tissue type prothallium Developmental stag...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914034|Adiantum capillus...s Res. 25:3389-3402. Query= BP914034|Adiantum capillus-veneris mRNA, clone: YMU00

  10. AcEST: BP914035 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_B07 572 Adiantum capillus-veneris mRNA. clone: YMU001_000039_B07. BP914035 - Show BP91403...is mRNA. clone: YMU001_000039_B07. Accession BP914035 Tissue type prothallium Developmental stage - Contig I...h programs, Nucleic Acids Res. 25:3389-3402. Query= BP914035|Adiantum capillus-ve... Nucleic Acids Res. 25:3389-3402. Query= BP914035|Adiantum capillus-veneris mRNA, clone: YMU001_000039_B07.

  11. AcEST: BP914037 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_B09 437 Adiantum capillus-veneris mRNA. clone: YMU001_000039_B09. BP914037 - Show BP91403...is mRNA. clone: YMU001_000039_B09. Accession BP914037 Tissue type prothallium Developmental stage - Contig I... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914037|Adia... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914037|Adia

  12. AcEST: BP914039 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_B11 577 Adiantum capillus-veneris mRNA. clone: YMU001_000039_B11. BP91403...9 CL791Contig1 Show BP914039 Clone id YMU001_000039_B11 Library YMU01 Length 577 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000039_B11. Accession BP914039 Tissue type prothallium Developmental stage... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914039|Adiantum capillus-ven...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91403

  13. AcEST: BP914030 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_A12 427 Adiantum capillus-veneris mRNA. clone: YMU001_000039_A12. BP914030 - Show BP91403...is mRNA. clone: YMU001_000039_A12. Accession BP914030 Tissue type prothallium Developmental stage - Contig I...ds Res. 25:3389-3402. Query= BP914030|Adiantum capillus-veneris mRNA, clone: YMU0...WNALISGFTVHLHGDGALQCYEQMRQEGF 403 VSWN +ISG++++ A++ + +M++ Sbjct: 211 WNVMIDGYMRL...ch programs, Nucleic Acids Res. 25:3389-3402. Query= BP914030|Adiantum capillus-v

  14. AcEST: BP916403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000087_C10 523 Adiantum capillus-veneris mRNA. clone: YMU001_000087_C10. BP916403... CL144Contig1 Show BP916403 Clone id YMU001_000087_C10 Library YMU01 Length 523 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000087_C10. Accession BP916403 Tissue type prothallium Developmental stage...ation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916403... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916403|Adiantum c

  15. AcEST: BP919403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_G01 499 Adiantum capillus-veneris mRNA. clone: YMU001_000124_G01. BP919403 - Show BP919403...is mRNA. clone: YMU001_000124_G01. Accession BP919403 Tissue type prothallium Developmental stage - Contig I...s. 25:3389-3402. Query= BP919403|Adiantum capillus-veneris mRNA, clone: YMU001_000124_G01. (499 letters) Dat...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919403

  16. AcEST: BP912403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_F06 462 Adiantum capillus-veneris mRNA. clone: YMU001_000018_F06. BP912403 - Show BP912403...is mRNA. clone: YMU001_000018_F06. Accession BP912403 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP912403|Adiantum capillus-veneris m...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912403|

  17. AcEST: BP915403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000071_B08 567 Adiantum capillus-veneris mRNA. clone: YMU001_000071_B08. BP915403 - Show BP915403...is mRNA. clone: YMU001_000071_B08. Accession BP915403 Tissue type prothallium Developmental stage - Contig I...s. 25:3389-3402. Query= BP915403|Adiantum capillus-veneris mRNA, clone: YMU001_000071_B08. (567 letters) Dat...s, Nucleic Acids Res. 25:3389-3402. Query= BP915403|Adiantum capillus-veneris mRNA, clone: YMU001_000071_B08

  18. AcEST: BP918403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_B03 531 Adiantum capillus-veneris mRNA. clone: YMU001_000113_B03. BP918403 - Show BP918403...is mRNA. clone: YMU001_000113_B03. Accession BP918403 Tissue type prothallium Developmental stage - Contig I...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918403...ucleic Acids Res. 25:3389-3402. Query= BP918403|Adiantum capillus-veneris mRNA, clone: YMU001_000113_B03. (5

  19. AcEST: BP914444 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_A03 493 Adiantum capillus-veneris mRNA. clone: YMU001_000059_A03. BP914444... CL1628Contig1 Show BP914444 Clone id YMU001_000059_A03 Library YMU01 Length 493 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_A03. Accession BP914444 Tissue type prothallium Developmental stag...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914444... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914444|Adiantum capillus-veneri

  20. AcEST: BP915008 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000065_D10 581 Adiantum capillus-veneris mRNA. clone: YMU001_000065_D10. BP915008 - Show BP91500...is mRNA. clone: YMU001_000065_D10. Accession BP915008 Tissue type prothallium Developmental stage - Contig I...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP915008|Adiantum capillus-veneris mRNA, clone: YMU001_0000...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915008|Adiant

  1. AcEST: BP917500 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000101_F01 537 Adiantum capillus-veneris mRNA. clone: YMU001_000101_F01. BP917500 - Show BP917500...is mRNA. clone: YMU001_000101_F01. Accession BP917500 Tissue type prothallium Developmental stage - Contig I...grams, Nucleic Acids Res. 25:3389-3402. Query= BP917500|Adiantum capillus-veneris mRNA, clone: YMU001_000101...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917500|Adiantum capillus-veneris

  2. AcEST: BP915500 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000072_D04 497 Adiantum capillus-veneris mRNA. clone: YMU001_000072_D04. BP915500... CL2883Contig1 Show BP915500 Clone id YMU001_000072_D04 Library YMU01 Length 497 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000072_D04. Accession BP915500 Tissue type prothallium Developmental stag...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915500...programs, Nucleic Acids Res. 25:3389-3402. Query= BP915500|Adiantum capillus-veneris mRNA, clone: YMU001_000

  3. AcEST: BP915002 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000065_D03 491 Adiantum capillus-veneris mRNA. clone: YMU001_000065_D03. BP91500...2 CL2712Contig1 Show BP915002 Clone id YMU001_000065_D03 Library YMU01 Length 491 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000065_D03. Accession BP915002 Tissue type prothallium Developmental stag...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91500...grams, Nucleic Acids Res. 25:3389-3402. Query= BP915002|Adiantum capillus-veneris

  4. AcEST: BP915009 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000065_D11 575 Adiantum capillus-veneris mRNA. clone: YMU001_000065_D11. BP915009 - Show BP91500...is mRNA. clone: YMU001_000065_D11. Accession BP915009 Tissue type prothallium Developmental stage - Contig I...se search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915009|Adiantum capillus-veneris mRNA, clone: ...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915009|

  5. AcEST: BP920500 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000137_G11 581 Adiantum capillus-veneris mRNA. clone: YMU001_000137_G11. BP920500... CL3073Contig1 Show BP920500 Clone id YMU001_000137_G11 Library YMU01 Length 581 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000137_G11. Accession BP920500 Tissue type prothallium Developmental stag...AST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920500...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920500|Adiantum capill

  6. AcEST: BP921010 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_E04 526 Adiantum capillus-veneris mRNA. clone: YMU001_000144_E04. BP921010 - Show BP921010...is mRNA. clone: YMU001_000144_E04. Accession BP921010 Tissue type prothallium Developmental stage - Contig I...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921010|Adiantum capillus-veneris mRNA...programs, Nucleic Acids Res. 25:3389-3402. Query= BP921010|Adiantum capillus-veneris mRNA, clone: YMU001_000...002030-PA (Fragment) OS=Anopheles gambiae GN=AGAP002030 PE=4 SV=4 Length = 2210 S

  7. AcEST: BP915555 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000073_A05 516 Adiantum capillus-veneris mRNA. clone: YMU001_000073_A05. BP915555 - Show BP915555...is mRNA. clone: YMU001_000073_A05. Accession BP915555 Tissue type prothallium Developmental stage - Contig I... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915555... Acids Res. 25:3389-3402. Query= BP915555|Adiantum capillus-veneris mRNA, clone: YMU001_000073_A05. (516 let

  8. AcEST: BP919975 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_E02 472 Adiantum capillus-veneris mRNA. clone: YMU001_000131_E02. BP919975 - Show BP919975...is mRNA. clone: YMU001_000131_E02. Accession BP919975 Tissue type prothallium Developmental stage - Contig I...ids Res. 25:3389-3402. Query= BP919975|Adiantum capillus-veneris mRNA, clone: YMU...cids Res. 25:3389-3402. Query= BP919975|Adiantum capillus-veneris mRNA, clone: YM

  9. AcEST: BP920157 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G01 550 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G01. BP92015...7 CL541Contig1 Show BP920157 Clone id YMU001_000133_G01 Library YMU01 Length 550 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000133_G01. Accession BP920157 Tissue type prothallium Developmental stage...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920157|Adiantum capillus-veneris mRNA,...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920157|Adiantum capillus-veneris

  10. AcEST: BP920152 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_F06 457 Adiantum capillus-veneris mRNA. clone: YMU001_000133_F06. BP920152 - Show BP92015...is mRNA. clone: YMU001_000133_F06. Accession BP920152 Tissue type prothallium Developmental stage - Contig I...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920152|Adiantu...Res. 25:3389-3402. Query= BP920152|Adiantum capillus-veneris mRNA, clone: YMU001_

  11. AcEST: BP920159 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G03 420 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G03. BP920159 - Show BP92015...is mRNA. clone: YMU001_000133_G03. Accession BP920159 Tissue type prothallium Developmental stage - Contig I... Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92015... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92015

  12. AcEST: BP920153 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_F08 540 Adiantum capillus-veneris mRNA. clone: YMU001_000133_F08. BP920153 - Show BP92015...is mRNA. clone: YMU001_000133_F08. Accession BP920153 Tissue type prothallium Developmental stage - Contig I...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920153|Adiantum capillus-veneris mRNA, clone: YMU...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920153|Adiantum capillus-ve

  13. AcEST: BP920156 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_F12 587 Adiantum capillus-veneris mRNA. clone: YMU001_000133_F12. BP92015...6 CL200Contig1 Show BP920156 Clone id YMU001_000133_F12 Library YMU01 Length 587 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000133_F12. Accession BP920156 Tissue type prothallium Developmental stage...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920156...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920156|Adiantum

  14. AcEST: BP920150 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_F04 550 Adiantum capillus-veneris mRNA. clone: YMU001_000133_F04. BP920150 - Show BP92015...is mRNA. clone: YMU001_000133_F04. Accession BP920150 Tissue type prothallium Developmental stage - Contig I...cids Res. 25:3389-3402. Query= BP920150|Adiantum capillus-veneris mRNA, clone: YMU001_000133_F04. (550 lette...c Acids Res. 25:3389-3402. Query= BP920150|Adiantum capillus-veneris mRNA, clone: YMU001_000133_F04. (550 le

  15. AcEST: BP920856 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000142_E09 470 Adiantum capillus-veneris mRNA. clone: YMU001_000142_E09. BP920856... CL4215Contig1 Show BP920856 Clone id YMU001_000142_E09 Library YMU01 Length 470 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000142_E09. Accession BP920856 Tissue type prothallium Developmental stag...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP920856|Adiantum capillus-... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920856|Adiantum capil

  16. AcEST: BP920000 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_G10 490 Adiantum capillus-veneris mRNA. clone: YMU001_000131_G10. BP920000 - Show BP920000...is mRNA. clone: YMU001_000131_G10. Accession BP920000 Tissue type prothallium Developmental stage - Contig I...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920000...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920000|Adiantum capil

  17. AcEST: BP920127 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_D02 541 Adiantum capillus-veneris mRNA. clone: YMU001_000133_D02. BP92012...7 CL3843Contig1 Show BP920127 Clone id YMU001_000133_D02 Library YMU01 Length 541 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000133_D02. Accession BP920127 Tissue type prothallium Developmental stag...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920127|Adiantum capillus-ve... database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920127|Adian

  18. AcEST: BP920124 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_C09 380 Adiantum capillus-veneris mRNA. clone: YMU001_000133_C09. BP920124 - Show BP92012...is mRNA. clone: YMU001_000133_C09. Accession BP920124 Tissue type prothallium Developmental stage - Contig I...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920124|Adiantum capillus-veneris ...ic Acids Res. 25:3389-3402. Query= BP920124|Adiantum capillus-veneris mRNA, clone: YMU001_000133_C09. (380 l

  19. AcEST: BP920120 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_C05 434 Adiantum capillus-veneris mRNA. clone: YMU001_000133_C05. BP920120 - Show BP92012...is mRNA. clone: YMU001_000133_C05. Accession BP920120 Tissue type prothallium Developmental stage - Contig I...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920120|Ad...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920120|

  20. AcEST: BP920125 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_C12 422 Adiantum capillus-veneris mRNA. clone: YMU001_000133_C12. BP920125 - Show BP92012...is mRNA. clone: YMU001_000133_C12. Accession BP920125 Tissue type prothallium Developmental stage - Contig I...nd PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92012...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92012

  1. AcEST: BP918377 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_G07 508 Adiantum capillus-veneris mRNA. clone: YMU001_000112_G07. BP9183...77 CL44Contig1 Show BP918377 Clone id YMU001_000112_G07 Library YMU01 Length 508 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000112_G07. Accession BP918377 Tissue type prothallium Developmental stage ...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918377|Adi

  2. AcEST: BP918324 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_B09 441 Adiantum capillus-veneris mRNA. clone: YMU001_000112_B09. BP918324 - Show BP9183...is mRNA. clone: YMU001_000112_B09. Accession BP918324 Tissue type prothallium Developmental stage - Contig I... PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918324|Adiantum capillus-veneris

  3. AcEST: BP915183 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000067_E04 303 Adiantum capillus-veneris mRNA. clone: YMU001_000067_E04. BP915183 - Show BP915183...is mRNA. clone: YMU001_000067_E04. Accession BP915183 Tissue type prothallium Developmental stage - Contig I...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915183...es. 25:3389-3402. Query= BP915183|Adiantum capillus-veneris mRNA, clone: YMU001_0

  4. AcEST: BP918359 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_E12 553 Adiantum capillus-veneris mRNA. clone: YMU001_000112_E12. BP9183...59 CL3958Contig1 Show BP918359 Clone id YMU001_000112_E12 Library YMU01 Length 553 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000112_E12. Accession BP918359 Tissue type prothallium Developmental stag... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918359|Adiantum capillus-veneri...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918359|Adiantum capillus-veneris mRNA, clone: Y

  5. AcEST: BP921832 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_F10 448 Adiantum capillus-veneris mRNA. clone: YMU001_000154_F10. BP921832 - Show BP92183...is mRNA. clone: YMU001_000154_F10. Accession BP921832 Tissue type prothallium Developmental stage - Contig I..., Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92183...s, Nucleic Acids Res. 25:3389-3402. Query= BP921832|Adiantum capillus-veneris mRNA, clone: YMU001_000154_F10

  6. AcEST: BP918353 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_E05 498 Adiantum capillus-veneris mRNA. clone: YMU001_000112_E05. BP9183...53 CL2530Contig1 Show BP918353 Clone id YMU001_000112_E05 Library YMU01 Length 498 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000112_E05. Accession BP918353 Tissue type prothallium Developmental stag...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP918353|Adiantum capillus-veneris mRNA, clone: YMU00

  7. AcEST: BP918311 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_A08 458 Adiantum capillus-veneris mRNA. clone: YMU001_000112_A08. BP918311 - Show BP9183...is mRNA. clone: YMU001_000112_A08. Accession BP918311 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP918311|Adiantum capillus-veneris mRNA, clone...ams, Nucleic Acids Res. 25:3389-3402. Query= BP918311|Adiantum capillus-veneris m

  8. AcEST: BP919183 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_B10 484 Adiantum capillus-veneris mRNA. clone: YMU001_000122_B10. BP919183 - Show BP919183...is mRNA. clone: YMU001_000122_B10. Accession BP919183 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP919183|Adiantum capillus-veneris m..., Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919183

  9. AcEST: BP921836 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_G02 401 Adiantum capillus-veneris mRNA. clone: YMU001_000154_G02. BP921836 - Show BP92183...is mRNA. clone: YMU001_000154_G02. Accession BP921836 Tissue type prothallium Developmental stage - Contig I...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921836|Adiantum capillus-vener...s. 25:3389-3402. Query= BP921836|Adiantum capillus-veneris mRNA, clone: YMU001_000154_G02. (401 letters) Dat...GWEDVTRNSIGLIHSLEEDGDVGIAFCFRSKPFRCSVTDVEKVPPFEVG 1183 Score = 45.4 bits (106), Expect(2) = 9e-05 Identities

  10. AcEST: BP921837 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_G03 210 Adiantum capillus-veneris mRNA. clone: YMU001_000154_G03. BP921837 - Show BP92183...is mRNA. clone: YMU001_000154_G03. Accession BP921837 Tissue type prothallium Developmental stage - Contig I... Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92183...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP921837|Adiantum capillus-veneris mRNA, clone: YMU0

  11. AcEST: BP918348 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_D12 438 Adiantum capillus-veneris mRNA. clone: YMU001_000112_D12. BP9183...48 CL3952Contig1 Show BP918348 Clone id YMU001_000112_D12 Library YMU01 Length 438 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000112_D12. Accession BP918348 Tissue type prothallium Developmental stag...ds Res. 25:3389-3402. Query= BP918348|Adiantum capillus-veneris mRNA, clone: YMU0...SI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  12. AcEST: BP918328 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_C02 530 Adiantum capillus-veneris mRNA. clone: YMU001_000112_C02. BP918328 - Show BP9183...is mRNA. clone: YMU001_000112_C02. Accession BP918328 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918328|Adiantum capillus-veneris...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918328|Adian

  13. AcEST: BP918368 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_F10 559 Adiantum capillus-veneris mRNA. clone: YMU001_000112_F10. BP918368 - Show BP9183...is mRNA. clone: YMU001_000112_F10. Accession BP918368 Tissue type prothallium Developmental stage - Contig I...rams, Nucleic Acids Res. 25:3389-3402. Query= BP918368|Adiantum capillus-veneris mRNA, clone: YMU001_000112_...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918368

  14. AcEST: BP918339 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_D02 499 Adiantum capillus-veneris mRNA. clone: YMU001_000112_D02. BP918339 - Show BP9183...is mRNA. clone: YMU001_000112_D02. Accession BP918339 Tissue type prothallium Developmental stage - Contig I...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918339|Adiantum capillus-veneris mRNA, c

  15. AcEST: BP918316 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_B01 479 Adiantum capillus-veneris mRNA. clone: YMU001_000112_B01. BP9183...16 CL1887Contig1 Show BP918316 Clone id YMU001_000112_B01 Library YMU01 Length 479 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000112_B01. Accession BP918316 Tissue type prothallium Developmental stag...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918316|Adia...SI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  16. AcEST: BP918333 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_C07 551 Adiantum capillus-veneris mRNA. clone: YMU001_000112_C07. BP918333 - Show BP9183...is mRNA. clone: YMU001_000112_C07. Accession BP918333 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP918333|Adiantum capillus-veneris mRNA, clone: YMU001_000112_C07. (5... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  17. AcEST: BP921830 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_F08 494 Adiantum capillus-veneris mRNA. clone: YMU001_000154_F08. BP92183...0 CL1991Contig1 Show BP921830 Clone id YMU001_000154_F08 Library YMU01 Length 494 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000154_F08. Accession BP921830 Tissue type prothallium Developmental stag... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92183...AST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92183

  18. AcEST: BP918392 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_A02 381 Adiantum capillus-veneris mRNA. clone: YMU001_000113_A02. BP918392 - Show BP9183...is mRNA. clone: YMU001_000113_A02. Accession BP918392 Tissue type prothallium Developmental stage - Contig I...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918392|Adiantum capillus-veneris ...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918392|...TAKLGPNVSISANARIGPGVRLVGCIILDDVEIKEN 355 Query: 183 KCCDNALYHWMEVL-HWKMRQ---EYRESAIMLPNWE*QYLVKMFLCEDEVVVTSC

  19. AcEST: BP918372 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_G02 505 Adiantum capillus-veneris mRNA. clone: YMU001_000112_G02. BP918372 - Show BP9183...is mRNA. clone: YMU001_000112_G02. Accession BP918372 Tissue type prothallium Developmental stage - Contig I...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918372... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918372|Adia

  20. AcEST: BP921833 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_F11 469 Adiantum capillus-veneris mRNA. clone: YMU001_000154_F11. BP921833 - Show BP92183...is mRNA. clone: YMU001_000154_F11. Accession BP921833 Tissue type prothallium Developmental stage - Contig I...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP921833|Adiantum capillus-veneris mRNA, clone: YMU00...), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92183

  1. AcEST: BP918300 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000111_H01 559 Adiantum capillus-veneris mRNA. clone: YMU001_000111_H01. BP918300 - Show BP9183...is mRNA. clone: YMU001_000111_H01. Accession BP918300 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP918300|Adiantum capillus-veneris mRNA, c...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  2. AcEST: BP913183 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000027_D11 553 Adiantum capillus-veneris mRNA. clone: YMU001_000027_D11. BP913183 - Show BP913183...is mRNA. clone: YMU001_000027_D11. Accession BP913183 Tissue type prothallium Developmental stage - Contig I...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913183|Adiantum capillus-veneris ...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913183

  3. AcEST: BP917183 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000097_D01 417 Adiantum capillus-veneris mRNA. clone: YMU001_000097_D01. BP917183 - Show BP917183...is mRNA. clone: YMU001_000097_D01. Accession BP917183 Tissue type prothallium Developmental stage - Contig I... and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917183...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917183|Adiantum capillus-veneris m

  4. AcEST: BP918321 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_B06 529 Adiantum capillus-veneris mRNA. clone: YMU001_000112_B06. BP9183...21 CL638Contig1 Show BP918321 Clone id YMU001_000112_B06 Library YMU01 Length 529 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000112_B06. Accession BP918321 Tissue type prothallium Developmental stage...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918321|Adiantum capillus-veneris mRNA, clo... Acids Res. 25:3389-3402. Query= BP918321|Adiantum capillus-veneris mRNA, clone:

  5. AcEST: BP918357 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_E09 576 Adiantum capillus-veneris mRNA. clone: YMU001_000112_E09. BP918357 - Show BP9183...is mRNA. clone: YMU001_000112_E09. Accession BP918357 Tissue type prothallium Developmental stage - Contig I...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918357|Adiantum capillus-veneris mRNA, c...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP918357|Adiantum capillus

  6. AcEST: BP918319 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_B04 586 Adiantum capillus-veneris mRNA. clone: YMU001_000112_B04. BP918319 - Show BP9183...is mRNA. clone: YMU001_000112_B04. Accession BP918319 Tissue type prothallium Developmental stage - Contig I...ew generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918319|Adiantum...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918319|Adiantu

  7. AcEST: BP918340 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_D03 538 Adiantum capillus-veneris mRNA. clone: YMU001_000112_D03. BP918340 - Show BP9183...is mRNA. clone: YMU001_000112_D03. Accession BP918340 Tissue type prothallium Developmental stage - Contig I...Acids Res. 25:3389-3402. Query= BP918340|Adiantum capillus-veneris mRNA, clone: YMU001_000112_D03. (524 lett... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  8. AcEST: BP918308 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_A05 514 Adiantum capillus-veneris mRNA. clone: YMU001_000112_A05. BP918308 - Show BP9183...is mRNA. clone: YMU001_000112_A05. Accession BP918308 Tissue type prothallium Developmental stage - Contig I...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  9. AcEST: BP918332 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_C06 222 Adiantum capillus-veneris mRNA. clone: YMU001_000112_C06. BP918332 - Show BP9183...is mRNA. clone: YMU001_000112_C06. Accession BP918332 Tissue type prothallium Developmental stage - Contig I...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918332|Adiantum capillus-veneris mRNA, clo

  10. AcEST: BP918364 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_F06 521 Adiantum capillus-veneris mRNA. clone: YMU001_000112_F06. BP918364 - Show BP9183...is mRNA. clone: YMU001_000112_F06. Accession BP918364 Tissue type prothallium Developmental stage - Contig I...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...ENAPVEDNVSHFSQ--------LKDQQPATLCYAPPLSTDDTAEILFTSG 183 Query: 372 TTSDPKGVVSSHRGAYIASLTACPVWGLKEGCIYLWTLPLFH...c Acids Res. 25:3389-3402. Query= BP918364|Adiantum capillus-veneris mRNA, clone:

  11. AcEST: BP918397 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_A08 462 Adiantum capillus-veneris mRNA. clone: YMU001_000113_A08. BP918397 - Show BP9183...is mRNA. clone: YMU001_000113_A08. Accession BP918397 Tissue type prothallium Developmental stage - Contig I...cids Res. 25:3389-3402. Query= BP918397|Adiantum capillus-veneris mRNA, clone: YM...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918397

  12. AcEST: BP918345 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_D08 477 Adiantum capillus-veneris mRNA. clone: YMU001_000112_D08. BP918345 - Show BP9183...is mRNA. clone: YMU001_000112_D08. Accession BP918345 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP918345|Adiantum capillus-veneris mRNA, c... 25:3389-3402. Query= BP918345|Adiantum capillus-veneris mRNA, clone: YMU001_000112_D08. (477 letters) Datab

  13. AcEST: BP918331 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_C05 460 Adiantum capillus-veneris mRNA. clone: YMU001_000112_C05. BP918331 - Show BP9183...is mRNA. clone: YMU001_000112_C05. Accession BP918331 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP918331|Adiantum capillus-veneris mRNA, clone...d PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  14. AcEST: BP918313 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_A10 512 Adiantum capillus-veneris mRNA. clone: YMU001_000112_A10. BP918313 - Show BP9183...is mRNA. clone: YMU001_000112_A10. Accession BP918313 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP918313|Adiantum capillus-veneris mRNA, clone: YMU001_000112_A...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918313|Adiantum capillus-veneris mR

  15. AcEST: BP918396 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_A07 400 Adiantum capillus-veneris mRNA. clone: YMU001_000113_A07. BP918396 - Show BP9183...is mRNA. clone: YMU001_000113_A07. Accession BP918396 Tissue type prothallium Developmental stage - Contig I...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918396|Adiantum capillus-veneris mRNA, clon... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918396|Adiantum c

  16. AcEST: BP918307 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_A04 589 Adiantum capillus-veneris mRNA. clone: YMU001_000112_A04. BP9183...07 CL4210Contig1 Show BP918307 Clone id YMU001_000112_A04 Library YMU01 Length 589 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000112_A04. Accession BP918307 Tissue type prothallium Developmental stag...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918307|Adiantum capi...rams, Nucleic Acids Res. 25:3389-3402. Query= BP918307|Adiantum capillus-veneris

  17. AcEST: BP918375 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_G05 494 Adiantum capillus-veneris mRNA. clone: YMU001_000112_G05. BP918375 - Show BP9183...is mRNA. clone: YMU001_000112_G05. Accession BP918375 Tissue type prothallium Developmental stage - Contig I...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918375|Adiantum capillus-...s, Nucleic Acids Res. 25:3389-3402. Query= BP918375|Adiantum capillus-veneris mRN

  18. AcEST: BP918344 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_D07 527 Adiantum capillus-veneris mRNA. clone: YMU001_000112_D07. BP918344 - Show BP9183...is mRNA. clone: YMU001_000112_D07. Accession BP918344 Tissue type prothallium Developmental stage - Contig I...ew generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...ch programs, Nucleic Acids Res. 25:3389-3402. Query= BP918344|Adiantum capillus-v

  19. AcEST: BP918373 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_G03 522 Adiantum capillus-veneris mRNA. clone: YMU001_000112_G03. BP918373 - Show BP9183...is mRNA. clone: YMU001_000112_G03. Accession BP918373 Tissue type prothallium Developmental stage - Contig I...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183

  20. AcEST: BP918388 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_H09 552 Adiantum capillus-veneris mRNA. clone: YMU001_000112_H09. BP918388 - Show BP9183...is mRNA. clone: YMU001_000112_H09. Accession BP918388 Tissue type prothallium Developmental stage - Contig I... Acids Res. 25:3389-3402. Query= BP918388|Adiantum capillus-veneris mRNA, clone: YMU001_000112_H09. (552 let...eic Acids Res. 25:3389-3402. Query= BP918388|Adiantum capillus-veneris mRNA, clone: YMU001_000112_H09. (552

  1. AcEST: BP920183 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000134_A07 427 Adiantum capillus-veneris mRNA. clone: YMU001_000134_A07. BP920183 - Show BP920183...is mRNA. clone: YMU001_000134_A07. Accession BP920183 Tissue type prothallium Developmental stage - Contig I...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920183...programs, Nucleic Acids Res. 25:3389-3402. Query= BP920183|Adiantum capillus-veneris mRNA, clone: YMU001_000

  2. AcEST: BP918315 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_A12 550 Adiantum capillus-veneris mRNA. clone: YMU001_000112_A12. BP918315 - Show BP9183...is mRNA. clone: YMU001_000112_A12. Accession BP918315 Tissue type prothallium Developmental stage - Contig I...ST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9183...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP918315|Adiantum capillus-veneris mRNA, clone: YMU001_0001

  3. AcEST: BP919570 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000126_F05 404 Adiantum capillus-veneris mRNA. clone: YMU001_000126_F05. BP91957...0 CL2080Contig1 Show BP919570 Clone id YMU001_000126_F05 Library YMU01 Length 404 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000126_F05. Accession BP919570 Tissue type prothallium Developmental stag...ST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919570|A... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919570|Adiantum c

  4. AcEST: BP919578 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000126_G03 472 Adiantum capillus-veneris mRNA. clone: YMU001_000126_G03. BP919578 - Show BP91957...is mRNA. clone: YMU001_000126_G03. Accession BP919578 Tissue type prothallium Developmental stage - Contig I...grams, Nucleic Acids Res. 25:3389-3402. Query= BP919578|Adiantum capillus-veneris...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919578|Adiantum capillus-veneris mRNA, clone: Y

  5. AcEST: BP919577 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000126_G02 494 Adiantum capillus-veneris mRNA. clone: YMU001_000126_G02. BP91957...7 CL2728Contig1 Show BP919577 Clone id YMU001_000126_G02 Library YMU01 Length 494 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000126_G02. Accession BP919577 Tissue type prothallium Developmental stag...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919577|Adiantum capill...Acids Res. 25:3389-3402. Query= BP919577|Adiantum capillus-veneris mRNA, clone: YMU001_000126_G02. (494 lett

  6. AcEST: BP911957 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_C07 599 Adiantum capillus-veneris mRNA. clone: YMU001_000011_C07. BP911957... CL144Contig1 Show BP911957 Clone id YMU001_000011_C07 Library YMU01 Length 599 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000011_C07. Accession BP911957 Tissue type prothallium Developmental stage...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911957|Adiantum capillus-ve... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911957|Adiant

  7. AcEST: BP916000 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000081_G02 533 Adiantum capillus-veneris mRNA. clone: YMU001_000081_G02. BP916000 - Show BP916000...is mRNA. clone: YMU001_000081_G02. Accession BP916000 Tissue type prothallium Developmental stage - Contig I...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916000...s Res. 25:3389-3402. Query= BP916000|Adiantum capillus-veneris mRNA, clone: YMU001_000081_G02. (533 letters)

  8. AcEST: BP912094 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000015_A09 564 Adiantum capillus-veneris mRNA. clone: YMU001_000015_A09. BP9120...94 CL2967Contig1 Show BP912094 Clone id YMU001_000015_A09 Library YMU01 Length 564 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000015_A09. Accession BP912094 Tissue type prothallium Developmental stag... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912094|Adiantum c...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  9. AcEST: BP912057 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_E09 528 Adiantum capillus-veneris mRNA. clone: YMU001_000012_E09. BP9120...57 CL1892Contig1 Show BP912057 Clone id YMU001_000012_E09 Library YMU01 Length 528 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000012_E09. Accession BP912057 Tissue type prothallium Developmental stag...Acids Res. 25:3389-3402. Query= BP912057|Adiantum capillus-veneris mRNA, clone: YMU001_000012_E09. (528 lett... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  10. AcEST: BP921209 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_A04 535 Adiantum capillus-veneris mRNA. clone: YMU001_000147_A04. BP921209 - Show BP92120...is mRNA. clone: YMU001_000147_A04. Accession BP921209 Tissue type prothallium Developmental stage - Contig I...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92120...grams, Nucleic Acids Res. 25:3389-3402. Query= BP921209|Adiantum capillus-veneris mRNA, clone: YMU001_000147

  11. AcEST: BP912061 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_F01 532 Adiantum capillus-veneris mRNA. clone: YMU001_000012_F01. BP912061 - Show BP9120...is mRNA. clone: YMU001_000012_F01. Accession BP912061 Tissue type prothallium Developmental stage - Contig I...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120...d BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  12. AcEST: BP912036 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_C09 555 Adiantum capillus-veneris mRNA. clone: YMU001_000012_C09. BP912036 - Show BP9120...is mRNA. clone: YMU001_000012_C09. Accession BP912036 Tissue type prothallium Developmental stage - Contig I...ms, Nucleic Acids Res. 25:3389-3402. Query= BP912036|Adiantum capillus-veneris mRNA, clone: YMU001_000012_C0... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912036|Adiantum capillus-ven

  13. AcEST: BP912025 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_B09 484 Adiantum capillus-veneris mRNA. clone: YMU001_000012_B09. BP9120...25 CL1441Contig1 Show BP912025 Clone id YMU001_000012_B09 Library YMU01 Length 484 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000012_B09. Accession BP912025 Tissue type prothallium Developmental stag...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  14. AcEST: BP912042 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_D05 541 Adiantum capillus-veneris mRNA. clone: YMU001_000012_D05. BP912042 - Show BP9120...is mRNA. clone: YMU001_000012_D05. Accession BP912042 Tissue type prothallium Developmental stage - Contig I...c Acids Res. 25:3389-3402. Query= BP912042|Adiantum capillus-veneris mRNA, clone: YMU001_000012_D05. (541 le...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912042|Adiantum capil

  15. AcEST: BP921208 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_A03 436 Adiantum capillus-veneris mRNA. clone: YMU001_000147_A03. BP921208 - Show BP92120...is mRNA. clone: YMU001_000147_A03. Accession BP921208 Tissue type prothallium Developmental stage - Contig I..., Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92120... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921208|Adiantum c

  16. AcEST: BP912056 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_E08 538 Adiantum capillus-veneris mRNA. clone: YMU001_000012_E08. BP912056 - Show BP9120...is mRNA. clone: YMU001_000012_E08. Accession BP912056 Tissue type prothallium Developmental stage - Contig I...base search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912056|Adiantum capillus-veneris mRNA, clone... Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  17. AcEST: BP921120 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000146_A02 427 Adiantum capillus-veneris mRNA. clone: YMU001_000146_A02. BP921120 - Show BP921120...is mRNA. clone: YMU001_000146_A02. Accession BP921120 Tissue type prothallium Developmental stage - Contig I... Acids Res. 25:3389-3402. Query= BP921120|Adiantum capillus-veneris mRNA, clone: ...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921120|Adian

  18. AcEST: BP912009 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_A03 561 Adiantum capillus-veneris mRNA. clone: YMU001_000012_A03. BP912009 - Show BP9120...is mRNA. clone: YMU001_000012_A03. Accession BP912009 Tissue type prothallium Developmental stage - Contig I...s, Nucleic Acids Res. 25:3389-3402. Query= BP912009|Adiantum capillus-veneris mRNA, clone: YMU001_000012_A03... database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912009|Adian

  19. AcEST: BP912030 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_C03 525 Adiantum capillus-veneris mRNA. clone: YMU001_000012_C03. BP912030 - Show BP9120...is mRNA. clone: YMU001_000012_C03. Accession BP912030 Tissue type prothallium Developmental stage - Contig I...ein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912030|Ad...cids Res. 25:3389-3402. Query= BP912030|Adiantum capillus-veneris mRNA, clone: YMU001_000012_C03. (513 lette

  20. AcEST: BP912050 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_E01 544 Adiantum capillus-veneris mRNA. clone: YMU001_000012_E01. BP912050 - Show BP9120...is mRNA. clone: YMU001_000012_E01. Accession BP912050 Tissue type prothallium Developmental stage - Contig I...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912050|Adiantum capillus-veneris mRNA, c.... 25:3389-3402. Query= BP912050|Adiantum capillus-veneris mRNA, clone: YMU001_000

  1. AcEST: BP915615 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000073_F08 475 Adiantum capillus-veneris mRNA. clone: YMU001_000073_F08. BP915615... CL3512Contig1 Show BP915615 Clone id YMU001_000073_F08 Library YMU01 Length 475 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000073_F08. Accession BP915615 Tissue type prothallium Developmental stag...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915615|Adiantum capill...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915615|Adiantum capillus-veneris mRNA, clon

  2. AcEST: BP915815 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000077_C11 552 Adiantum capillus-veneris mRNA. clone: YMU001_000077_C11. BP915815... CL3742Contig1 Show BP915815 Clone id YMU001_000077_C11 Library YMU01 Length 552 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000077_C11. Accession BP915815 Tissue type prothallium Developmental stag...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP915815|Adiantum capillus-veneris mRNA, clone: YMU001... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915815|Adiant

  3. AcEST: BP915155 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000067_B08 468 Adiantum capillus-veneris mRNA. clone: YMU001_000067_B08. BP91515...5 CL2592Contig1 Show BP915155 Clone id YMU001_000067_B08 Library YMU01 Length 468 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000067_B08. Accession BP915155 Tissue type prothallium Developmental stag... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915155|Adiantum capillus-ven...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915

  4. AcEST: BP917474 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000101_C07 287 Adiantum capillus-veneris mRNA. clone: YMU001_000101_C07. BP917474... CL2332Contig1 Show BP917474 Clone id YMU001_000101_C07 Library YMU01 Length 287 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000101_C07. Accession BP917474 Tissue type prothallium Developmental stag...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917474|Adiantum capil...ch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917474|Adiantum capillus-veneris mRNA, clone: YMU001_

  5. Analysis list: Irf2bp2 [Chip-atlas[Archive

    Lifescience Database Archive (English)

    Full Text Available Irf2bp2 Blood + mm9 http://dbarchive.biosciencedbc.jp/kyushu-u/mm9/target/Irf2bp2.1....tsv http://dbarchive.biosciencedbc.jp/kyushu-u/mm9/target/Irf2bp2.5.tsv http://dbarchive.biosciencedbc.jp/kyushu-u/mm9/target/Irf...2bp2.10.tsv http://dbarchive.biosciencedbc.jp/kyushu-u/mm9/colo/Irf2bp2.Blood.tsv http://dbarchive.biosciencedbc.jp/kyushu-u/mm9/colo/Blood.gml ...

  6. AcEST: BP921521 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000150_H10 495 Adiantum capillus-veneris mRNA. clone: YMU001_000150_H10. BP921521... CL1722Contig1 Show BP921521 Clone id YMU001_000150_H10 Library YMU01 Length 495 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000150_H10. Accession BP921521 Tissue type prothallium Developmental stag... PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921521...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921521|Adia

  7. AcEST: BP921219 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_B05 600 Adiantum capillus-veneris mRNA. clone: YMU001_000147_B05. BP92121...9 CL3191Contig1 Show BP921219 Clone id YMU001_000147_B05 Library YMU01 Length 600 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000147_B05. Accession BP921219 Tissue type prothallium Developmental stag...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921219|Adiantum capillus-...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92121

  8. AcEST: BP921216 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_B01 347 Adiantum capillus-veneris mRNA. clone: YMU001_000147_B01. BP921216 - Show BP92121...is mRNA. clone: YMU001_000147_B01. Accession BP921216 Tissue type prothallium Developmental stage - Contig I... programs, Nucleic Acids Res. 25:3389-3402. Query= BP921216|Adiantum capillus-veneris mRNA, clone: YMU001_00...tities = 12/32 (37%), Positives = 18/32 (56%) Frame = -1 Query: 116 LLQTLIVTGYISFDEHLHNPHLSKHSALHITK 21 L LI...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92121

  9. AcEST: BP921211 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_A08 189 Adiantum capillus-veneris mRNA. clone: YMU001_000147_A08. BP921211 - Show BP92121...is mRNA. clone: YMU001_000147_A08. Accession BP921211 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921211|Adiantum capillus-veneris... 25:3389-3402. Query= BP921211|Adiantum capillus-veneris mRNA, clone: YMU001_000147_A08. (189 letters) Datab

  10. AcEST: BP921821 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_E10 497 Adiantum capillus-veneris mRNA. clone: YMU001_000154_E10. BP921821 - Show BP921821...is mRNA. clone: YMU001_000154_E10. Accession BP921821 Tissue type prothallium Developmental stage - Contig I...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921821|Adiantum capill...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921821|Adiantum capillus-veneris mRNA, clone: Y...ct: 159 PTSLIQPSIVTSKKEETGIDEIIRGMRDLQIKFAKLEEKGQSPRISTKQKPRLMEGVVHR 218 Query: 237 CIWCDSTDHGRRDC 196 C+WCD+ DH RR+C Sbjct: 21

  11. AcEST: BP921021 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_F03 449 Adiantum capillus-veneris mRNA. clone: YMU001_000144_F03. BP921021... CL4025Contig1 Show BP921021 Clone id YMU001_000144_F03 Library YMU01 Length 449 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000144_F03. Accession BP921021 Tissue type prothallium Developmental stag...Acids Res. 25:3389-3402. Query= BP921021|Adiantum capillus-veneris mRNA, clone: Y...ein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921021|Adiantum capillus-veneris mRN

  12. AcEST: BP915100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000066_E04 551 Adiantum capillus-veneris mRNA. clone: YMU001_000066_E04. BP915100... CL3103Contig1 Show BP915100 Clone id YMU001_000066_E04 Library YMU01 Length 551 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000066_E04. Accession BP915100 Tissue type prothallium Developmental stag...ation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915100|Adiantum capillu...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP915100|Adiantum capillus-veneris mRNA, clone: YMU001

  13. AcEST: BP919100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000121_C03 561 Adiantum capillus-veneris mRNA. clone: YMU001_000121_C03. BP919100 - Show BP919100...is mRNA. clone: YMU001_000121_C03. Accession BP919100 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP919100|Adiantum capillus-veneris mRNA, clone: YMU001_000121_C03. (5...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919100

  14. AcEST: BP921003 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_D08 457 Adiantum capillus-veneris mRNA. clone: YMU001_000144_D08. BP92100...3 CL1992Contig1 Show BP921003 Clone id YMU001_000144_D08 Library YMU01 Length 457 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000144_D08. Accession BP921003 Tissue type prothallium Developmental stag...ds Res. 25:3389-3402. Query= BP921003|Adiantum capillus-veneris mRNA, clone: YMU0...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921003|Adiantum capillus-vener

  15. AcEST: BP921006 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_D12 494 Adiantum capillus-veneris mRNA. clone: YMU001_000144_D12. BP921006 - Show BP92100...is mRNA. clone: YMU001_000144_D12. Accession BP921006 Tissue type prothallium Developmental stage - Contig I...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921006|Adiantum capillus-...ch programs, Nucleic Acids Res. 25:3389-3402. Query= BP921006|Adiantum capillus-veneris mRNA, clone: YMU001_

  16. AcEST: BP917100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000095_H06 514 Adiantum capillus-veneris mRNA. clone: YMU001_000095_H06. BP917100 - Show BP917100...is mRNA. clone: YMU001_000095_H06. Accession BP917100 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917100|... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917100

  17. AcEST: BP921007 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_E01 460 Adiantum capillus-veneris mRNA. clone: YMU001_000144_E01. BP92100...7 CL57Contig1 Show BP921007 Clone id YMU001_000144_E01 Library YMU01 Length 460 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000144_E01. Accession BP921007 Tissue type prothallium Developmental stage ...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921007|Adiantum capill... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921007|Adiantum capillus-veneri

  18. AcEST: BP917432 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000100_G02 450 Adiantum capillus-veneris mRNA. clone: YMU001_000100_G02. BP917432... CL1686Contig1 Show BP917432 Clone id YMU001_000100_G02 Library YMU01 Length 450 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000100_G02. Accession BP917432 Tissue type prothallium Developmental stag...Acids Res. 25:3389-3402. Query= BP917432|Adiantum capillus-veneris mRNA, clone: Y...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917432|Adiantum capillu

  19. AcEST: BP914326 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_F07 599 Adiantum capillus-veneris mRNA. clone: YMU001_000057_F07. BP91432...6 CL274Contig1 Show BP914326 Clone id YMU001_000057_F07 Library YMU01 Length 599 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000057_F07. Accession BP914326 Tissue type prothallium Developmental stage...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914326...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91432

  20. AcEST: BP914321 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_F02 534 Adiantum capillus-veneris mRNA. clone: YMU001_000057_F02. BP914321 - Show BP91432...is mRNA. clone: YMU001_000057_F02. Accession BP914321 Tissue type prothallium Developmental stage - Contig I... 25:3389-3402. Query= BP914321|Adiantum capillus-veneris mRNA, clone: YMU001_000057_F02. (534 letters) Datab...leic Acids Res. 25:3389-3402. Query= BP914321|Adiantum capillus-veneris mRNA, clone: YMU001_000057_F02. (534

  1. AcEST: BP914432 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_G12 488 Adiantum capillus-veneris mRNA. clone: YMU001_000058_G12. BP914432... CL2573Contig1 Show BP914432 Clone id YMU001_000058_G12 Library YMU01 Length 488 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000058_G12. Accession BP914432 Tissue type prothallium Developmental stag...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914432|...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914432|Adiantum ca

  2. AcEST: BP914324 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_F05 457 Adiantum capillus-veneris mRNA. clone: YMU001_000057_F05. BP91432...4 CL2609Contig1 Show BP914324 Clone id YMU001_000057_F05 Library YMU01 Length 457 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000057_F05. Accession BP914324 Tissue type prothallium Developmental stag...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP914324|Adiantum capillus-vener...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91432

  3. AcEST: BP913432 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000030_B10 512 Adiantum capillus-veneris mRNA. clone: YMU001_000030_B10. BP913432 - Show BP913432...is mRNA. clone: YMU001_000030_B10. Accession BP913432 Tissue type prothallium Developmental stage - Contig I...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913432|Adiantum ... TY A +T+C Sbjct: 1417 TTVSPKTYTTATVTQC 1432 >sp|Q6ZRP5|YD019_HUMAN Putative uncharacterized protein FLJ4620...ucleic Acids Res. 25:3389-3402. Query= BP913432|Adiantum capillus-veneris mRNA, clone: YMU001_000030_B10. (5

  4. AcEST: BP914328 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_F09 454 Adiantum capillus-veneris mRNA. clone: YMU001_000057_F09. BP914328 - Show BP91432...is mRNA. clone: YMU001_000057_F09. Accession BP914328 Tissue type prothallium Developmental stage - Contig I...), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91432...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91432

  5. AcEST: BP914320 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000057_F01 393 Adiantum capillus-veneris mRNA. clone: YMU001_000057_F01. BP914320 - Show BP91432...is mRNA. clone: YMU001_000057_F01. Accession BP914320 Tissue type prothallium Developmental stage - Contig I...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914320|Adiantum capillus-veneris mRNA, clone: Y...apped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91432

  6. AcEST: BP920432 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000137_A06 513 Adiantum capillus-veneris mRNA. clone: YMU001_000137_A06. BP920432 - Show BP920432...is mRNA. clone: YMU001_000137_A06. Accession BP920432 Tissue type prothallium Developmental stage - Contig I... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920432...eic Acids Res. 25:3389-3402. Query= BP920432|Adiantum capillus-veneris mRNA, clone: YMU001_000137_A06. (513

  7. AcEST: BP911938 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_A06 103 Adiantum capillus-veneris mRNA. clone: YMU001_000011_A06. BP911938 - Show BP911938...is mRNA. clone: YMU001_000011_A06. Accession BP911938 Tissue type prothallium Developmental stage - Contig I...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911938|Adiantum ca...programs, Nucleic Acids Res. 25:3389-3402. Query= BP911938|Adiantum capillus-veneris mRNA, clone: YMU001_000

  8. AcEST: BP919384 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E05 553 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E05. BP919384 - Show BP91938...is mRNA. clone: YMU001_000124_E05. Accession BP919384 Tissue type prothallium Developmental stage - Contig I... generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91938...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91938

  9. AcEST: BP919381 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E02 515 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E02. BP919381 - Show BP91938...is mRNA. clone: YMU001_000124_E02. Accession BP919381 Tissue type prothallium Developmental stage - Contig I...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91938...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919381|Adiantum capillus-veneris

  10. AcEST: BP919386 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E08 575 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E08. BP919386 - Show BP91938...is mRNA. clone: YMU001_000124_E08. Accession BP919386 Tissue type prothallium Developmental stage - Contig I...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP919386|Adiantum capillus-veneris mRNA, clone: YMU001...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919386|Adiantum capillus-veneris mRNA, clo

  11. AcEST: BP919385 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E07 296 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E07. BP919385 - Show BP91938...is mRNA. clone: YMU001_000124_E07. Accession BP919385 Tissue type prothallium Developmental stage - Contig I...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91938...25:3389-3402. Query= BP919385|Adiantum capillus-veneris mRNA, clone: YMU001_00012...1997), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res.

  12. AcEST: BP919388 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E10 530 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E10. BP919388 - Show BP91938...is mRNA. clone: YMU001_000124_E10. Accession BP919388 Tissue type prothallium Developmental stage - Contig I... Nucleic Acids Res. 25:3389-3402. Query= BP919388|Adiantum capillus-veneris mRNA, clone: YMU001_000124_E10. ...cleic Acids Res. 25:3389-3402. Query= BP919388|Adiantum capillus-veneris mRNA, cl

  13. AcEST: BP919387 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_E09 378 Adiantum capillus-veneris mRNA. clone: YMU001_000124_E09. BP919387 - Show BP91938...is mRNA. clone: YMU001_000124_E09. Accession BP919387 Tissue type prothallium Developmental stage - Contig I...grams, Nucleic Acids Res. 25:3389-3402. Query= BP919387|Adiantum capillus-veneris mRNA, clone: YMU001_000124... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919387|Adia

  14. AcEST: BP920052 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E03 500 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E03. BP92005...2 CL183Contig1 Show BP920052 Clone id YMU001_000132_E03 Library YMU01 Length 500 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000132_E03. Accession BP920052 Tissue type prothallium Developmental stage...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92005...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920052|Adian

  15. AcEST: BP920053 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E04 141 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E04. BP92005...3 CL323Contig1 Show BP920053 Clone id YMU001_000132_E04 Library YMU01 Length 141 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000132_E04. Accession BP920053 Tissue type prothallium Developmental stage... Nucleic Acids Res. 25:3389-3402. Query= BP920053|Adiantum capillus-veneris mRNA,...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920053

  16. AcEST: BP920058 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E09 507 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E09. BP92005...8 CL621Contig1 Show BP920058 Clone id YMU001_000132_E09 Library YMU01 Length 507 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000132_E09. Accession BP920058 Tissue type prothallium Developmental stage... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92005...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920058|Adiantu

  17. AcEST: BP920059 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E10 367 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E10. BP920059 - Show BP92005...is mRNA. clone: YMU001_000132_E10. Accession BP920059 Tissue type prothallium Developmental stage - Contig I...s, Nucleic Acids Res. 25:3389-3402. Query= BP920059|Adiantum capillus-veneris mRNA, clone: YMU001_000132_E10... programs, Nucleic Acids Res. 25:3389-3402. Query= BP920059|Adiantum capillus-veneris mRNA, clone: YMU001_00

  18. AcEST: BP920056 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E07 303 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E07. BP92005...6 CL779Contig1 Show BP920056 Clone id YMU001_000132_E07 Library YMU01 Length 303 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000132_E07. Accession BP920056 Tissue type prothallium Developmental stage... 25:3389-3402. Query= BP920056|Adiantum capillus-veneris mRNA, clone: YMU001_000132_E07. (303 letters) Datab... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92005

  19. AcEST: BP920051 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000132_E02 361 Adiantum capillus-veneris mRNA. clone: YMU001_000132_E02. BP92005...1 CL2821Contig1 Show BP920051 Clone id YMU001_000132_E02 Library YMU01 Length 361 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000132_E02. Accession BP920051 Tissue type prothallium Developmental stag... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920051|Adiant... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92005

  20. AcEST: BP919684 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000127_H09 516 Adiantum capillus-veneris mRNA. clone: YMU001_000127_H09. BP919684 - Show BP91968...is mRNA. clone: YMU001_000127_H09. Accession BP919684 Tissue type prothallium Developmental stage - Contig I...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919684...BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91968

  1. AcEST: BP919685 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000127_H10 544 Adiantum capillus-veneris mRNA. clone: YMU001_000127_H10. BP919685 - Show BP91968...is mRNA. clone: YMU001_000127_H10. Accession BP919685 Tissue type prothallium Developmental stage - Contig I... Res. 25:3389-3402. Query= BP919685|Adiantum capillus-veneris mRNA, clone: YMU001_000127_H10. (544 letters) ...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91968

  2. AcEST: BP919687 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000128_A01 517 Adiantum capillus-veneris mRNA. clone: YMU001_000128_A01. BP919687 - Show BP91968...is mRNA. clone: YMU001_000128_A01. Accession BP919687 Tissue type prothallium Developmental stage - Contig I...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91968...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91968

  3. AcEST: BP919681 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000127_H06 556 Adiantum capillus-veneris mRNA. clone: YMU001_000127_H06. BP919681 - Show BP91968...is mRNA. clone: YMU001_000127_H06. Accession BP919681 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919681|Adiantum capillus-veneris m...ucleic Acids Res. 25:3389-3402. Query= BP919681|Adiantum capillus-veneris mRNA, clone: YMU001_000127_H06. (5

  4. AcEST: BP919683 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000127_H08 545 Adiantum capillus-veneris mRNA. clone: YMU001_000127_H08. BP919683 - Show BP91968...is mRNA. clone: YMU001_000127_H08. Accession BP919683 Tissue type prothallium Developmental stage - Contig I...Acids Res. 25:3389-3402. Query= BP919683|Adiantum capillus-veneris mRNA, clone: YMU001_000127_H08. (545 lett... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919683|Adiantum capillus-veneri

  5. AcEST: BP917220 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000097_G09 125 Adiantum capillus-veneris mRNA. clone: YMU001_000097_G09. BP917220 - Show BP917220...is mRNA. clone: YMU001_000097_G09. Accession BP917220 Tissue type prothallium Developmental stage - Contig I...T and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917220...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917220|Adiantum capillus-veneris

  6. AcEST: BP913220 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000027_G12 489 Adiantum capillus-veneris mRNA. clone: YMU001_000027_G12. BP913220 - Show BP913220...is mRNA. clone: YMU001_000027_G12. Accession BP913220 Tissue type prothallium Developmental stage - Contig I...grams, Nucleic Acids Res. 25:3389-3402. Query= BP913220|Adiantum capillus-veneris...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913220

  7. AcEST: BP915220 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000067_H10 510 Adiantum capillus-veneris mRNA. clone: YMU001_000067_H10. BP915220 - Show BP915220...is mRNA. clone: YMU001_000067_H10. Accession BP915220 Tissue type prothallium Developmental stage - Contig I...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915220...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915220|Adiantum capillus-veneris mRNA, clone: YMU

  8. AcEST: BP921220 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000147_B06 550 Adiantum capillus-veneris mRNA. clone: YMU001_000147_B06. BP921220 - Show BP921220...is mRNA. clone: YMU001_000147_B06. Accession BP921220 Tissue type prothallium Developmental stage - Contig I...base search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921220|Adiantum capillus-veneris mRNA, clone...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921220|Adiantum capillus-veneris mRNA, c

  9. AcEST: BP912209 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000016_D06 540 Adiantum capillus-veneris mRNA. clone: YMU001_000016_D06. BP912209 - Show BP91220...is mRNA. clone: YMU001_000016_D06. Accession BP912209 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912209|Adiantum capillus-veneris... programs, Nucleic Acids Res. 25:3389-3402. Query= BP912209|Adiantum capillus-veneris mRNA, clone: YMU001_00

  10. AcEST: BP912220 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000016_E08 357 Adiantum capillus-veneris mRNA. clone: YMU001_000016_E08. BP912220 - Show BP912220...is mRNA. clone: YMU001_000016_E08. Accession BP912220 Tissue type prothallium Developmental stage - Contig I...), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912220...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912220

  11. AcEST: BP912200 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000016_C08 572 Adiantum capillus-veneris mRNA. clone: YMU001_000016_C08. BP91220...0 CL3270Contig1 Show BP912200 Clone id YMU001_000016_C08 Library YMU01 Length 572 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000016_C08. Accession BP912200 Tissue type prothallium Developmental stag...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912200|Adiantum capillus-veneris mRNA, clo...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP912200|Adiantum capillus-vener

  12. AcEST: BP912206 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000016_D03 484 Adiantum capillus-veneris mRNA. clone: YMU001_000016_D03. BP912206 - Show BP91220...is mRNA. clone: YMU001_000016_D03. Accession BP912206 Tissue type prothallium Developmental stage - Contig I...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912206|Adiantum capi...-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91220

  13. AcEST: BP919883 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C06 445 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C06. BP91988...3 CL74Contig1 Show BP919883 Clone id YMU001_000130_C06 Library YMU01 Length 445 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000130_C06. Accession BP919883 Tissue type prothallium Developmental stage ...s Res. 25:3389-3402. Query= BP919883|Adiantum capillus-veneris mRNA, clone: YMU00...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919883|Adiantum capillus-veneris mRNA, clo

  14. AcEST: BP919888 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C11 410 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C11. BP919888 - Show BP91988...is mRNA. clone: YMU001_000130_C11. Accession BP919888 Tissue type prothallium Developmental stage - Contig I...ation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919888|Adiantum capillu...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919888|Adiantum capillus-

  15. AcEST: BP919885 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C08 326 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C08. BP91988...5 CL2Contig2 Show BP919885 Clone id YMU001_000130_C08 Library YMU01 Length 326 Definition Adiantum capil...lus-veneris mRNA. clone: YMU001_000130_C08. Accession BP919885 Tissue type prothallium Developmental stage -...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP919885|Adiantum capillus-veneris mRNA, clone: YMU001_0001... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91988

  16. AcEST: BP911988 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_F12 484 Adiantum capillus-veneris mRNA. clone: YMU001_000011_F12. BP911988 - Show BP911988...is mRNA. clone: YMU001_000011_F12. Accession BP911988 Tissue type prothallium Developmental stage - Contig I...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP911988|Adiantum capillus...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP911988|Adiantum capillus-veneris mRNA, clone: YMU0

  17. AcEST: BP919881 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C04 528 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C04. BP919881 - Show BP91988...is mRNA. clone: YMU001_000130_C04. Accession BP919881 Tissue type prothallium Developmental stage - Contig I...rams, Nucleic Acids Res. 25:3389-3402. Query= BP919881|Adiantum capillus-veneris mRNA, clone: YMU001_000130_..., Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91988

  18. AcEST: BP919882 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C05 413 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C05. BP919882 - Show BP91988...is mRNA. clone: YMU001_000130_C05. Accession BP919882 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919882|Adiantum capillus-veneris m... Nucleic Acids Res. 25:3389-3402. Query= BP919882|Adiantum capillus-veneris mRNA, clone: YMU001_000130_C05.

  19. AcEST: BP919886 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_C09 570 Adiantum capillus-veneris mRNA. clone: YMU001_000130_C09. BP919886 - Show BP91988...is mRNA. clone: YMU001_000130_C09. Accession BP919886 Tissue type prothallium Developmental stage - Contig I...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919886|Adiantum capillus-vener... Res. 25:3389-3402. Query= BP919886|Adiantum capillus-veneris mRNA, clone: YMU001_000130_C09. (570 letters)

  20. AcEST: BP917072 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000095_E09 516 Adiantum capillus-veneris mRNA. clone: YMU001_000095_E09. BP917072 - Show BP91707...is mRNA. clone: YMU001_000095_E09. Accession BP917072 Tissue type prothallium Developmental stage - Contig I... Acids Res. 25:3389-3402. Query= BP917072|Adiantum capillus-veneris mRNA, clone: YMU001_000095_E09. (516 let...LAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91707