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Sample records for bp deletion induced

  1. Alterations of mtDNA number and 4977 bp deletion induced by ionizing radiation in human peripheral blood

    International Nuclear Information System (INIS)

    Alterations of mitochondria DNA (mtDNA) 4977 bp common deletion (CD) and mtDNA copy number induced by ionizing radiation were observed in human different cell lines and total body irradiation patients. However, only few experiments have evaluated the levels of the CD and mtDNA copy number in human peripheral blood exposed to ionizing radiation till now. The aim of this study is to analyze the mtDNA alterations in irradiated human peripheral blood from healthy donors as well as to explore their feasibility as biomarkers for constructing new biodosimeter. Peripheral blood samples were collected from six healthy donors, and exposed to 60Co gamma ray with the doses of 0 Gy, 1 Gy, 2 Gy, 3 Gy, 4 Gy and 5 Gy. Levels of the CD and mtDNA copy number in irradiated samples after 2h or 24 h incubation were detected using TaqMan real-time PCR, and the CD ratio was calculated. The results showed that the mean of the CD ratio and the CD copy number exhibited a dose-dependent increase 2 h in the dose range from 0-5 Gy, and of the mtDNA copy number significantly increased 24 h in irradiated groups compared with 0 Gy group after irradiation. It indicates that the parameters in human peripheral blood may be considered as molecular biomarkers to applying construction of new biodosimeter. (authors)

  2. Prevalence of the 4977-bp and 4408-bp mitochondrial DNA deletions in mesenteric arteries from patients with colorectal cancer.

    Science.gov (United States)

    Li, Tao; Chen, Gui-Lan; Lan, Huan; Mao, Liang; Zeng, Bo

    2016-09-01

    Mitochondrial DNA (mtDNA) deletions are found in many diseased tissues and lead to impairment of mitochondrial functions. In this study, we found wide presence of the common 4977-bp and a novel 4408-bp deletion in the mtDNA of mesenteric arteries from patients with colorectal cancer. These two deletions were also detected in samples from healthy individuals. The content of mtDNA with the 4977-bp deletion was significantly lower in healthy controls than cancer-associated samples, and there was no significant difference for the 4408-bp deletion between the two groups. These results suggest that mtDNA in blood vessels around cancer cells may be strongly affected by oxidative stress and tend to accumulate more large-scale variations. PMID:26332461

  3. 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...

  4. 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.

  5. 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.

  6. 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...

  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 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

  12. Time-effect relationship of mitochondrial DNA 4977bp deletion in human peripheral blood cell after X ray irradiation

    International Nuclear Information System (INIS)

    To investigate the time-effect of mitochondrial DNA 4977bp deletion in human peripheral blood cells exposed to X ray, human peripheral whole blood samples were collected from two healthy individuals, and exposed to X rays with dose from 0 to 10 Gy. The genomic DNAs were isolated from the whole-blood samples, and the levels of mtDNA 4977bp deletion and copy number of total mtDNA in the DNA samples were detected by Real-time PCR after irradiation at 2, 12, 24, 48 and 72 h, respectively. The results showed that the copy number of mtDNA 4977bp deletion and total mtDNA, and the rates of mtDNA 4977bp deletion increase with incubation time with dose at 5 Gy after irradiation. Moreover, they increased with dose from 0 to 10 Gy after irradiation at 24 h and 72 h, respectively. The results suggested that the levels of mtDNA 4977bp deletion and the copy number of total mtDNA in human peripheral blood cells exposed to X ray were accumulated with incubation time and dose increase, respectively. (authors)

  13. 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).

  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. 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...

  16. A novel 26 bp deletion [HBB: c.20_45del26bp] in exon 1 of the β-globin gene causing β-thalassemia major.

    Science.gov (United States)

    Edison, Eunice S; Venkatesan, Rajkumar S; Govindanattar, Sankari Devi; George, Biju; Shaji, Ramachandran V

    2012-01-01

    Molecular characterization of β-thalassemia (β-thal) is essential in prevention and in understanding the biology of the disease. Deletion mutations are relatively uncommon in β-thal. In this report, we describe a novel 26 bp deletion from codon 6 to codon 14 in the β-globin in a consanguineous family from Tamil Nadu, India. This novel mutation causes a shift in the normal reading frame of the β-globin coding sequence, and consequently, a premature chain termination of translation due to the creation of a stop codon at the position of codon 21. The identification of this novel deletional mutation adds to the repertoire of β-thal mutations in India. PMID:22233277

  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. Radiosensitivity evaluation of human tumor cell lines by detecting 4977 bp deletion in mitochondrial DNA and comet assay

    International Nuclear Information System (INIS)

    Objective: To explore the feasibility of determining radiosensitivity of human tumor cell lines in vitro using the assay of mtDNA 4977 bp deletion and comet assay. Methods: Three human tumor cell lines were selected in this study, HepG2, EC-9706 and MCF-7. The surviving fraction(SF), the ratio of mtDNA 4977 bp deletion and DNA damage were detected by MTY assay, nested PCR technique and comet assay, respectively. Results: The results of MTT assay showed that the radiosensitivity of HepG2 and EC-9706 was higher than that of MCF-7. The ratio of mtDNA 4977 bp deletion of HepG2 and EC-9706 was higher significantly than that of MCF-7 (P2 and EC-9706 was higher than that of MCF-7. The difference of radiosensitivity among these three tumor cell lines was significant after 8 Gy γ-ray irradiation. Conclusions: Combination of many biological parameter is helpful to evaluate the radiosensitivity of tumor cells more accurately. (authors)

  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. PMID:25619305

  20. Association between sHLA-G and HLA-G 14-bp deletion/insertion polymorphism in Crohn's disease.

    Science.gov (United States)

    Zidi, Inès; Ben Yahia, Hamza; Bortolotti, Daria; Mouelhi, Leila; Laaribi, Ahmed Baligh; Ayadi, Shema; Zidi, Nour; Houissa, Fatma; Debbech, Radhouane; Boudabous, Abdellatif; Najjar, Taoufik; Di Luca, Dario; Rizzo, Roberta

    2015-06-01

    The aim of this study was to evaluate the association between the HLA-G 14-bp deletion/insertion (Del/Ins) polymorphism and soluble (s) HLA-G production in patients with Crohn's disease (CD). We analyzed also the sHLA-G molecules by ELISA and western blot in plasma samples. Among unselected patients, the 14-bp Del/Ins polymorphism was not significantly associated with increased CD risk neither for alleles (P = 0.371) nor for genotypes (P = 0.625). However, a significant association was reported between the 14-bp Del/Ins polymorphism and CD, in particular in young-onset CD patients for alleles [P = 0.020, odds ratio (OR) = 2.438, 95% confidence interval (CI): 1.13-5.25] but not with adult-onset CD patients. A significant association was reported concerning the genotype Ins/Ins for young-onset CD patients (P = 0.029, OR = 3.257, 95% CI: 1.08-9.77). We observed also a significant increase in sHLA-G measured by ELISA in CD patients compared to controls (P = 0.002). The 14-bp Del/Del and 14-bp Del/Ins genotypes are the high HLA-G producers. Among sHLA-G(positive) patients, 43% of subjects present dimers of HLA-G. The presence of dimers seems to be related to the advanced stages of the disease. The 14-bp Del/Ins polymorphism is associated with an increased risk of CD particularly in young-onset CD patients and controls sHLA-G plasma levels. Dimers of sHLA-G are frequent in advanced disease stages. The above findings indicate that the genetic 14-bp Del/Ins polymorphism in exon 8 of the HLA-G gene is associated with the risk of CD and suggest a role for sHLA-G as a prognostic marker for progressive disease. PMID:25577194

  1. 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

  2. Mitochondrial DNA control region sequence variation suggests an independent origin of an {open_quotes}Asian-specific{close_quotes} 9-bp deletion in Africans

    Energy Technology Data Exchange (ETDEWEB)

    Soodyall, H.; Redd, A.; Vigilant [Pennsylvania State Univ., Univeristy Park, PA (United States)] [and others

    1994-09-01

    The intergenic noncoding region between the cytochrome oxidase II and lysyl tRNA genes of human mitochondrial DNA (mtDNA) is associated with two tandemly arranged copies of a 9-bp sequence. A deletion of one of these repeats has been found at varying frequencies in populations of Asian descent, and is commonly referred to as an {open_quotes}Asian-specific{close_quotes} marker. We report here that the 9-bp deletion is also found at a frequency of 10.2% (66/649) in some indigenous African populations, with frequencies of 28.6% (20/70) in Pygmies, 26.6% (12/45) in Malawians and 15.4% (31/199) in southeastern Bantu-speaking populations. The deletion was not found in 123 Khoisan individuals nor in 209 western Bantu-speaking individuals, with the exception of 3 individuals from one group that was admixed with Pygmies. Sequence analysis of the two hypervariable segments of the mtDNA control region reveals that the types associated with the African 9-bp deletion are different from those found in Asian-derived populations with the deletion. Phylogenetic analysis separates the {open_quotes}African{close_quotes} and {open_quotes}Asian{close_quotes} 9-bp deletion types into two different clusters which are statistically supported. Mismatch distributions based on the number of differences between pairs of mtDNA types are consistent with this separation. These findings strongly support the view that the 9-bp deletion originated independently in Africa and in Asia.

  3. Genotyping of the 19-bp insertion/deletion polymorphism in the 5' flank of beta-hydroxylase gene by dissociation analysis of allele-specific PCR products

    DEFF Research Database (Denmark)

    Rasmussen, Henrik Berg; Werge, Thomas

    2005-01-01

    The 19-bp insertion/deletion polymorphism in the 5' flank of the dopamine beta-hydroxylase (DBH) gene has been associated with psychiatric disorders. We have developed a simple, reliable and inexpensive closed-tube assay for genotyping of this polymorphism based upon T(m) determination of amplified...

  4. 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...

  5. 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...

  6. 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.

  7. 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.

  8. Blocking rpS6 Phosphorylation Exacerbates Tsc1 Deletion-Induced Kidney Growth.

    Science.gov (United States)

    Wu, Huijuan; Chen, Jianchun; Xu, Jinxian; Dong, Zheng; Meyuhas, Oded; Chen, Jian-Kang

    2016-04-01

    The molecular mechanisms underlying renal growth and renal growth-induced nephron damage remain poorly understood. Here, we report that in murine models, deletion of the tuberous sclerosis complex protein 1 (Tsc1) in renal proximal tubules induced strikingly enlarged kidneys, with minimal cystogenesis and occasional microscopic tumorigenesis. Signaling studies revealed hyperphosphorylation of eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and increased phosphorylation of ribosomal protein S6 (rpS6) in activated renal tubules. Notably, knockin of a nonphosphorylatable rpS6 in theseTsc1-mutant mice exacerbated cystogenesis and caused drastic nephron damage and renal fibrosis, leading to kidney failure and a premature death rate of 67% by 9 weeks of age. In contrast,Tsc1single-mutant mice were all alive and had far fewer renal cysts at this age. Mechanistic studies revealed persistent activation of mammalian target of rapamycin complex 1 (mTORC1) signaling causing hyperphosphorylation and consequent accumulation of 4E-BP1, along with greater cell proliferation, in the renal tubules ofTsc1andrpS6double-mutant mice. Furthermore, pharmacologic treatment ofTsc1single-mutant mice with rapamycin reduced hyperphosphorylation and accumulation of 4E-BP1 but also inhibited phosphorylation of rpS6. Rapamycin also exacerbated cystic and fibrotic lesions and impaired kidney function in these mice, consequently leading to a premature death rate of 40% within 2 weeks of treatment, despite destroying tumors and decreasing kidney size. These findings indicate that Tsc1 prevents aberrant renal growth and tumorigenesis by inhibiting mTORC1 signaling, whereas phosphorylated rpS6 suppresses cystogenesis and fibrosis inTsc1-deleted kidneys. PMID:26296742

  9. A 6-bp deletion in exon 8 and two mutations in introns of TYRP1 are associated with blond coat color in Liangshan pigs.

    Science.gov (United States)

    Wu, Xiaoqian; Zhang, Yi; Shen, Linyuan; Du, Jingjing; Luo, Jia; Liu, Chendong; Pu, Qiang; Yang, Runlin; Li, Xuewei; Bai, Lin; Tang, Guoqing; Zhang, Shunhua; Zhu, Li

    2016-03-01

    Melanocortin receptor 1 (MC1R), Agouti signaling protein (ASIP), and Tyrosinase-related protein 1 (TYRP1) are reported critical genes that regulate pheomelanin and eumelanin synthesis in mammals. Liangshan pig is a special Chinese indigenous pig breed with two completely different coat colors, solid black and blond. In this study, we detected polymorphisms of the above three genes and assessed the relationships between the variations and coat color phenotypes in Liangshan pigs. The findings revealed that the blond phenotype of Liangshan pig was related to dominant mutations in TYRP1, but not related to mutations in MC1R or ASIP. We found three closely linked mutations in TYRP1, g.8406G>A in intron 4, g.11100A>G in intron 5, and g.17599_17604del in exon 8, that were completely associated with blond coat color in Liangshan pigs. Further analysis revealed that a 6-bp deletion mutation resulted in deletion of Met and Gly residues at positions 495 and 496 in TYRP1 protein, and altered the structure of transmembrane domain of TYRP1. Together, our findings indicated that these three mutations in TYRP1 cause the blond phenotype in Liangshan pigs. PMID:26680103

  10. SSCP analysis and sequencing of the human prion protein gene (PRNP) detects two different 24 bp deletions in an atypical Alzheimer`s disease family

    Energy Technology Data Exchange (ETDEWEB)

    Perry, R.T.; Go, R.C.P.; Harrell, L.E.; Acton, R.T. [Univ. of Alabama, Birmingham, AL (United States)

    1995-02-27

    Alzheimer`s disease (AD) is a progressive, degenerative neurological disorder of the central nervous system. AD is the fourth leading cause of death in elderly persons 65 years or older in Western industrialized societies. The etiology of AD is unknown, but clinical, pathological, epidemiological, and molecular investigations suggest it is etiologically heterogeneous. Mutations in the amyloid protein are rare and segregate with the disease in a few early-onset familial AD (FAD) families. Similarities between AD and the unconventional viral (UCV) diseases, and between the amyloid and prion proteins, implicate the human prion protein gene (PRNP) as another candidate gene. Single strand conformation polymorphism (SSCP) analysis was used to screen for mutations at this locus in 82 AD patients from 54 families (30 FAD), vs. 39 age-matched controls. A 24-bp deletion around codon 68 that codes for one of five Gly-Pro rich octarepeats was identified in two affected sibs and one offspring of one late-onset FAD family. Two other affected sibs, three unaffected sibs, and three offspring from this family, in addition to one sporadic AD patient and three age-matched controls, were heterozygous for another octarepeat deletion located around codon 82. Two of the four affected sibs had features of PD, including one who was autopsy-verified AD and PD. Although these deletions were found infrequently in other AD patients and controls, they appear to be a rare polymorphism that is segregating in this FAD family. It does not appear that mutations at the PRNP locus are frequently associated with AD in this population. 54 refs., 4 figs.

  11. Arachnomelia syndrome in Simmental cattle is caused by a homozygous 2-bp deletion in the molybdenum cofactor synthesis step 1 gene (MOCS1

    Directory of Open Access Journals (Sweden)

    Semmer Jördis

    2011-01-01

    Full Text Available Abstract Background Arachnomelia syndrome is an autosomal recessive inherited disease in cattle. Affected calves die around birth and show malformations of the skeleton mainly affecting the legs, the spinal column and the skull. A number of arachnomelia syndrome affected Simmental calves were recently detected by a surveillance system of anomalies with a peak of more than 120 recorded cases in the year 2006. The causative mutation was previously mapped to a 9 cM-region on bovine chromosome 23. We herein report the fine-mapping and identification of the gene causing arachnomelia syndrome in Simmental cattle. Results By using a dense set of markers, the arachnomelia syndrome linked region could be refined to 1.5 cM harbouring three protein coding genes. Comparative sequencing of these genes revealed a two-bp-deletion in the bovine MOCS1 gene resulting in a frame-shift and a premature termination codon. We genotyped affected calves and their ancestors and found that all affected were homozygous for the deletion whereas all carriers were heterozygous. Furthermore, cattle from the same population, but not directly related to known carriers mostly showed the wild type genotype. Conclusions MOCS1 encodes two proteins that are involved in the first synthesis step of molybdenum cofactor. A non functional sulfite-oxydase, one of the enzymes requiring molybdenum cofactor, leads to a similar pathology in Brown Swiss cattle. In combination the perfect association of the mutation with the phenotype and the obvious disruption of protein translation provide strong evidence for the causality of the MOCS1 mutation. Our results are the first example for an oligogenic lethal inherited disease in cattle. Furthermore, they show the potential involvement of sulfite metabolism in aberrant bone development.

  12. 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.

  13. 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.

  14. 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.

    Science.gov (United States)

    Thyssen, Gregory N; Fang, David D; Zeng, Linghe; Song, Xianliang; Delhom, Christopher D; Condon, Tracy L; Li, Ping; Kim, Hee Jin

    2016-01-01

    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. PMID:27172184

  15. 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.

  16. Conditional deletion of ferritin H in mice induces loss of iron storage and liver damage

    OpenAIRE

    Darshan, Deepak; Vanoaica, Liviu; Richman, Larry; Beermann, Friedrich; Kühn, Lukas C.

    2009-01-01

    Ferritin plays a central role in iron metabolism by acting both as iron storage and detoxifying protein. We have generated a ferritin H allele with loxP sites and studied the conditional ferritin H deletion in adult mice. Ten days after Mx-Cre induced deletion, ferritin H mRNA was below 5% in the liver, spleen and bone marrow of deleted mice compared to control littermates. Mice lost their cellular iron stores indicating the requirement of ferritin H in iron deposition. Serum iron and...

  17. 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.

  18. 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.

  19. 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.

  20. CacyBP/SIP inhibits Doxourbicin-induced apoptosis of glioma cells due to activation of ERK1/2.

    Science.gov (United States)

    Tang, Yuan; Zhan, Wenjian; Cao, Tong; Tang, Tianjin; Gao, Yong; Qiu, Zhichao; Fu, Chunling; Qian, Fengyuan; Yu, Rutong; Shi, Hengliang

    2016-03-01

    Calcyclin-binding protein or Siah-1-interacting protein (CacyBP/SIP) was previously reported to promote the proliferation of glioma cells. However, the effect of CacyBP/SIP on apoptosis of glioma is poorly understood. Here, our study shows that CacyBP/SIP plays a role in inhibiting doxorubicin (DOX) induced apoptosis of glioma cells U251 and U87. Overexpression of CacyBP/SIP obviously suppressed the DOX-induced cell apoptosis. On the contrary, silencing of CacyBP/SIP significantly promoted it. Further investigation indicated that inhibition of apoptosis by CacyBP/SIP was relevant to its nuclear translocation in response to the DOX treatment. Importantly, we found that the level of p-ERK1/2 in nuclei was related to the nuclear accumulation of CacyBP/SIP. Finally, the role of CacyBP/SIP was confirmed in vivo in a mouse model with the cell line stably silencing CacyBP/SIP. Taken together, our results suggest that CacyBP/SIP plays an important role in inhibiting apoptosis of glioma cells which might be mediated by ERK1/2 signaling pathway, which will provide some guidance for the treatment of glioma. PMID:26825673

  1. 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.

  2. Neuronal Deletion of Ghrelin Receptor Almost Completely Prevents Diet-Induced Obesity.

    Science.gov (United States)

    Lee, Jong Han; Lin, Ligen; Xu, Pingwen; Saito, Kenji; Wei, Qiong; Meadows, Adelina G; Bongmba, Odelia Y N; Pradhan, Geetali; Zheng, Hui; Xu, Yong; Sun, Yuxiang

    2016-08-01

    Ghrelin signaling has major effects on energy and glucose homeostasis, but it is unknown whether ghrelin's functions are centrally and/or peripherally mediated. The ghrelin receptor, growth hormone secretagogue receptor (GHS-R), is highly expressed in the brain and detectable in some peripheral tissues. To understand the roles of neuronal GHS-R, we generated a mouse line where Ghsr gene is deleted in all neurons using synapsin 1 (Syn1)-Cre driver. Our data showed that neuronal Ghsr deletion abolishes ghrelin-induced spontaneous food intake but has no effect on total energy intake. Remarkably, neuronal Ghsr deletion almost completely prevented diet-induced obesity (DIO) and significantly improved insulin sensitivity. The neuronal Ghsr-deleted mice also showed improved metabolic flexibility, indicative of better adaption to different fuels. In addition, gene expression analysis suggested that hypothalamus and/or midbrain might be the sites that mediate the effects of GHS-R in thermogenesis and physical activity, respectively. Collectively, our results indicate that neuronal GHS-R is a crucial regulator of energy metabolism and a key mediator of DIO. Neuronal Ghsr deletion protects against DIO by regulating energy expenditure, not by energy intake. These novel findings suggest that suppressing central ghrelin signaling may serve as a unique antiobesity strategy. PMID:27207529

  3. 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.

  4. Genomics meets induced mutations in citrus: identification of deleted genes through comparative genomic hybridization

    International Nuclear Information System (INIS)

    We report on the use of genomic approaches to identify pivotal genes in induced citrus mutants. Citrus is the most economically important fruit crop in the world while Spain is the first fresh citrus producer. The survival of the Citrus industry is critically dependent on genetically superior cultivars but improvements in fruit quality traits through traditional techniques are extremely difficult due to the unusual combination of biological characteristics of citrus. Genomic science, however, holds promise of improvements in breeding. In this work, we reported the successful identification of genes included in hemizygous deletions induced by fast neutron irradiation on Citrus clementina. Microarray-based CGH was used to identify underrepresented genes in a citrus mutant that shows color break delay. Subsequent confirmation of gene doses through quantitative PCR and comparison of best hits of putative deleted citrus genes against annotated genomes from other eudicots, specially poplar, enabled the prediction that these genes were clustered into a 700 kb fragment. The availability of Citrus BAC end sequences helped to draw a partial physical map of the deletion. Furthermore, gene content and order in the deleted segment was established by PCR location of gene hits on the physical map. Finally, a lower chlorophyll a/b ratio was found in green tissues from the mutant, an observation that can be related to the hemizygous deletion of a ClpC-like gene, coding a putative subunit of a multifunctional protease complex located into the chloroplast. Analysis of gene content and order inside this Citrus deletion led to the conclusion that microsynteny and local gene colinearity with Populus trichocarpa were higher than with the phylogenetically closer Arabidopsis thaliana genome. In conclusion, a combined strategy including genomics tools and induced citrus mutations has been proved to be a successful approach to identify genes with major roles in citrus fruit development

  5. Genomics Meets Induced Mutations in Citrus: Identification of Deleted Genes Through Comparative Genomic Hybridization

    International Nuclear Information System (INIS)

    We report on the use of genomic approaches to identify pivotal genes in induced citrus mutants. Citrus is the most economically important fruit crop in the world and Spain is the first fresh citrus producer. The survival of the citrus industry is critically dependent on genetically superior cultivars but improvements in fruit quality traits through traditional techniques are extremely difficult due to the unusual combination of biological characteristics of citrus. Genomic science, however, holds promise of improvements in breeding. In this work, we reported the successful identification of genes included in hemizygous deletions induced by fast neutron irradiation on Citrus clementina. Microarray-based CGH was used to identify underrepresented genes in a citrus mutant that shows color break delay. Subsequent confirmation of gene doses through quantitative PCR and comparison of best hits of putative deleted citrus genes against annotated genomes from other eudicots, specially poplar, enabled the prediction that these genes were clustered into a 700 kb fragment. The availability of Citrus BAC end sequences helped to draw a partial physical map of the deletion. Furthermore, gene content and order in the deleted segment was established by PCR location of gene hits on the physical map. Finally, a lower chlorophyll a/b ratio was found in green tissues from the mutant, an observation that can be related to the hemizygous deletion of a ClpC-like gene, coding a putative subunit of a multifunctional protease complex located into the chloroplast. Analysis of gene content and order inside this Citrus deletion led to the conclusion that microsynteny and local gene colinearity with Populus trichocarpa were higher than with the phylogenetically closer Arabidopsis thaliana genome. In conclusion, a combined strategy including genomics tools and induced citrus mutations has been proved to be a successful approach to identify genes with major roles in citrus fruit development

  6. [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.

  7. 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

  8. Molecular analysis and comparison of radiation-induced large deletions of the HPRT locus in primary human skin fibroblasts

    Science.gov (United States)

    Yamada, Y.; Park, M. S.; Okinaka, R. T.; Chen, D. J.

    1996-01-01

    Genetic alterations in gamma-ray- and alpha-particle-induced HPRT mutants were examined by multiplex polymerase chain reaction (PCR) analysis. A total of 39-63% of gamma-ray-induced and 31-57% of alpha-particle-induced mutants had partial or total deletions of the HPRT gene. The proportion of these deletion events was dependent on radiation dose, and at the resolution limits employed there were no significant differences between the spectra induced by equitoxic doses of alpha particles (0.2-0.4 Gy) and gamma rays (3 Gy). The molecular nature of the deletions was analyzed by the use of sequence tagged site (STS) primers and PCR amplification as a "probe" for specific regions of the human X chromosome within the Xq26 region. These STSs were closely linked and spanned regions approximately 1.7 Mbp from the telomeric side and 1.7 Mbp from the centromeric side of the HPRT gene. These markers include: DXS53, 299R, DXS79, yH3L, 3/19, PR1, PR25, H2, yH3R, 1/44, 1/67, 1/1, DXS86, D8C6, DXS10 and DXS144. STS analyses indicated that the maximum size of total deletions in radiation-induced HPRT mutants can be greater than 2.7 Mbp and deletion size appears to be dependent on radiation dose. There were no apparent differences in the sizes of the deletions induced by alpha particles or gamma rays. On the other hand, deletions containing portions of the HPRT gene were observed to be 800 kbp or less, and the pattern of the partial deletion induced by alpha particles appeared to be different from that induced by gamma rays.

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

    Science.gov (United States)

    Tsai, Shih-Yin; Rodriguez, Ariana A; Dastidar, Somasish G; Del Greco, Elizabeth; Carr, Kaili Lia; Sitzmann, Joanna M; Academia, Emmeline C; Viray, Christian Michael; Martinez, Lizbeth Leon; Kaplowitz, Brian Stephen; Ashe, Travis D; La Spada, Albert R; Kennedy, Brian K

    2016-08-16

    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. PMID:27498874

  10. 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.

  11. 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

    Interferons (IFNs) are a family of cytokines with growth inhibitory, and antiviral functions. IFNs exert their biological actions through the expression of more than 1000 IFN stimulated genes, ISGs. ISG12 is an IFN type I induced gene encoding a protein of Mr 12,000. We have identified a novel, IFN...... 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...

  12. 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...

  13. Immunogenic response induced by wzm and wzt gene deletion mutants from Brucella abortus S19.

    Science.gov (United States)

    Wang, Xiu-Ran; Yan, Guang-Mou; Zhang, Rui; Lang, Xu-Long; Yang, Yan-Ling; Li, Xiao-Yan; Chen, Si; Qian, Jing; Wang, Xing-Long

    2014-02-01

    Brucellosis is an infectious disease affecting humans and animals worldwide. Effective methods of control include inducing immunity in animals by vaccination and elimination. Brucella abortus S19 is one of the popular vaccines for control of cattle brucellosis, as it has low virulence. In this paper, allelic exchange plasmids of wzm and wzt genes were constructed and partially knocked out to evaluate the effects on the induction of immunity to Brucella abortus S19 mutants. Cytokine secretion in vitro, INF-γ induction in vivo and antibody dynamics were evaluated. These data suggested that the immunity-eliciting ability of the wzm and wzt gene deletion mutants was similar, although reduced compared with the S19 strain. The results demonstrated that the wzt gene may be more important in the regulation of the induction of immunity than the wzm gene. PMID:24247358

  14. 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.

  15. Consequences of PAI-1 specific deletion in endothelium on radiation-induced intestinal damage

    International Nuclear Information System (INIS)

    Radiation-induced injury to healthy tissues is a real public health problem, since they are one of the most limiting factors that restrict efficiency of radiation therapy. This problematic is also part of the French Cancer Plan 2014-2017, and involves clinical research. Concepts surrounding the development of radiation-induced damage have gradually evolved into a contemporary and integrated view of the pathogenesis, involving all compartments of target tissue. Among them, endothelium seems to be central in the sequence of interrelated events that lead to the development of radiation-induced damage, although there are rare concrete elements that support this concept. By using new transgenic mouse models, this PhD project provides a direct demonstration of an endothelium-dependent continuum in evolution of radiation-induced intestinal damage. Indeed, changes in the endothelial phenotype through targeted deletion of the gene SERPINE1, chosen because of its key role in the development of radiation enteritis, influences various parameters of the development of the disease. Thus, lack of PAI-1 secretion by endothelial cells significantly improves survival of the animals, and limits severity of early and late tissue damage after a localized small bowel irradiation. Furthermore, these mice partially KO for PAI-1 showed a decrease in the number of apoptotic intestinal stem cells in the hours following irradiation, a decrease in the macrophages infiltrate density one week after irradiation, and a change in the polarization of macrophages throughout the pathophysiological process. In an effort to protect healthy tissues from radiation therapy side effects, without hindering the cancer treatment, PAI-1 seems to be an obvious therapeutic target. Conceptually, this work represents the direct demonstration of the link between endothelium phenotype and radiation enteritis pathogenesis. (author)

  16. 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.

  17. Selective deletion of Pten in pancreatic beta cells leads to increased islet mass and resistance to STZ-induced diabetes.

    Science.gov (United States)

    Stiles, Bangyan L; Kuralwalla-Martinez, Christine; Guo, Wei; Gregorian, Caroline; Wang, Ying; Tian, Jide; Magnuson, Mark A; Wu, Hong

    2006-04-01

    Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a lipid phosphatase. PTEN inhibits the action of phosphatidylinositol-3-kinase and reduces the levels of phosphatidylinositol triphosphate, a crucial second messenger for cell proliferation and survival, as well as insulin signaling. In this study, we deleted Pten specifically in the insulin producing beta cells during murine pancreatic development. Pten deletion leads to increased cell proliferation and decreased cell death, without significant alteration of beta-cell differentiation. Consequently, the mutant pancreas generates more and larger islets, with a significant increase in total beta-cell mass. PTEN loss also protects animals from developing streptozotocin-induced diabetes. Our data demonstrate that PTEN loss in beta cells is not tumorigenic but beneficial. This suggests that modulating the PTEN-controlled signaling pathway is a potential approach for beta-cell protection and regeneration therapies. PMID:16537919

  18. 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.

  19. Induction of Mitochondrial DNA Deletion by Ionizing Radiation in Human Lung Fibroblast IMR-90 Cells

    Energy Technology Data Exchange (ETDEWEB)

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

    2009-06-15

    Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging and also contributes to their unfavorable effects in cultured cells and animal tissues. This study was conducted to investigate the effect of ionizing radiation (IR) on mtDNA deletion and the involvement of reactive oxygen species (ROS) in this process in human lung fibroblast (IMR-90) cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated with {sup 137}Cs -rays and the intracellular ROS level was determined by 2',7'-dichlorofluorescein diacetate (DCFH-DA) and mtDNA common deletion (4977bp) was detected by nested PCR. Old cells at PD 55 and H{sub 2}O{sub 2}-treated young cells were compared as the positive control. IR increased the intracellular ROS level and mtDNA 4977 bp deletion in IMR-90 cells dose-dependently. The increases of ROS level and mtDNA deletion were also observed in old cells and H{sub 2}O{sub 2}-treated young cells. To confirm the increased ROS level is essential for mtDNA deletion in irradiated cells, the effects of N-acetylcysteine (NAC) on IRinduced ROS and mtDNA deletion were examined. 5 mM NAC significantly attenuated the IR-induced ROS increase and mtDNA deletion. These results suggest that IR induces the mtDNA deletion and this process is mediated by ROS in IMR-90 cells.

  20. 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

  1. 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,

  2. 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.

  3. 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.

  4. 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.

  5. 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.

  6. 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.

  7. Time-effect Relationship of Mitochondrial DNA 4977bp Deletion in Human Peripheral Blood Cell after X Ray Irradiation%X射线致人外周血线粒体DNA 4977bp缺失的时效关系研究

    Institute of Scientific and Technical Information of China (English)

    王金合; 王平; 姜峰; 韩林; 王喜爱; 吕玉民

    2011-01-01

    To investigate the time-effect of mitochondfial DNA 4977bp deletion in human peripheral blood cells exposed to X ray, human peripheral whole blood samples were collected from two healthy individuals, and exposed to X rays with dose from 0 to 10 Gy. The genomic DNAs were isolated from the whole-blood samples, and the levels of mtDNA 4977bp deletion and copy number of total mtDNA in the DNA samples were detected by Real-time PCR after irradiation at 2, 12, 24, 48, and 72 h, respectively. The results showed that the copy number of mtDNA 4977bp deletion and total mtDNA, and the rates of mtDNA 4977bp deletion increase with incubation time with dose at 5 Gy after irradiation. Moreover, they increased with dose from 0 to 10 Gy after irradiation at 24 h and 72 h, respectively. The results suggested that the levels of mtDNA 4977bp deletion and the copy number of total mtDNA in human peripheral blood cells exposed to X ray were accumulated with incubation time and dose increase, respectively.%采集2名25岁健康男性外周血进行不同剂量(0~10 Gy)单次X射线照射,于照后取不同时间点(2、12、24、48和72 h)培养的细胞提取基因组DNA,利用实时定量PCR检测不同时间点线粒体DNA(mtDNA)4977bp缺失情况,探讨X射线致人外周血mtDNA 4977bp缺失的时间效应关系。结果表明,受照剂量为5 Gy时,随着照射后培养时间的增加,mtDNA 4977bp缺失拷贝数、mtDNA总拷贝数和mtDNA 4977bp缺失率均有增加趋势。培养时间为24 h和72 h时,在0~10 Gy剂量范围内mtDNA 4977bp缺失拷贝数、mtDNA总拷贝数和mtDNA 4977bp缺失率随着受照剂量的增加而增加。提示X射线诱发的mtDNA 4977bp缺失和mtDNA总拷贝数具有时间和剂量累积性。

  8. The deletion of residues 268-292 of E1 impairs the ability of HCV envelope proteins to induce pore formation.

    Science.gov (United States)

    Lombana, Laura; Ortega-Atienza, Sara; Gómez-Gutiérrez, Julián; Yélamos, Belén; Peterson, Darrell L; Gavilanes, Francisco

    2016-06-01

    We have obtained a chimeric protein containing the ectodomains of hepatitis C virus (HCV) envelope proteins but lacking the region 268-292 of E1. All its structural properties are coincident with those of the corresponding full length chimera. The deleted and entire chimeras were compared in terms of their membrane destabilizing properties. No differences were found in their ability to induce vesicle aggregation and lipid mixing but the deleted chimera showed a reduced capacity to promote leakage. The role of the deletion was also studied by obtaining HCV pseudoparticles (HCVpp). Both E1 and E2, and also the E1 deleted mutant, were incorporated into HCVpp to a similar level. However, HCVpp containing the E1 deleted protein are almost unable to infect Huh7 cells. These results point to the involvement of the region 268-292 in the formation of pores in the membrane necessary for the complete fusion of the membranes. PMID:26945847

  9. Adipocyte-Specific Deletion of Manganese Superoxide Dismutase Protects From Diet-Induced Obesity Through Increased Mitochondrial Uncoupling and Biogenesis.

    Science.gov (United States)

    Han, Yong Hwan; Buffolo, Márcio; Pires, Karla Maria; Pei, Shaobo; Scherer, Philipp E; Boudina, Sihem

    2016-09-01

    Obesity and insulin resistance are associated with oxidative stress (OS). The causal role of adipose OS in the pathogenesis of these conditions is unknown. To address this issue, we generated mice with an adipocyte-selective deletion of manganese superoxide dismutase (MnSOD). When fed a high-fat diet (HFD), the AdSod2 knockout (KO) mice exhibited less adiposity, reduced adipocyte hypertrophy, and decreased circulating leptin. The resistance to diet-induced adiposity was the result of an increased metabolic rate and energy expenditure. Furthermore, palmitate oxidation was elevated in the white adipose tissue (WAT) and brown adipose tissue of AdSod2 KO mice fed an HFD, and the expression of key fatty acid oxidation genes was increased. To gain mechanistic insight into the increased fat oxidation in HFD-fed AdSod2 KO mice, we quantified the mitochondrial function and mitochondrial content in WAT and found that MnSOD deletion increased mitochondrial oxygen consumption and induced mitochondrial biogenesis. This effect was preserved in cultured adipocytes from AdSod2 KO mice in vitro. As expected from the enhanced fat oxidation, circulating levels of free fatty acids were reduced in the HFD-fed AdSod2 KO mice. Finally, HFD-fed AdSod2 KO mice were protected from hepatic steatosis, adipose tissue inflammation, and glucose and insulin intolerance. Taken together, these results demonstrate that MnSOD deletion in adipocytes triggered an adaptive stress response that activated mitochondrial biogenesis and enhanced mitochondrial fatty acid oxidation, thereby preventing diet-induced obesity and insulin resistance. PMID:27284109

  10. Reduced cocaine-induced serotonin, but not dopamine and noradrenaline, release in rats with a genetic deletion of serotonin transporters.

    Science.gov (United States)

    Verheij, Michel M M; Karel, Peter; Cools, Alexander R; Homberg, Judith R

    2014-11-01

    It has recently been proposed that the increased reinforcing properties of cocaine and ecstasy observed in rats with a genetic deletion of serotonin transporters are the result of a reduction in the psychostimulant-induced release of serotonin. Here we provide the neurochemical evidence in favor of this hypothesis and show that changes in synaptic levels of dopamine or noradrenaline are not very likely to play an important role in the previously reported enhanced psychostimulant intake of these serotonin transporter knockout rats. The results may very well explain why human subjects displaying a reduced expression of serotonin transporters have an increased risk to develop addiction. PMID:25261262

  11. Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo.

    Science.gov (United States)

    Németh, Tamás; Futosi, Krisztina; Sitaru, Cassian; Ruland, Jürgen; Mócsai, Attila

    2016-01-01

    Neutrophils are terminally differentiated cells with limited transcriptional activity. The biological function of their gene expression changes is poorly understood. CARD9 regulates transcription during antifungal immunity but its role in sterile inflammation is unclear. Here we show that neutrophil CARD9 mediates pro-inflammatory chemokine/cytokine but not lipid mediator release during non-infectious inflammation. Genetic deficiency of CARD9 suppresses autoantibody-induced arthritis and dermatitis in mice. Neutrophil-specific deletion of CARD9 is sufficient to induce that phenotype. Card9(-/-) neutrophils show defective immune complex-induced gene expression changes and pro-inflammatory chemokine/cytokine release but normal LTB4 production and other short-term responses. In vivo deletion of CARD9 reduces tissue levels of pro-inflammatory chemokines and cytokines but not LTB4. The CARD9-mediated signalling pathway involves Src-family kinases, Syk, PLCγ2, Bcl10/Malt1 and NFκB. Collectively, CARD9-mediated gene expression changes within neutrophils play important roles during non-infectious inflammation in vivo and CARD9 acts as a divergence point between chemokine/cytokine and lipid mediator release. PMID:27032818

  12. CFTR Deletion in Mouse Testis Induces VDAC1 Mediated Inflammatory Pathway Critical for Spermatogenesis

    Science.gov (United States)

    Huijuan, Liao; Jiang, Xie; Ming, Yang; Huaqin, Sun; Wenming, Xu

    2016-01-01

    Cystic fibrosis is the most common genetic disease among Caucasians and affects tissues including lung, pancreas and reproductive tracts. It has been shown that Endoplasmic Reticulum (ER) stress and heat shock response are two major deregulated functional modules related to CFTR dysfunction. To identify the impact of CFTR deletion during spermatogenesis, we examined the expression of spermiogenesis-related genes in the testis of CFTR mutant mice (CF mice). We confirmed expression changes of MSY2, a germ cell specific RNA binding protein, resulting from deletion of CFTR in testis. Furthermore, real time PCR and Western blot results showed that an inflammatory response was activated in CF mice testis, as reflected by the altered expression of cytokines. We demonstrate for the first time that expression of MSY2 is decreased in CF mice. Our results suggest that CFTR deletion in testis influences inflammatory responses and these features are likely to be due to the unique environment of the seminiferous tubule during the spermatogenesis process. The current study also suggests avenues to understand the pathophysiology of CFTR during spermatogenesis and provides targets for the possible treatment of CFTR-related infertility. PMID:27483469

  13. CFTR Deletion in Mouse Testis Induces VDAC1 Mediated Inflammatory Pathway Critical for Spermatogenesis.

    Science.gov (United States)

    Yan, Chen; Lang, Qin; Huijuan, Liao; Jiang, Xie; Ming, Yang; Huaqin, Sun; Wenming, Xu

    2016-01-01

    Cystic fibrosis is the most common genetic disease among Caucasians and affects tissues including lung, pancreas and reproductive tracts. It has been shown that Endoplasmic Reticulum (ER) stress and heat shock response are two major deregulated functional modules related to CFTR dysfunction. To identify the impact of CFTR deletion during spermatogenesis, we examined the expression of spermiogenesis-related genes in the testis of CFTR mutant mice (CF mice). We confirmed expression changes of MSY2, a germ cell specific RNA binding protein, resulting from deletion of CFTR in testis. Furthermore, real time PCR and Western blot results showed that an inflammatory response was activated in CF mice testis, as reflected by the altered expression of cytokines. We demonstrate for the first time that expression of MSY2 is decreased in CF mice. Our results suggest that CFTR deletion in testis influences inflammatory responses and these features are likely to be due to the unique environment of the seminiferous tubule during the spermatogenesis process. The current study also suggests avenues to understand the pathophysiology of CFTR during spermatogenesis and provides targets for the possible treatment of CFTR-related infertility. PMID:27483469

  14. 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.

  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. 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.

  17. APP-BP1 mediates APP-induced apoptosis and DNA synthesis and is increased in Alzheimer's disease brain

    OpenAIRE

    Chen, Yuzhi; Liu,Wenyun; McPhie, Donna L.; Hassinger, Linda; Neve, Rachael L

    2003-01-01

    APP-BP1, first identified as an amyloid precursor protein (APP) binding protein, is the regulatory subunit of the activating enzyme for the small ubiquitin-like protein NEDD8. We have shown that APP-BP1 drives the S- to M-phase transition in dividing cells, and causes apoptosis in neurons (Chen, Y., D.L. McPhie, J. Hirschberg, and R.L. Neve. 2000. J. Biol. Chem. 275:8929–8935). We now demonstrate that APP-BP1 binds to the COOH-terminal 31 amino acids of APP (C31) and colocalizes with APP in a...

  18. Deletion of CB2 cannabinoid receptor induces schizophrenia-related behaviors in mice.

    Science.gov (United States)

    Ortega-Alvaro, Antonio; Aracil-Fernández, Auxiliadora; García-Gutiérrez, María S; Navarrete, Francisco; Manzanares, Jorge

    2011-06-01

    The possible role of the CB(2) receptor (CB(2)r) in psychiatric disorders has been considered. Several animal models use knockout (KO) mice that display schizophrenia-like behaviors and this study evaluated the role of CB(2)r in the regulation of such behaviors. Mice lacking the CB(2)r (CB(2)KO) were challenged in open field, light-dark box, elevated plus-maze, tail suspension, step down inhibitory avoidance, and pre-pulse inhibition tests (PPI). Furthermore, the effects of treatment with cocaine and risperidone were evaluated using the OF and the PPI test. Gene expression of dopamine D(2) (D(2)r), adrenergic-α(2C) (α(2C)r), serotonergic 5-HT(2A) and 5-HT(2C) receptors (5-HT(2A)r and 5-HT(2C)r) were studied by RT-PCR in brain regions related to schizophrenia. Deletion of CB(2)r decreased motor activity in the OF test, but enhanced response to acute cocaine and produced mood-related alterations, PPI deficit, and cognitive impairment. Chronic treatment with risperidone tended to impair PPI in WT mice, whereas it 'normalized' the PPI deficit in CB(2)KO mice. CB(2)KO mice presented increased D(2)r and α(2C)r gene expressions in the prefrontal cortex (PFC) and locus coeruleus (LC), decreased 5-HT(2C)r gene expression in the dorsal raphe (DR), and 5-HT(2A)r gene expression in the PFC. Chronic risperidone treatment in WT mice left α(2C)r gene expression unchanged, decreased D(2)r gene expression (15 μg/kg), and decreased 5-HT(2C)r and 5-HT(2A)r in PFC and DR. In CB(2)KO, the gene expression of D(2)r in the PFC, of α(2C)r in the LC, and of 5-HT(2C)r and 5-HT(2A)r in PFC was reduced; 5-HT(2C)r and 5-HT(2A)r gene expressions in DR were increased after treatment with risperidone. These results suggest that deletion of CB(2)r has a relation with schizophrenia-like behaviors. Pharmacological manipulation of CB(2)r may merit further study as a potential therapeutic target for the treatment of schizophrenia-related disorders. PMID:21430651

  19. 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.

  20. Deletion of Metallothionein Exacerbates Intermittent Hypoxia-Induced Oxidative and Inflammatory Injury in Aorta

    Directory of Open Access Journals (Sweden)

    Shanshan Zhou

    2014-01-01

    Full Text Available The present study was to explore the effect of metallothionein (MT on intermittent hypoxia (IH induced aortic pathogenic changes. Markers of oxidative damages, inflammation, and vascular remodeling were observed by immunohistochemical staining after 3 days and 1, 3, and 8 weeks after IH exposures. Endogenous MT was induced after 3 days of IH but was significantly decreased after 8 weeks of IH. Compared with the wild-type mice, MT knock-out mice exhibited earlier and more severe pathogenic changes of oxidative damages, inflammatory responses, and cellular apoptosis, as indicated by the significant accumulation of collagen, increased levels of connective tissue growth factor, transforming growth factor β1, tumor necrosis factor-alpha, vascular cell adhesion molecule 1,3-nitrotyrosine, and 4-hydroxy-2-nonenal in the aorta. These findings suggested that chronic IH may lead to aortic damages characterized by oxidative stress and inflammation, and MT may play a pivotal role in the above pathogenesis process.

  1. HLA-G基因14bp插入/缺失多态性与不明原因复发性流产患者相关性的病例对照研究%Association between HLA-G 14-bp Insertion/Deletion Polymorphism and Women with Recurrent Spontaneous Abortions

    Institute of Scientific and Technical Information of China (English)

    张惠湘; 朱永生

    2012-01-01

    目的 探讨HLA-G基因3'非翻译区14bp插入/缺失多态性与不明原因复发性流产患者的相关性.方法 选择343名不明原因复发性流产患者,按照不同流产次数分为流产2次组(n=152),流产3次组(n=132),流产4次及以上组(n=59);268名正常妊娠妇女作为健康对照组.采用聚合酶链反应(PCR)及8%非变性聚丙烯酰胺凝胶电泳分离技术检测HLA-G基因14bp插入/缺失多态性位点在不明原因复发性流产患者及正常妊娠组中的基因型频率分布.结果 HLA-G基因14bp插入/缺失多态性位点的基因型频率分布在流产4次及以上组与正常妊娠组差异有统计学意义(χ2=6.941,P=0.031),流产4次及以上组+14bp等位基因频率分布显著高于正常妊娠组(χ2=4.956,P=0.026,OR=1.573,95%CI:1.054~2.349).结论 H LA-G 14 bp 缺失多态性在维持正常的妊娠中可能有重要作用.%Objective To investigate the association between HLA - G gene 14 - bp insertion/deletion polymorphism in 3 UTR and recurrent spontaneous abortions. Methods In this study, a total of 611 Chinese women were genotyped for the + 14 - bp/14 - bp polymorphism, including 343 who had recurrent spontaneous abortions (two miscarriages; 152, three miscarriages; 132, four or more miscarriages; 59) , 268 women with normal fertility as controls. Results To our knowledge, this is the first report that Significant difference was observed in the distribution of + 14 - bp/ + 14 - bp genotype between controls and the recurrent abortion group with four or more abortions ( X2 = 6. 941, P - 0. 031 ) . The + 14 - bp homozygote sequence was more prominent among those with recurrent spontaneous abortions (four or more recurrent miscarriages) in contrast to fertile control women (X2 = 4.956, P=0.026, OR =1.573, 95%CI: 1.054 ~2. 349). Conclusion A 14 - bp insertion/deletion polymorphism in exon 8 has a possible role in HLA ?G expression in certain cases of recurrent spontaneous abortions. However, additional

  2. 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.

  3. Hematopoietic Cell–Restricted Deletion of CD36 Reduces High-Fat Diet–Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue

    OpenAIRE

    Nicholls, Hayley T.; Kowalski, Greg; Kennedy, David J.; Risis, Steve; Zaffino, Lee A.; Watson, Nadine; Kanellakis, Peter; Watt, Matthew J.; Bobik, Alex; Bonen, Arend; Febbraio, Maria; Lancaster, Graeme I.; Febbraio, Mark A.

    2011-01-01

    OBJECTIVE The fatty acid translocase and scavenger receptor CD36 is important in the recognition and uptake of lipids. Accordingly, we hypothesized that it plays a role in saturated fatty acid–induced macrophage lipid accumulation and proinflammatory activation. RESEARCH DESIGN AND METHODS In vitro, the effect of CD36 inhibition and deletion in lipid-induced macrophage inflammation was assessed using the putative CD36 inhibitor, sulfosuccinimidyl oleate (SSO), and bone marrow–derived macropha...

  4. Zinc transporter 3 (ZnT3) gene deletion reduces spinal cord white matter damage and motor deficits in a murine MOG-induced multiple sclerosis model.

    Science.gov (United States)

    Choi, Bo Young; Kim, In Yeol; Kim, Jin Hee; Kho, A Ra; Lee, Song Hee; Lee, Bo Eun; Sohn, Min; Koh, Jae-Young; Suh, Sang Won

    2016-10-01

    The present study aimed to evaluate the role of zinc transporter 3 (ZnT3) on multiple sclerosis (MS) pathogenesis. Experimental autoimmune encephalomyelitis (EAE), a disease model of multiple sclerosis, was induced by immunization with myelin oligodendrocyte glycoprotein (MOG35-55) in female mice. Three weeks after the initial immunization, demyelination, immune cell infiltration and blood brain barrier (BBB) disruption in the spinal cord were analyzed. Clinical signs of EAE first appeared on day 11 and reached a peak level on day 19 after the initial immunization. ZnT3 gene deletion profoundly reduced the daily clinical score of EAE. The ZnT3 gene deletion-mediated inhibition of the clinical course of EAE was accompanied by suppression of inflammation and demyelination in the spinal cord. The motor deficit accompanying neuropathological changes associated with EAE were mild in ZnT3 gene deletion mice. This reduction in motor deficit was accompanied by coincident reductions in demyelination and infiltration of encephalitogenic immune cells including CD4+ T cells, CD8+ T cells, CD20+ B cells and F4/80+ microglia in the spinal cord. These results demonstrate that ZnT3 gene deletion inhibits the clinical features and neuropathological changes associated with EAE. ZnT3 gene deletion also remarkably inhibited formation of EAE-associated aberrant synaptic zinc patches, matrix metalloproteinases-9 (MMP-9) activation and BBB disruption. Therefore, amelioration of EAE-induced clinical and neuropathological changes by ZnT3 gene deletion suggests that vesicular zinc may be involved in several steps of MS pathogenesis. PMID:27370228

  5. 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.

  6. 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

  7. The Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Modifies Exercise-Induced Muscle Metabolism.

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    David Vaughan

    Full Text Available A silencer region (I-allele within intron 16 of the gene for the regulator of vascular perfusion, angiotensin-converting enzyme (ACE, is implicated in phenotypic variation of aerobic fitness and the development of type II diabetes. We hypothesised that the reportedly lower aerobic performance in non-carriers compared to carriers of the ACE I-allele, i.e. ACE-DD vs. ACE-ID/ACE-II genotype, is associated with alterations in activity-induced glucose metabolism and capillarisation in exercise muscle.Fifty-three, not-specifically trained Caucasian men carried out a one-legged bout of cycling exercise to exhaustion and/or participated in a marathon, the aim being to identify and validate genotype effects on exercise metabolism. Respiratory exchange ratio (RER, serum glucose and lipid concentration, glycogen, and metabolite content in vastus lateralis muscle based on ultra-performance lipid chromatography-mass spectrometry (UPLC-MS, were assessed before and after the cycling exercise in thirty-three participants. Serum metabolites were measured in forty subjects that completed the marathon. Genotype effects were assessed post-hoc.Cycling exercise reduced muscle glycogen concentration and this tended to be affected by the ACE I-allele (p = 0.09. The ACE-DD genotype showed a lower maximal RER and a selective increase in serum glucose concentration after exercise compared to ACE-ID and ACE-II genotypes (+24% vs. +2% and -3%, respectively. Major metabolites of mitochondrial metabolism (i.e. phosphoenol pyruvate, nicotinamide adenine dinucleotide phosphate, L-Aspartic acid, glutathione were selectively affected in vastus lateralis muscle by exercise in the ACE-DD genotype. Capillary-to-fibre ratio was 24%-lower in the ACE-DD genotype. Individuals with the ACE-DD genotype demonstrated an abnormal increase in serum glucose to 7.7 mM after the marathon.The observations imply a genetically modulated role for ACE in control of glucose import and oxidation in

  8. Gene Deletion by Synthesis in Yeast.

    Science.gov (United States)

    Kim, Jinsil; Kim, Dong-Uk; Hoe, Kwang-Lae

    2017-01-01

    Targeted gene deletion is a useful tool for understanding the function of a gene and its protein product. We have developed an efficient and robust gene deletion approach in yeast that employs oligonucleotide-based gene synthesis. This approach requires a deletion cassette composed of three modules: a central 1397-bp KanMX4 selection marker module and two 366-bp gene-specific flanking modules. The invariable KanMX4 module can be used in combination with different pairs of flanking modules targeting different genes. The two flanking modules consist of both sequences unique to each cassette (chromosomal homologous regions and barcodes) and those common to all deletion constructs (artificial linkers and restriction enzyme sites). Oligonucleotides for each module and junction regions are designed using the BatchBlock2Oligo program and are synthesized on a 96-well basis. The oligonucleotides are ligated into a single deletion cassette by ligase chain reaction, which is then amplified through two rounds of nested PCR to obtain sufficient quantities for yeast transformation. After removal of the artificial linkers, the deletion cassettes are transformed into wild-type diploid fission yeast SP286 cells. Verification of correct clone and gene deletion is achieved by performing check PCR and tetrad analysis. This method with proven effectiveness, as evidenced by a high success rate of gene deletion, can be potentially applicable to create systematic gene deletion libraries in a variety of yeast species. PMID:27671940

  9. Adult-Onset Deletion of β-Catenin in (10kb)Dmp1-Expressing Cells Prevents Intermittent PTH-Induced Bone Gain.

    Science.gov (United States)

    Kedlaya, Rajendra; Kang, Kyung Shin; Hong, Jung Min; Bettagere, Vidya; Lim, Kyung-Eun; Horan, Daniel; Divieti-Pajevic, Paola; Robling, Alexander G

    2016-08-01

    β-Catenin (βcat) is a major downstream signaling node in canonical Wingless-related integration site (Wnt) signaling pathway, and its activity is crucial for canonical Wnt signal transduction. Wnt signaling has recently been implicated in the osteo-anabolic response to PTH, a potent calcium-regulating factor. We investigated whether βcat is essential for the anabolic action of intermittent PTH by generating male mice with adult-onset deletion of βcat in a subpopulation of bone cells (osteocytes and late-stage osteoblasts), treating them with an anabolic regimen of PTH, and measuring the skeletal responses. Male (10kb)Dmp1-CreERt2 transgenic mice that also harbored floxed loss-of-function βcat alleles (βcat(f/f)) were induced for Cre activity using tamoxifen, then injected daily with human PTH 1-34 (30 μg/kg) or vehicle for 5 weeks. Mice in which βcat was deleted showed either total lack of bone mineral density (BMD) gain, or BMD loss, and did not respond to PTH treatment. However, bone mass measurements in the trabecular compartment of the femur and spine revealed PTH-induced bone gain whether βcat was deleted or not. PTH-stimulated increases in periosteal and cancellous bone formation rates were not impaired by βcat deletion, but resorption markers and cortical porosity were significantly increased in induced mice, particularly induced mice treated with PTH. These results suggest that βcat is required for net-positive BMD effects of PTH therapy but that the anabolic effects per se of PTH treatment might not require osteocytic/osteoblastic βcat. PMID:27253995

  10. 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

    2016-01-01

    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). PMID:27401954

  11. 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).

  12. Identification of a novel functional deletion variant in the 5'-UTR of the DJ-1 gene

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    Warnich Louise

    2009-10-01

    Full Text Available Abstract Background DJ-1 forms part of the neuronal cellular defence mechanism against oxidative insults, due to its ability to undergo self-oxidation. Oxidative stress has been implicated in the pathogenesis of central nervous system damage in different neurodegenerative disorders including Alzheimer's disease and Parkinson's disease (PD. Various mutations in the DJ-1 (PARK7 gene have been shown to cause the autosomal recessive form of PD. In the present study South African PD patients were screened for mutations in DJ-1 and we aimed to investigate the functional significance of a novel 16 bp deletion variant identified in one patient. Methods The possible effect of the deletion on promoter activity was investigated using a Dual-Luciferase Reporter assay. The DJ-1 5'-UTR region containing the sequence flanking the 16 bp deletion was cloned into a pGL4.10-Basic luciferase-reporter vector and transfected into HEK293 and BE(2-M17 neuroblastoma cells. Promoter activity under hydrogen peroxide-induced oxidative stress conditions was also investigated. Computational (in silico cis-regulatory analysis of DJ-1 promoter sequence was performed using the transcription factor-binding site database, TRANSFAC via the PATCH™ and rVISTA platforms. Results A novel 16 bp deletion variant (g.-6_+10del was identified in DJ-1 which spans the transcription start site and is situated 93 bp 3' from a Sp1 site. The deletion caused a reduction in luciferase activity of approximately 47% in HEK293 cells and 60% in BE(2-M17 cells compared to the wild-type (P Conclusion This is the first report of a functional DJ-1 promoter variant, which has the potential to influence transcript stability or translation efficiency. Further work is necessary to determine the extent to which the g.-6_+10del variant affects the normal function of the DJ-1 promoter and whether this variant confers a risk for PD.

  13. 儿童淋巴瘤患者EBV-LMP1基因C末端30bp缺失突变检测%Detection of C-terminal 30 bp-deletion mutation of latent membrane protein 1 of EBV in childhood lymphoma

    Institute of Scientific and Technical Information of China (English)

    谢正德; 周春菊; 王琳; 申昆玲

    2008-01-01

    Objective To study C-terminal 30 bp-deletion mutation of latent membrane protein 1 of the virus from childhood lymphoma. Methods Nested-PCR was used to amplify C-terminal of EBV-LMP1 from childhood lymphoma and non-lymphoma associated to EBV,including Hodgkin lymphoma (HL),non-Hodgkin lymphoma (NHL)and reactive hyperplasia of lymph node (RL). Sequence analysis was performed on the positive PCR product.Results LMP1 with 30 bp deletion in C-terminal was detected in 11/25 HL,3/8 NHL and 5/15 RL cases respectively .There were no significant differences among HL,NHL and RL (P = 0.793 ). Sequence analysis showed that LMP1 detected in this study belongs to the following three subgroups: B95.8,China1 and China2. Conclusion LMP1 with 30 bp deletion in C-terminal widely existed in childhood HL,NHL and RL.There was no correlation between special types of LMP1 and the diseases. There were 3 LMP1 subgroups of EBV in children's lymphoma in the cases studied,including B95.8,Chinal and China 2.%目的 研究儿童淋巴瘤来源的EBV-LMP1基因C末端30 bp缺失突变情况并分析其意义.方法 应用巢式聚合酶链反应技术(Nested-PCR)扩增免疫组化检测EBV-LMP1或原位杂交检测EBV.EBERS阳性的霍奇金淋巴瘤、非霍奇金淋巴瘤和淋巴结反应性增生病理标本中EBV-LMP1基因,并进行序列分析.结果 EBV-LMP1羧基端30 bp缺失的del-LMP1的检出率在霍奇金淋巴瘤、非霍奇金淋巴瘤和淋巴结反应性增生分别为11/25、3/8和5/15,三组间差异无统计学意义(P=0.793,X2=0.463).经序列分析发现,所扩增的EBV-LmP1基因型可分为三个亚型:B95.8、China1和China2.结论 EBV羧基端30 bp缺失的del-LMP1基因型广泛存在EBV阳性的儿童霍奇金淋巴瘤、非霍奇金淋巴瘤和淋巴结反应性增生病例中,与疾病本身没有关系.儿童来源的EBV-LMP1基因型主要可分为B95.8、China1和China2三个亚型.

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

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    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.

  15. 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.

  16. The vaccine properties of a Brazilian BHV-1 strain with an induced deletion of the gE gene

    International Nuclear Information System (INIS)

    Full text: A Brazilian strain of bovine herpesvirus type 1.2a with a deletion of the glycoprotein E (gE) gene was constructed (BHV-1.2a gE-). The deletion was introduced by the co-transfection of a deletion fragment containing the 5' and 3' gE flanking regions and genomic DNA of wild type BHV-1 into bovine cells. Identification of gE deletion mutant was performed by immunoperoxidase staining with an anti-gE monoclonal antibody. This gE deletion mutant was plaque purified and further examined by restriction endonuclesase digestion and Southern blot hybridization. The in vitro growth characteristics of this gE negative mutant were studied and compared with the parental strain. The results of these experiments showed that the BHV- 1.2a gE- had a significantly reduced cell-to-cell spread in three different host cells. No statistical differences were observed when single step growth curves or penetration assays were performed using the BHV-1.2a gE- and the parental strain. In vivo studies were performed to access the potential of this virus as a vaccinal strain. In order to examine its attenuation for cattle, four BHV-1 seronegative calves were inoculated intranasally with 2x105,3 TCID50 of the gE- virus. Another group of three calves was inoculated with 5x107 TCID50 of the wild type virus. Two other calves were kept as uninfected controls. The deletion mutant had a markedly reduced virulence for calves, whereas the wild type virus was highly virulent. The gE- virus was excreted to lower titres and for a shorter period of time than the wild type virus. Calves immunized with gE- virus and challenged with 5x107 TCID50 of wild type virus developed very mild clinical disease with a significant reduction in virus excretion. These results show that the gE- recombinant was attenuated and capable of prevent clinical disease upon challenge. The gE- deletion mutant is a promising candidate virus for a differential vaccine to BHV-1 infections. (author)

  17. 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.

  18. Genetic Deletion of the Neuronal Glutamate Transporter, EAAC1, Results in Decreased Neuronal Death after Pilocarpine-Induced Status Epilepticus

    OpenAIRE

    Lane, Meredith C.; Jackson, Joshua G.; Krizman, Elizabeth N.; Rothstein, Jeffery D.; Porter, Brenda E.; Robinson, Michael B.

    2013-01-01

    Excitatory amino acid carrier 1 (EAAC1, also called EAAT3) is a Na+-dependent glutamate transporter expressed by both glutamatergic and GABAergic neurons. It provides precursors for the syntheses of glutathione and GABA and contributes to the clearance of synaptically released glutamate. Mice deleted of EAAC1 are more susceptible to neurodegeneration in models of ischemia, Parkinson’s disease, and aging. Antisense knock-down of EAAC1 causes an absence seizure-like phenotype. Additionally, EAA...

  19. 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

    2015-01-01

    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. PMID:26214481

  20. 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.

  1. Deletion of Protein Tyrosine Phosphatase 1B (PTP1B Enhances Endothelial Cyclooxygenase 2 Expression and Protects Mice from Type 1 Diabetes-Induced Endothelial Dysfunction.

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    David J Herren

    Full Text Available Protein tyrosine phosphatase 1B (PTP1B dephosphorylates receptors tyrosine kinase and acts as a molecular brake on insulin signaling pathway. Conditions of metabolic dysfunction increase PTP1B, when deletion of PTP1B protects against metabolic disorders by increasing insulin signaling. Although vascular insulin signaling contributes to the control of glucose disposal, little is known regarding the direct role of PTP1B in the control of endothelial function. We hypothesized that metabolic dysfunctions increase PTP1B expression in endothelial cells and that PTP1B deletion prevents endothelial dysfunction in situation of diminished insulin secretion. Type I diabetes (T1DM was induced in wild-type (WT and PTP1B-deficient mice (KO with streptozotocin (STZ injection. After 28 days of T1DM, KO mice exhibited a similar reduction in body weight and plasma insulin levels and a comparable increase in glycemia (WT: 384 ± 20 vs. Ko: 432 ± 29 mg/dL, cholesterol and triglycerides, as WT mice. T1DM increased PTP1B expression and impaired endothelial NO-dependent relaxation, in mouse aorta. PTP1B deletion did not affect baseline endothelial function, but preserved endothelium-dependent relaxation, in T1DM mice. NO synthase inhibition with L-NAME abolished endothelial relaxation in control and T1DM WT mice, whereas L-NAME and the cyclooxygenases inhibitor indomethacin were required to abolish endothelium relaxation in T1DM KO mice. PTP1B deletion increased COX-2 expression and PGI2 levels, in mouse aorta and plasma respectively, in T1DM mice. In parallel, simulation of diabetic conditions increased PTP1B expression and knockdown of PTP1B increased COX-2 but not COX-1 expression, in primary human aortic endothelial cells. Taken together these data indicate that deletion of PTP1B protected endothelial function by compensating the reduction in NO bioavailability by increasing COX-2-mediated release of the vasodilator prostanoid PGI2, in T1DM mice.

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

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    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

  3. Radiation-induced chromosome aberrations in ataxia telangiectasia cells: high frequency of deletions and misrejoining detected by fluorescence in situ hybridization

    Science.gov (United States)

    Kawata, Tetsuya; Ito, Hisao; George, Kerry; Wu, Honglu; Uno, Takashi; Isobe, Kouichi; Cucinotta, Francis A.

    2003-01-01

    The mechanisms underlying the hyper-radiosensitivity of AT cells were investigated by analyzing chromosome aberrations in the G(2) and M phases of the cell cycle using a combination of chemically induced premature chromosome condensation (PCC) and fluorescence in situ hybridization (FISH) with chromosome painting probes. Confluent cultures of normal fibroblast cells (AG1522) and fibroblast cells derived from an individual with AT (GM02052) were exposed to gamma rays and allowed to repair at 37 degrees C for 24 h. At doses that resulted in 10% survival, GM02052 cells were approximately five times more sensitive to gamma rays than AG1522 cells. For a given dose, GM02052 cells contained a much higher frequency of deletions and misrejoining than AG1522 cells. For both cell types, a good correlation was found between the percentage of aberrant cells and cell survival. The average number of color junctions, which represent the frequency of chromosome misrejoining, was also found to correlate well with survival. However, in a similar surviving population of GM02052 and AG1522 cells, induced by 1 Gy and 6 Gy, respectively, AG1522 cells contained four times more color junctions and half as many deletions as GM02052 cells. These results indicate that both repair deficiency and misrepair may be involved in the hyper-radiosensitivity of AT cells.

  4. 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.

  5. 鸡胚低分子提取物对D-半乳糖拟衰老小鼠线粒体DNA缺失突变的影响%Effect of low molecular weight substance extracted from chick embryo on mitochondrial DNA deletion in aging mice induced by D-galactose

    Institute of Scientific and Technical Information of China (English)

    陈姝; 何蕴韶; 程刚; 高劲松

    2008-01-01

    Objective To investigate the effect of low molecular weight substance extracted from chick embryo on mitochondrial DNA(mtDNA)deletion in senile mice induced bv D-galactose.Methods Senile mice induced by D-galactose were treated with low molecular weight substance extracted from chick embryo.The deleted fragment of mtDNA was examined by using polymerase chain reaction technique and agarose gel electrophoresis.A relative quantitation of band densities was performed by using densitometry scanning techniques.The deletion was identified by using direct sequencing analysis. Results The 4239 bD mtDNA deletion were present in liver,cerebral cortex and hippocampus tissues in all of the mice.and it was significantly higher in senile model mice than in control mice(all P<0.01).Low molecular weight substance extracted from chick embryo reduced the mtDNA deletion in various tissues in senile model mice(all P<0.05).Deletion was more abundant in liver than in cerebral cortex and hippoeampus. Conclusions The 4239 bp mtDNA deletion is a common deletion,and low molecular weight substance extracted from chick embryo could decrease the incidence of 4239 bD mtDNA deletion.%目的 探讨鸡胚低分子提取物对D-半乳糖诱导的衰老小鼠线粒体DNA(mtDNA)缺失突变的影响.方法 采用D-半乳糖诱导制备衰老小鼠模型并用鸡胚低分子提取物处理.用聚合酶链反应技术和琼脂糖凝胶电泳检测mtDNA缺失片段,密度扫描技术对扩增片段进行相对定量.缺失片段构建质粒后,直接测序进行鉴定.结果 全部小鼠的肝、大脑皮质与海马组织内均存在4239 bp的mtDNA缺失片段.衰老模型鼠不同组织mtDNA缺失的相对百分含量均明显高于正常对照组(均为P%0.01),而鸡胚低分子提取物可明显降低模型鼠肝、大脑皮质与海马组织内mtDNA缺失的比例(均为P<0.05).肝组织中mtDNA缺失的比例较大脑皮质和海马组织更高.结论 4239 bp的mtDNA缺失片段普遍存在

  6. 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

  7. 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.

  8. 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.

  9. Targeted deletion of the murine Lgr4 gene decreases lens epithelial cell resistance to oxidative stress and induces age-related cataract formation.

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    Jun Zhu

    Full Text Available Oxidative stress contributes to the formation of cataracts. The leucine rich repeat containing G protein-coupled receptor 4 (LGR4, also known as GPR48, is important in many developmental processes. Since deletion of Lgr4 has previously been shown to lead to cataract formation in mice, we sought to determine the specific role that Lgr4 plays in the formation of cataracts. Initially, the lens opacities of Lgr4(-/- mice at different ages without ocular anterior segment dysgenesis (ASD were evaluated with slit-lamp biomicroscopy. Lenses from both Lgr4(-/- and wild-type mice were subjected to oxidation induced protein denaturation to assess the ability of the lens to withstand oxidation. The expression of antioxidant enzymes was evaluated with real-time quantitative PCR. Phenotypically, Lgr4(-/- mice showed earlier onset of lens opacification and higher incidence of cataract formation compared with wild-type mice of similar age. In addition, Lgr4(-/- mice demonstrated increased sensitivity to environmental oxidative damage, as evidenced by altered protein expression. Real-time quantitative PCR showed that two prominent antioxidant defense enzymes, catalase (CAT and superoxidase dismutase-1 (SOD1, were significantly decreased in the lens epithelial cells of Lgr4(-/- mice. Our results suggest that the deletion of Lgr4 can lead to premature cataract formation, as well as progressive deterioration with aging. Oxidative stress and altered expression of several antioxidant defense enzymes contribute to the formation of cataracts.

  10. Targeted deletion of the murine Lgr4 gene decreases lens epithelial cell resistance to oxidative stress and induces age-related cataract formation.

    Science.gov (United States)

    Zhu, Jun; Hou, Qiang; Dong, Xiang Da; Wang, Zhenlian; Chen, Xiaoyan; Zheng, Dandan; Zhou, Linglin; He, Chao; Liu, Mingyao; Tu, LiLi; Qu, Jia

    2015-01-01

    Oxidative stress contributes to the formation of cataracts. The leucine rich repeat containing G protein-coupled receptor 4 (LGR4, also known as GPR48), is important in many developmental processes. Since deletion of Lgr4 has previously been shown to lead to cataract formation in mice, we sought to determine the specific role that Lgr4 plays in the formation of cataracts. Initially, the lens opacities of Lgr4(-/-) mice at different ages without ocular anterior segment dysgenesis (ASD) were evaluated with slit-lamp biomicroscopy. Lenses from both Lgr4(-/-) and wild-type mice were subjected to oxidation induced protein denaturation to assess the ability of the lens to withstand oxidation. The expression of antioxidant enzymes was evaluated with real-time quantitative PCR. Phenotypically, Lgr4(-/-) mice showed earlier onset of lens opacification and higher incidence of cataract formation compared with wild-type mice of similar age. In addition, Lgr4(-/-) mice demonstrated increased sensitivity to environmental oxidative damage, as evidenced by altered protein expression. Real-time quantitative PCR showed that two prominent antioxidant defense enzymes, catalase (CAT) and superoxidase dismutase-1 (SOD1), were significantly decreased in the lens epithelial cells of Lgr4(-/-) mice. Our results suggest that the deletion of Lgr4 can lead to premature cataract formation, as well as progressive deterioration with aging. Oxidative stress and altered expression of several antioxidant defense enzymes contribute to the formation of cataracts. PMID:25811370

  11. PP2C-like Promoter and Its Deletion Variants Are Induced by ABA but Not by MeJA and SA in Arabidopsis thaliana

    Science.gov (United States)

    Bhalothia, Purva; Sangwan, Chetna; Alok, Anshu; Mehrotra, Sandhya; Mehrotra, Rajesh

    2016-01-01

    Gene expression is mediated through interaction between cis regulatory elements and its cognate transcription factors. Cis regulatory elements are defined as non-coding DNA sequences that provide the binding sites for transcription factors and are clustered in the upstream region of genes. ACGT cis regulatory element is one of the important cis regulatory elements found to be involved in diverse biological processes like auxin response, salicylic acid (SA) response, UV light response, ABA response and jasmonic acid (JA) response. We identified through in silico analysis that the upstream region of protein phosphatase 2C (PP2C) gene has a distinct genetic architecture of ACGT elements. In the present study, the activation of the full length promoter and its deletion constructs like 900 base pair, 500 base pair, 400 base pair and NRM (Nathji Rajesh Mehrotra) were examined by stable transformation in Arabidopsis thaliana using β-glucuronidase as the reporter gene. Evaluation of deletion constructs of PP2C-like promoter was carried out in the presence of phytohormones like abscisic acid (ABA), SA and JA. Our result indicated that the full length and 900 base pair promoter-reporter constructs of PP2C-like promoter was induced in response to ABA but not to methyl jasmonate and SA. PMID:27200023

  12. 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. PMID:27019998

  13. Translation of the radioresistance kinase TLK1B is induced by γ-irradiation through activation of mTOR and phosphorylation of 4E-BP1

    Directory of Open Access Journals (Sweden)

    De Benedetti Arrigo

    2004-04-01

    Full Text Available Abstract Background The mammalian protein kinase TLK1 is a homologue of Tousled, a gene involved in flower development in Arabidopsis thaliana. The function of TLK1 is not well known, although knockout of the gene in Drosophila, or expression of a dominant negative mutant in mouse cells causes loss of nuclear divisions and chromosome missegregation probably due to alterations in chromatin remodeling capacity. Overexpression of TLK1B, a spliced variant of the TLK1 mRNA, in a model mouse cell line increases their resistance to ionizing radiation, also likely through changes in chromatin remodeling. The TLK1B mRNA is translationally repressed by its 5'UTR and is regulated by the availability of eIF4E. We now report that radiation or doxorubicin result in an increase in the translation of TLK1B, and we have uncovered the likely mechanism for this effect. Results Radiation causes a shift in the polysomal distribution of TLK1B mRNA, from the untranslated region and small polysomes to the large polysomes, concomitant with an increase in the expression of TLK1B protein. This change is preceded by an increase in phosphorylation of the eIF4E inhibitory protein 4E-BP1, which releases eIF4E when it is phosphorylated. The phosphorylation of 4E-BP1 depends on mTOR, since rapamycin blocked the increase in phosphorylation induced by radiation, and prevented the increase in TLK1B protein expression. The activation of mTOR was likely due to the rapid activation of Akt following radiation. The activation of Akt could be inhibited with wortmannin, an inhibitor of PI3 kinase, hence placing PI3 kinase upstream of Akt as a very early event following radiation. Wortmannin also inhibited translation of TLK1B mRNA following activation by IR. This was shown both by western blot and by measuring the initiation capacity of the mRNA, as indicated by its distribution on polysomes. Conclusions The translational upregulation of TLK1B elicited by DNA double strand breaks

  14. 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.

  15. 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

  16. 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

  17. Deletion of the msdS/AfmsdC gene induces abnormal polarity and septation in Aspergillus fumigatus.

    Science.gov (United States)

    Li, Yanjie; Zhang, Lei; Wang, Depeng; Zhou, Hui; Ouyang, Haomiao; Ming, Jia; Jin, Cheng

    2008-07-01

    alpha-Mannosidases play an important role in the processing of mannose-containing glycans in eukaryotes. A deficiency in alpha-mannosidase is lethal in humans and cattle. In contrast to mammals, Saccharomyces cerevisiae does not require the endoplasmic reticulum alpha-mannosidase gene for growth. However, little is known of the consequence of loss of function of class I alpha-mannosidases in filamentous fungi. In this study, the msdS/AfmsdC gene was identified to encode 1,2-alpha-mannosidase MsdS in Aspergillus fumigatus. Soluble MsdS expressed in Escherichia coli was characterized as a typical class I alpha-mannosidase. The msdS gene was deleted by replacement of the msdS gene with a pyrG gene. Although the mutant showed a defect in N-glycan processing, as well as a reduction of cell wall components and a reduced ability of conidiation, it appeared that the rate of hyphal growth was not affected. Morphology analysis revealed abnormal polarity and septation at the stages of germination, hyphal growth and conidiation. Although the mechanism by which the N-glycan processing affects polarity and septation is unclear, our results show that msdS is involved in polarity and septation in A. fumigatus. PMID:18599824

  18. 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...

  19. Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis

    Science.gov (United States)

    Alves, C. Henrique; Ober-Blöbaum, Julia L.; Brouwers-Haspels, Inge; Asmawidjaja, Patrick S.; Mus, Adriana M. C.; Razawy, Wida; Molendijk, Marlieke; Clausen, Björn E.; Lubberts, Erik

    2015-01-01

    Dendritic cells (DCs) are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The β-catenin pathway has been suggested to promote a regulatory DC phenotype. The aim of this study was to unravel the role of β-catenin signalling to control DC function in the autoimmune collagen-induced arthritis model (CIA). Deletion of β-catenin specifically in DCs was achieved by crossing conditional knockout mice with a CD11c-Cre transgenic mouse line. Bone marrow-derived DCs (BMDCs) were generated and used to study the maturation profile of these cells in response to a TLR2 or TLR4 ligand stimulation. CIA was induced by intra-dermal immunization with 100 μg chicken type II collagen in complete Freund’s adjuvant on days 0 and 21. CIA incidence and severity was monitored macroscopically and by histology. The T cell profile as well as their cytokine production were analysed by flow cytometry. Lack of β-catenin specifically in DCs did not affect the spontaneous, TLR2- or TLR4-induced maturation and activation of BMDCs or their cytokine production. Moreover, no effect on the incidence and severity of CIA was observed in mice lacking β-catenin in CD11c+ cells. A decreased frequency of splenic CD3+CD8+ T cells and of regulatory T cells (Tregs) (CD4+CD25highFoxP3+), but no changes in the frequency of splenic Th17 (CCR6+CXCR3-CCR4+), Th2 (CCR6-CXCR3-CCR4+) and Th1 (CCR6-CXCR3+CCR4-) cells were observed in these mice under CIA condition. Furthermore, the expression of IL-17A, IL-17F, IL-22, IL-4 or IFNγ was also not affected. Our data indicate that ablation of β-catenin expression in DCs did not alter the course and severity of CIA. We conclude that although deletion of β-catenin resulted in a lower frequency of Tregs, this decrease was not sufficient to aggravate the onset and severity of CIA. PMID:26587585

  20. Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis.

    Directory of Open Access Journals (Sweden)

    C Henrique Alves

    Full Text Available Dendritic cells (DCs are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The β-catenin pathway has been suggested to promote a regulatory DC phenotype. The aim of this study was to unravel the role of β-catenin signalling to control DC function in the autoimmune collagen-induced arthritis model (CIA. Deletion of β-catenin specifically in DCs was achieved by crossing conditional knockout mice with a CD11c-Cre transgenic mouse line. Bone marrow-derived DCs (BMDCs were generated and used to study the maturation profile of these cells in response to a TLR2 or TLR4 ligand stimulation. CIA was induced by intra-dermal immunization with 100 μg chicken type II collagen in complete Freund's adjuvant on days 0 and 21. CIA incidence and severity was monitored macroscopically and by histology. The T cell profile as well as their cytokine production were analysed by flow cytometry. Lack of β-catenin specifically in DCs did not affect the spontaneous, TLR2- or TLR4-induced maturation and activation of BMDCs or their cytokine production. Moreover, no effect on the incidence and severity of CIA was observed in mice lacking β-catenin in CD11c+ cells. A decreased frequency of splenic CD3+CD8+ T cells and of regulatory T cells (Tregs (CD4+CD25highFoxP3+, but no changes in the frequency of splenic Th17 (CCR6+CXCR3-CCR4+, Th2 (CCR6-CXCR3-CCR4+ and Th1 (CCR6-CXCR3+CCR4- cells were observed in these mice under CIA condition. Furthermore, the expression of IL-17A, IL-17F, IL-22, IL-4 or IFNγ was also not affected. Our data indicate that ablation of β-catenin expression in DCs did not alter the course and severity of CIA. We conclude that although deletion of β-catenin resulted in a lower frequency of Tregs, this decrease was not sufficient to aggravate the onset and severity of CIA.

  1. Inhibiting heat shock protein 90 (HSP90 limits the formation of liver cysts induced by conditional deletion of Pkd1 in mice.

    Directory of Open Access Journals (Sweden)

    Zachary B Smithline

    Full Text Available Polycystic liver disease (PLD occurs in 75-90% of patients affected by autosomal dominant polycystic kidney disease (ADPKD, which affects 1∶400-1,000 adults and arises from inherited mutations in the PKD1 or PKD2 genes. PLD can lead to bile duct obstructions, infected or bleeding cysts, and hepatomegaly, which can diminish quality of life. At present, no effective, approved therapy exists for ADPKD or PLD. We recently showed that inhibition of the molecular chaperone heat shock protein 90 (HSP90 with a small molecule inhibitor, STA-2842, induced the degradation of multiple HSP90-dependent client proteins that contribute to ADPKD pathogenesis and slowed the progression of renal cystogenesis in mice with conditional deletion of Pkd1. Here, we analyzed the effects of STA-2842 on liver size and cystic burden in Pkd-/- mice with established PLD. Using magnetic resonance imaging over time, we demonstrate that ten weeks of STA-2842 treatment significantly reduced both liver mass and cystic index suggesting selective elimination of cystic tissue. Pre-treatment cystic epithelia contain abundant HSP90; the degree of reduction in cysts was accompanied by inhibition of proliferation-associated signaling proteins EGFR and others, and induced cleavage of caspase 8 and PARP1, and correlated with degree of HSP90 inhibition and with inactivation of ERK1/2. Our results suggest that HSP90 inhibition is worth further evaluation as a therapeutic approach for patients with PLD.

  2. Functional clonal deletion versus suppressor cell-induced transplantation tolerance in chimeras prepared with a short course of total-lymphoid irradiation

    International Nuclear Information System (INIS)

    Allogeneic bone marrow (BM) chimeras induced by infusion of BM cells into recipients conditioned with total lymphoid irradiation (TLI) were shown to develop humoral and cell-mediated tolerance to host and donor-type alloantigens by a number of in vitro and in vivo assays. Spleen cells of tolerant chimeras exhibited suppressive activity of mixed lymphocyte reaction (MLR). MLR suppression was not abrogated by depletion of Lyt-2 cells, and neither could Lyt-2-positive cells sorted from the spleens of tolerant chimeras suppress MLR or attenuate graft-versus-host reactivity in vivo. Likewise, specifically unresponsive spleen cells obtained from chimeras could not be induced to respond in MLR against tolerizing host-type cells following depletion of Lyt-2 or passage through a nylon-wool column. Tolerance of chimera spleen cells to host alloantigens, best documented by permanent survival of donor-type skin allografts, could be adoptively transferred into syngeneic recipients treated by heavy irradiation but not into untreated or mildly irradiated recipients. Adoptive transfer of tolerance seemed to be associated with experimental conditions favoring engraftment of tolerant cells rather than suppression of host reactivity. We speculate that although host and/or donor-derived suppressor cells may be operating in reducing the pool of specific alloreactive clones by blocking cell proliferation in response to allogeneic challenge, the final outcome in tolerant chimeras is actual or functional deletion of alloreactive clones

  3. Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo

    OpenAIRE

    Németh, Tamás; Futosi, Krisztina; Sitaru, Cassian; Ruland, Jürgen; Mócsai, Attila

    2016-01-01

    Neutrophils are terminally differentiated cells with limited transcriptional activity. The biological function of their gene expression changes is poorly understood. CARD9 regulates transcription during antifungal immunity but its role in sterile inflammation is unclear. Here we show that neutrophil CARD9 mediates pro-inflammatory chemokine/cytokine but not lipid mediator release during non-infectious inflammation. Genetic deficiency of CARD9 suppresses autoantibody-induced arthritis and derm...

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

    OpenAIRE

    M. Chen; S. Li; Xie, W.; Wang, B; Chen, D.

    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...

  5. Deletion of running-induced hippocampal neurogenesis by irradiation prevents development of an anxious phenotype in mice.

    Directory of Open Access Journals (Sweden)

    Johannes Fuss

    Full Text Available Recent evidence postulates a role of hippocampal neurogenesis in anxiety behavior. Here we report that elevated levels of neurogenesis elicit increased anxiety in rodents. Mice performing voluntary wheel running displayed both highly elevated levels of neurogenesis and increased anxiety in three different anxiety-like paradigms: the open field, elevated O-maze, and dark-light box. Reducing neurogenesis by focalized irradiation of the hippocampus abolished this exercise-induced increase of anxiety, suggesting a direct implication of hippocampal neurogenesis in this phenotype. On the other hand, irradiated mice explored less frequently the lit compartment of the dark-light box test irrespective of wheel running, suggesting that irradiation per se induced anxiety as well. Thus, our data suggest that intermediate levels of neurogenesis are related to the lowest levels of anxiety. Moreover, using c-Fos immunocytochemistry as cellular activity marker, we observed significantly different induction patterns between runners and sedentary controls when exposed to a strong anxiogenic stimulus. Again, this effect was altered by irradiation. In contrast, the well-known induction of brain-derived neurotrophic factor (BDNF by voluntary exercise was not disrupted by focal irradiation, indicating that hippocampal BDNF levels were not correlated with anxiety under our experimental conditions. In summary, our data demonstrate to our knowledge for the first time that increased neurogenesis has a causative implication in the induction of anxiety.

  6. 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.

  7. 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

  8. 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.

  9. 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.

  10. 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.

  11. 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.

  12. 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. PMID:26974397

  13. 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.

  14. Age-associated reduction of cell spreading induces mitochondrial DNA common deletion by oxidative stress in human skin dermal fibroblasts: implication for human skin connective tissue aging

    OpenAIRE

    Quan, Chunji; Cho, Moon Kyun; Perry, Daniel; Quan, Taihao

    2015-01-01

    Background Reduced cell spreading is a prominent feature of aged dermal fibroblasts in human skin in vivo. Mitochondrial DNA (mtDNA) common deletion has been reported to play a role in the human aging process, however the relationship between age-related reduced cell spreading and mtDNA common deletion has not yet been reported. Results To examine mtDNA common deletion in the dermis of aged human skin, the epidermis was removed from full-thickness human skin samples using cryostat. mtDNA comm...

  15. 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.

  16. 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

  17. 3p deletion syndrome.

    Science.gov (United States)

    Kaur, Anupam; Khetarpal, S

    2013-08-01

    3p deletion is a rare cytogenetic finding. Here we describe a 3 months old male with congenital malformations. His karyotype revealed 3p deletion 46,XY,del(3)(p25-pter). The child had flexion deformity of wrist and elbow which has never been reported before. PMID:24036645

  18. 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...

  19. 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.

  20. 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...

  1. Molecular basis of human growth hormone gene deletions

    International Nuclear Information System (INIS)

    Crossover sites resulting from unequal recombination within the human growth hormone (GH) gene cluster that cause GH1 gene deletions and isolated GH deficiency type 1A were localized in nine patients. In eight unrelated subjects homozygous for 6.7-kilobase (kb) deletions, the breakpoints are within two blocks of highly homologous DNA sequences that lie 5' and 3' to the GH1 gene. In seven of these eight cases, the breakpoints map within a 1,250-base-pair (bp) region composed of 300-bp Alu sequences of 86% homology and flanking non-Alu sequences that are 600 and 300 bp in length and are of 96% and 88% homology, respectively. In the eighth patient, the breakpoints are 5' to these Alu repeats and are most likely within a 700-bp-region of 96% homologous DNA sequences. In the ninth patient homozygous for a 7.6-kb deletion, the breakpoints are contained with a 29-bp perfect repeat lying 5' to GH1 and the human chorionic somatomammotropin pseudogene (CSHP1). Together, these results indicate that the presence of highly homologous DNA sequences flanking GH1 predispose to recurrent unequal recombinational events presumably through chromosomal misalignment

  2. 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.

  3. 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.

  4. On fixed-parameter algorithms for Split Vertex Deletion

    OpenAIRE

    CYGAN, Marek; Pilipczuk, Marcin

    2012-01-01

    In the Split Vertex Deletion problem, given a graph G and an integer k, we ask whether one can delete k vertices from the graph G to obtain a split graph (i.e., a graph, whose vertex set can be partitioned into two sets: one inducing a clique and the second one inducing an independent set). In this paper we study fixed-parameter algorithms for Split Vertex Deletion parameterized by k: we show that, up to a factor quasipolynomial in k and polynomial in n, the Split Vertex Deletion problem can ...

  5. 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

  6. Role of Evaluating MGMT Status and 1p36 Deletion in Radiosurgery-Induced Anaplastic Ependymoma That Rapidly and Completely Resolved by Temozolomide Alone: Case Report and Review of the Literature.

    Science.gov (United States)

    Hirono, Seiichiro; Iwadate, Yasuo; Kambe, Michiyo; Hiwasa, Takaki; Takiguchi, Masaki; Nakatani, Yukio; Saeki, Naokatsu

    2015-07-01

    Stereotactic gamma knife surgery (GKS)-induced brain tumors are extremely rare, and no ependymal tumors induced by GKS have been reported. Therefore, little is known about their clinical, pathologic, and genetic features. In addition, a regimen of adjuvant chemotherapy for anaplastic ependymoma (AE) has not been established. A 77-year-old man presented with a gait disturbance and left-side cerebellar ataxia more than 19 years after GKS performed for a cerebellar arteriovenous malformation. Imaging studies demonstrated an enhancing mass in the irradiated field with signs of intraventricular dissemination. Surgical resection confirmed the diagnosis of AE. Temozolomide (TMZ) was administrated postoperatively because the methylated promoter region of O(6)-methylguanine-DNA methyltransferase (MGMT) and 1p36 deletion were observed. Surprisingly, images 16 days after TMZ initiation demonstrated a complete resolution of the residual tumor that was maintained after three cycles of TMZ. This first case report of GKS-induced AE emphasizes the importance of genetic evaluation of MGMT and chromosomal deletion of 1p36 that are not commonly performed in primary ependymal tumors. In addition, it is speculated that a GKS-induced tumor may have a different genetic background compared with the primary tumor because the pathogenesis of the tumors differed. PMID:26251808

  7. Feature Analysis and Recognition of Induced Uranium Components Fission Signal Based on BP Neural Network%基于BP神经网络的诱发铀部件裂变信号特征分析及识别

    Institute of Scientific and Technical Information of China (English)

    谢军华; 刘知贵; 任立学; 张活力

    2012-01-01

    The paper presents feature parameter analysis and processing in fission time-dependent signal of induced uranium components based on BP-Neural Networks through the analysis of the measuring princi- ple and signal characteristics of induced uranium components fission signal. The auto correlation functions and cross correlation functions are calculated by using unbiased estimate, and then the feature parameters of fission signal in different status are extracted by using feature abstraction method, comparative method and derivative method, and then applied to training and prediction by means of BP-neural networks based on pattern recognition. Theoretical analysis and the results show that, it is effective to obtain feature pa- rameters of induced uranium component fission signal via comparative method and derivative method. Using BP neural network to tiveness and reasonability of recognize patter of fission signal, we got good results that verified the effec the method.%在对诱发铀部件裂变信号的测量原理及特点分析的基础上,开展了基于BP神经网络的诱发铀部件裂变时间关联信号特征参量分析处理的研究工作。采用无偏估计方法,计算信号的自相关函数和互相关函数,再利用比较法和导数法两种特征量提取方法,提取出不同状态下裂变信号的特征参量,借助于BP神经网络模式识别应用原理进行训练和预测。理论分析和研究结果表明:基于比较法和导数法获得的特征参量能较好地反映诱发铀部件裂变信号的特征;用BP神经网络对裂变信号进行模式识别,取得了较高的正确率,验证了此方法的有效性和合理性。

  8. 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.

  9. 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

    between 35,000 and 15,000 years BP, and kaolinite is the dominant clay mineral during this period. During most of the Holocene and >35,000 years BP, Al/Mg is comparable to today and smectites (Holocene) and illites (MIS 3) are the most abundant clay minerals. The clay mineralogy suggests deeper soil erosion during wet interglacials and more surficial erosion during dry glacial climate conditions. These findings imply that erosion and element cycling are mainly driven by changes in precipitation amount and terrestrial runoff in Towuti's catchment. The Al/Mg ratio on the other hand points to a stronger (lesser) contribution of relatively unweathered sediments sourced from the Mahalona River catchment during dry (wet) phases, likely as a result of lake-level changes and associated changes in shoreline proximity to our coring sites.

  10. 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.

  11. 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...

  12. 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...

  13. 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.

  14. Mucopolysaccharidosis type IVA: Common double deletion in the N-Acetylgalactosamine-6-sulfatase gene (GALNS)

    Energy Technology Data Exchange (ETDEWEB)

    Hori, Toshinori; Tomatsu, Shunji; Fukuda, Seiji [Gifu Univ. School of Medicine, Gifu (Japan)] [and others

    1995-04-10

    Mucopolysaccharidosis IVA (MPS IVA) is an autosomal recessive disorder caused by a deficiency in N-acetylgalactosamine-6-sulfatase (GALNS). We found two separate deletions of nearly 8.0 and 6.0 kb in the GALNS gene, including some exons. There are Alu repetitive elements near the breakpoints of the 8.0-kb deletion, and this deletion resulted from an Alu-Alu recombination. The other 6.0-kb deletion involved illegitimate recombinational events between incomplete short direct repeats of 8 bp at deletion breakpoints. The same rearrangement has been observed in a heteroallelic state in four unrelated patients. This is the first documentation of a common double deletion a gene that is not a member of a gene cluster. 39 refs., 5 figs.

  15. Deletion of GPR40 Impairs Glucose-Induced Insulin Secretion In Vivo in Mice Without Affecting Intracellular Fuel Metabolism in Islets

    Energy Technology Data Exchange (ETDEWEB)

    Alquier, Thierry; Peyot, Marie-Line; Latour, M. G.; Kebede, Melkam; Sorensen, Christina M.; Gesta, Stephane; Kahn, C. R.; Smith, Richard D.; Jetton, Thomas L.; Metz, Thomas O.; Prentki, Marc; Poitout, Vincent J.

    2009-11-01

    The G protein-coupled receptor GPR40 mediates fatty-acid potentiation of glucose-stimulated insulin secretion, but its contribution to insulin secretion in vivo and mechanisms of action remain uncertain. This study was aimed to ascertain whether GPR40 controls insulin secretion in vivo and modulates intracellular fuel metabolism in islets. We observed that glucose- and arginine-stimulated insulin secretion, assessed by hyperglycemic clamps, was decreased by approximately 60% in GPR40 knock-out (KO) fasted and fed mice, without changes in insulin sensitivity assessed by hyperinsulinemic-euglycemic clamps. Glucose and palmitate metabolism were not affected by GPR40 deletion. Lipid profiling revealed a similar increase in triglyceride and decrease in lysophosphatidylethanolamine species in WT and KO islets in response to palmitate. These results demonstrate that GPR40 regulates insulin secretion in vivo not only in response to fatty acids but also to glucose and arginine, without altering intracellular fuel metabolism.

  16. Human Immunodeficiency Virus Type 1 Vpr-Binding Protein VprBP, a WD40 Protein Associated with the DDB1-CUL4 E3 Ubiquitin Ligase, Is Essential for DNA Replication and Embryonic Development▿

    Science.gov (United States)

    McCall, Chad M.; Miliani de Marval, Paula L.; Chastain, Paul D.; Jackson, Sarah C.; He, Yizhou J.; Kotake, Yojiro; Cook, Jeanette Gowen; Xiong, Yue

    2008-01-01

    Damaged DNA binding protein 1, DDB1, bridges an estimated 90 or more WD40 repeats (DDB1-binding WD40, or DWD proteins) to the CUL4-ROC1 catalytic core to constitute a potentially large number of E3 ligase complexes. Among these DWD proteins is the human immunodeficiency virus type 1 (HIV-1) Vpr-binding protein VprBP, whose cellular function has yet to be characterized but has recently been found to mediate Vpr-induced G2 cell cycle arrest. We demonstrate here that VprBP binds stoichiometrically with DDB1 through its WD40 domain and through DDB1 to CUL4A, subunits of the COP9/signalsome, and DDA1. The steady-state level of VprBP remains constant during interphase and decreases during mitosis. VprBP binds to chromatin in a DDB1-independent and cell cycle-dependent manner, increasing from early S through G2 before decreasing to undetectable levels in mitotic and G1 cells. Silencing VprBP reduced the rate of DNA replication, blocked cells from progressing through the S phase, and inhibited proliferation. VprBP ablation in mice results in early embryonic lethality. Conditional deletion of the VprBP gene in mouse embryonic fibroblasts results in severely defective progression through S phase and subsequent apoptosis. Our studies identify a previously unknown function of VprBP in S-phase progression and suggest the possibility that HIV-1 Vpr may divert an ongoing chromosomal replication activity to facilitate viral replication. PMID:18606781

  17. Genomic deletions and precise removal of transposable elements mediated by short identical DNA segments in primates

    OpenAIRE

    Louie N van de Lagemaat; Gagnier, Liane; Medstrand, Patrik; Mager, Dixie L.

    2005-01-01

    Insertion of transposable elements is a major cause of genomic expansion in eukaryotes. Less is understood, however, about mechanisms underlying contraction of genomes. In this study, we show that retroelements can, in rare cases, be precisely deleted from primate genomes, most likely via recombination between 10- to 20-bp target site duplications (TSDs) flanking the retroelement. The deleted loci are indistinguishable from pre-integration sites, effectively reversing the insertion. Through h...

  18. 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.

  19. 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.

  20. Edit Distance with Block Deletions

    OpenAIRE

    Dana Shapira; Storer, James A.

    2011-01-01

    Several variants of the edit distance problem with block deletions are considered. Polynomial time optimal algorithms are presented for the edit distance with block deletions allowing character insertions and character moves, but without block moves. We show that the edit distance with block moves and block deletions is NP-complete (Nondeterministic Polynomial time problems in which any given solution to such problem can be verified in polynomial time, and any NP problem can be converted into...

  1. Functional Profiling Using the Saccharomyces Genome Deletion Project Collections.

    Science.gov (United States)

    Nislow, Corey; Wong, Lai Hong; Lee, Amy Huei-Yi; Giaever, Guri

    2016-01-01

    The ability to measure and quantify the fitness of an entire organism requires considerably more complex approaches than simply using traditional "omic" methods that examine, for example, the abundance of RNA transcripts, proteins, or metabolites. The yeast deletion collections represent the only systematic, comprehensive set of null alleles for any organism in which such fitness measurements can be assayed. Generated by the Saccharomyces Genome Deletion Project, these collections allow the systematic and parallel analysis of gene functions using any measurable phenotype. The unique 20-bp molecular barcodes engineered into the genome of each deletion strain facilitate the massively parallel analysis of individual fitness. Here, we present functional genomic protocols for use with the yeast deletion collections. We describe how to maintain, propagate, and store the deletion collections and how to perform growth fitness assays on single and parallel screening platforms. Phenotypic fitness analyses of the yeast mutants, described in brief here, provide important insights into biological functions, mechanisms of drug action, and response to environmental stresses. It is important to bear in mind that the specific assays described in this protocol represent some of the many ways in which these collections can be assayed, and in this description particular attention is paid to maximizing throughput using growth as the phenotypic measure. PMID:27587776

  2. 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

  3. 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.

  4. 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.

  5. Intestine-Specific Mttp Deletion Decreases Mortality and Prevents Sepsis-Induced Intestinal Injury in a Murine Model of Pseudomonas aeruginosa Pneumonia

    OpenAIRE

    Dominguez, Jessica A.; Xie, Yan; Dunne, W. Michael; Yoseph, Benyam P.; Burd, Eileen M.; Coopersmith, Craig M.; Davidson, Nicholas O

    2012-01-01

    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 out...

  6. Deletion of dopamine D1 and D3 receptors differentially affects spontaneous behaviour and cocaine-induced locomotor activity, reward and CREB phosphorylation.

    Science.gov (United States)

    Karasinska, Joanna M; George, Susan R; Cheng, Regina; O'Dowd, Brian F

    2005-10-01

    Co-localization of dopamine D1 and D3 receptors in striatal neurons suggests that these two receptors interact at a cellular level in mediating dopaminergic function including psychostimulant-induced behaviour. To study D1 and D3 receptor interactions in cocaine-mediated effects, cocaine-induced locomotion and reward in mice lacking either D1, D3 or both receptors were analysed. Spontaneous locomotor activity was increased in D1-/- and D1-/-D3-/- mice and D1-/-D3-/- mice did not exhibit habituation of spontaneous rearing activity. Cocaine (20 mg/kg) increased locomotor activity in wild-type and D3-/- mice, failed to stimulate activity in D1-/- mice and reduced activity in D1-/-D3-/- mice. In the conditioned place preference, all groups exhibited reward at 5, 10 and 20 mg/kg of cocaine. D1-/-D3-/- mice did not demonstrate preference at 2.5 mg/kg of cocaine although preference was observed in wild-type, D1-/- and D3-/- mice. The transcription factor cAMP-responsive element binding protein (CREB) is activated by phosphorylation in striatal regions following dopamine receptor activation. Striatal pCREB levels following acute cocaine were increased in wild-type and D3-/- mice and decreased in D1-/- and D1-/-D3-/- mice. After repeated administration of 2.5 mg/kg of cocaine, D1-/- mice had lower pCREB levels in caudate-putamen and nucleus accumbens. Our findings suggest that, although spontaneous and cocaine-induced horizontal activity depended mainly on the presence of the D1 receptor, there may be crosstalk between D1 and D3 receptors in rearing habituation and the perception of cocaine reward at low doses of the drug. Furthermore, alterations in pCREB levels were associated with changes in cocaine-induced locomotor activity but not reward. PMID:16197514

  7. Deletion of Nuclear Factor kappa B p50 Subunit Decreases Inflammatory Response and Mildly Protects Neurons from Transient Forebrain Ischemia-induced Damage.

    Science.gov (United States)

    Rolova, Taisia; Dhungana, Hiramani; Korhonen, Paula; Valonen, Piia; Kolosowska, Natalia; Konttinen, Henna; Kanninen, Katja; Tanila, Heikki; Malm, Tarja; Koistinaho, Jari

    2016-08-01

    Transient forebrain ischemia induces delayed death of the hippocampal pyramidal neurons, particularly in the CA2 and medial CA1 area. Early pharmacological inhibition of inflammatory response can ameliorate neuronal death, but it also inhibits processes leading to tissue regeneration. Therefore, research efforts are now directed to modulation of post-ischemic inflammation, with the aim to promote beneficial effects of inflammation and limit adverse effects. Transcription factor NF-κB plays a key role in the inflammation and cell survival/apoptosis pathways. In the brain, NF-κB is predominantly found in the form of a heterodimer of p65 (RelA) and p50 subunit, where p65 has a transactivation domain while p50 is chiefly involved in DNA binding. In this study, we subjected middle-aged Nfkb1 knockout mice (lacking p50 subunit) and wild-type controls of both sexs to 17 min of transient forebrain ischemia and assessed mouse performance in a panel of behavioral tests after two weeks of post-operative recovery. We found that ischemia failed to induce clear memory and motor deficits, but affected spontaneous locomotion in genotype- and sex-specific way. We also show that both the lack of the NF-κB p50 subunit and female sex independently protected CA2 hippocampal neurons from ischemia-induced cell death. Additionally, the NF-κB p50 subunit deficiency significantly reduced ischemia-induced microgliosis, astrogliosis, and neurogenesis. Lower levels of hippocampal microgliosis significantly correlated with faster spatial learning. We conclude that NF-κB regulates the outcome of transient forebrain ischemia in middle-aged subjects in a sex-specific way, having an impact not only on neuronal death but also specific inflammatory responses and neurogenesis. PMID:27493832

  8. 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.

  9. The oil palm metallothionein promoter contains a novel AGTTAGG motif conferring its fruit-specific expression and is inducible by abiotic factors.

    Science.gov (United States)

    Omidvar, Vahid; Abdullah, Siti Nor Akmar; Izadfard, Amir; Ho, Chai Ling; Mahmood, Maziah

    2010-09-01

    The 1,053-bp promoter of the oil palm metallothionein gene (so-called MSP1) and its 5' deletions were fused to the GUS reporter gene, and analysed in transiently transformed oil palm tissues. The full length promoter showed sevenfold higher activity in the mesocarp than in leaves and 1.5-fold more activity than the CaMV35S promoter in the mesocarp. The 1,053-bp region containing the 5' untranslated region (UTR) gave the highest activity in the mesocarp, while the 148-bp region was required for minimal promoter activity. Two positive regulatory regions were identified at nucleotides (nt) -953 to -619 and -420 to -256 regions. Fine-tune deletion of the -619 to -420 nt region led to the identification of a 21-bp negative regulatory sequence in the -598 to -577 nt region, which is involved in mesocarp-specific expression. Gel mobility shift assay revealed a strong interaction of the leaf nuclear extract with the 21-bp region. An AGTTAGG core-sequence within this region was identified as a novel negative regulatory element controlling fruit-specificity of the MSP1 promoter. Abscisic acid (ABA) and copper (Cu(2+)) induced the activity of the promoter and its 5' deletions more effectively than methyl jasmonate (MeJa) and ethylene. In the mesocarp, the full length promoter showed stronger inducibility in response to ABA and Cu(2+) than its 5' deletions, while in leaves, the -420 nt fragment was the most inducible by ABA and Cu(2+). These results suggest that the MSP1 promoter and its regulatory regions are potentially useful for engineering fruit-specific and inducible gene expression in oil palm. PMID:20635097

  10. 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.

  11. 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.

  12. Deletion of the V2 vasopressin receptor gene in two Chinese patients with nephrogenic diabetes insipidus

    Directory of Open Access Journals (Sweden)

    Yin Jun

    2006-11-01

    Full Text Available Abstract Background Congenital nephrogenic diabetes insipidus (NDI is a rare X-linked inherited disorder characterized by the excretion of large volumes of diluted urine and caused by mutations in arginine vasopressin receptor 2 (AVPR2 gene. To investigate the mutation of AVPR2 gene in a Chinese family with congenital NDI, we screened AVPR2 gene in two NDI patients and eight family members by PCR amplification and direct sequencing. Results Five specific fragments, covering entire coding sequence and their flanking intronic sequences of AVPR2 gene, were not observed in both patients, while those fragments were all detected in the control subjects. Several different fragments around the AVPR2 locus were amplified step by step. It was revealed that a genomic fragment of 5,995-bp, which contained the entire AVPR2 gene and the last exon (exon 22 of the C1 gene, was deleted and a 3-bp (GAG was inserted. Examination of the other family members showed that the mothers and the grandmother were carriers for this deletion. Conclusion Our findings suggest that the two patients in a Chinese family suffering from congenital NDI had a 5,995-bp deletion and 3-bp (GAG insertion at Xq28. The deletion contained the entire AVPR2 gene and exon 22 of the C1 gene.

  13. PLASMID DELETION FORMATION BETWEEN SHORT DIRECT REPEATS IN BACILLUS-SUBTILIS IS STIMULATED BY SINGLE-STRANDED ROLLING-CIRCLE REPLICATION INTERMEDIATES

    NARCIS (Netherlands)

    BRON, S; HOLSAPPEL, S; VENEMA, G; PEETERS, BPH

    1991-01-01

    The effects of the rolling-circle mode of replication and the generation of single-stranded DNA (ss DNA) on plasmid deletion formation between short direct repeats in Bacillus subtilis were studied. Deletion units consisting of direct repeats (9, 18, or 27 bp) that do or do not flank inverted repeat

  14. 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.

  15. EST Table: BP123183 [KAIKOcDNA[Archive

    Lifescience Database Archive (English)

    Full Text Available BP123183 epV30681 10/09/28 44 %/109 aa ref|XP_967427.2| PREDICTED: similar to hypoxia....h 10/09/10 44 %/109 aa gi|189237669|ref|XP_967427.2| PREDICTED: similar to hypoxia-inducible factor 1 alpha [Tribolium castaneum] FS913906 epV3 ...

  16. Influence of BP Ultimate on engine cleanliness

    OpenAIRE

    Mieghem, R.S.P. van

    2007-01-01

    During early 2005, BP introduced two new fuels in the Netherlands. These new products are called BP Ultimate 98 Unleaded and BP Ultimate Diesel. These fuels were formulated to offer several benefits compared to ordinary fuels, specifically in engine cleanliness. TNO was asked to evaluate the test results from BP, examine the stated claims and, if proven, to give a specific endorsement of calculated claims of the product(s). In order to understand the performed research and the arising conclus...

  17. Research On Coagulation Zone Prediction Induced By Cooled-tip Radiofrequency Ablation Base On The BP Neural Network%基于BP神经网络的冷极射频消融凝固灶预测研究

    Institute of Scientific and Technical Information of China (English)

    郑丹平; 朱名日; 刘文彬; 姚鑫; 潘凯

    2014-01-01

    射频消融过程非常复杂,它的疗效影响因素多且关系复杂。在冷极射频消融仪治疗肿瘤过程中,射频输出功率和循环水泵转速起着重要作用。为扩大消融范围,达到一次性灭活肿瘤细胞,在治疗前,需选择适当的治疗参数。将BP神经网络模型引入射频消融中,建立冷极射频消融凝固灶预测的模型,并对效果进行检验。结果表明:检验样本中消融凝固灶与实际值的线性相关系数为0.988。针对消融横径,其相对误差的平均值为0.01。该模型对射频消融参数设置起到一定的支持作用,具有一定的实际参考价值。%The process of radiofrequency ablation is very complicated, there are many factors to influence the ef-fect and the relation is complex. The power output by RF and circulating pump speed plays an important role in the process of treatment by cooled-tip RFA. To expand the scope of ablation, the appropriate parameters should be se-lected to achieve one-time inactivated tumor cells before treatment. The BP neural network is introduced in the radiofrequency ablation. A model of coagulation zone prediction induced by cooled-tip radiofrequency ablation is built. The results show that the test sample correlation coefficient of linear ablation lesion and actual value is 0.988. For ablation diameter, the average value of the relative error is 0.01.The model plays a supporting role on parameter setting of radiofrequency ablation, which has some practical value.

  18. Expression of the Transcription Factor E4BP4 in Human Basophils

    DEFF Research Database (Denmark)

    Jensen, Bettina Margrethe; Gohr, Maria; Poulsen, Lars Kærgaard

    2014-01-01

    Rationale The cytokine IL-3 plays an important role for human basophil development, function and survival. IL-3 is also reported to induce the expression of the transcription factor E4BP4, but it is not known whether E4BP4 is expressed in basophils and influences basophil responsiveness. The aim...... the transcription factor E4BP4 which might have an impact on basophil histamine release....

  19. ATLAS DQ2 DELETION SERVICE

    CERN Document Server

    Oleynik, D; The ATLAS collaboration; Garonne, V; Campana, S

    2012-01-01

    ATLAS DQ2 Deletion service is a sub system of the ATLAS Distributed Data Management (DDM) project DQ2. DDM DQ2 responsible for the replication, access and bookkeeping of ATLAS data across more than 130 distributed grid sites. It also enforces data management policies decided on by the collaboration and defined in the ATLAS computing model. Responsibility of ATLAS DQ2 Deletion service is serving deletion requests on the grid by interacting with grid middleware and the DQ2 catalogues. Furthermore, it also takes care of retry strategies, check-pointing transactions, load management and fault tolerance. In this talk special attention is paid to the technical details, which are used to achieve the high performance of service, accomplished without overloading either site storage, catalogues or other DQ2 components. Also specialty of database backend implementation will be described. Special section will be devote to the deletion monitoring service that allows operators a detailed view of the working system.

  20. ATLAS DQ2 Deletion Service

    CERN Document Server

    OLEYNIK, D; The ATLAS collaboration; GARONNE, V; CAMPANA, S

    2012-01-01

    The ATLAS Distributed Data Management project DQ2 is responsible for the replication, access and bookkeeping of ATLAS data across more than 100 distributed grid sites. It also enforces data management policies decided on by the collaboration and defined in the ATLAS computing model. The DQ2 deletion service is one of the most important DDM services. This distributed service interacts with 3rd party grid middleware and the DQ2 catalogs to serve data deletion requests on the grid. Furthermore, it also takes care of retry strategies, check-pointing transactions, load management and fault tolerance. In this paper special attention is paid to the technical details which are used to achieve the high performance of service (peaking at more than 4 millions files deleted per day), accomplished without overloading either site storage, catalogs or other DQ2 components. Special attention is also paid to the deletion monitoring service that allows operators a detailed view of the working system.

  1. 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 ...

  2. 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- ...

  3. 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- ...

  4. 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- ...

  5. Genetic deletion of the adenosine A(2A) receptor prevents nicotine-induced upregulation of α7, but not α4β2* nicotinic acetylcholine receptor binding in the brain.

    Science.gov (United States)

    Metaxas, Athanasios; Al-Hasani, Ream; Farshim, Pamela; Tubby, Kristina; Berwick, Amy; Ledent, Catherine; Hourani, Susanna; Kitchen, Ian; Bailey, Alexis

    2013-08-01

    Considerable evidence indicates that adenosine A(2A) receptors (A(2A)Rs) modulate cholinergic neurotransmission, nicotinic acetylcholine receptor (nAChR) function, and nicotine-induced behavioural effects. To explore the interaction between A(2A) and nAChRs, we examined if the complete genetic deletion of adenosine A(2A)Rs in mice induces compensatory alterations in the binding of different nAChR subtypes, and whether the long-term effects of nicotine on nAChR regulation are altered in the absence of the A(2A)R gene. Quantitative autoradiography was used to measure cytisine-sensitive [¹²⁵I]epibatidine and [¹²⁵I]α-bungarotoxin binding to α4β2* and α7 nAChRs, respectively, in brain sections of drug-naïve (n = 6) or nicotine treated (n = 5-7), wild-type and adenosine A(2A)R knockout mice. Saline or nicotine (7.8 mg/kg/day; free-base weight) were administered to male CD1 mice via subcutaneous osmotic minipumps for a period of 14 days. Blood plasma levels of nicotine and cotinine were measured at the end of treatment. There were no compensatory developmental alterations in nAChR subtype distribution or density in drug-naïve A(2A)R knockout mice. In nicotine treated wild-type mice, both α4β2* and α7 nAChR binding sites were increased compared with saline treated controls. The genetic ablation of adenosine A(2A)Rs prevented nicotine-induced upregulation of α7 nAChRs, without affecting α4β2* receptor upregulation. This selective effect was observed at plasma levels of nicotine that were within the range reported for smokers (10-50 ng ml⁻¹). Our data highlight the involvement of adenosine A(2A)Rs in the mechanisms of nicotine-induced α7 nAChR upregulation, and identify A(2A)Rs as novel pharmacological targets for modulating the long-term effects of nicotine on α7 receptors. PMID:23583933

  6. 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...

  7. 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.

  8. A 76-bp deletion in the Mip gene causes autosomal dominant cataract in Hfi mice.

    NARCIS (Netherlands)

    Sidjanin, D.J.; Parker-Wilson, D.M.; Neuhauser-Klaus, A.; Pretsch, W.; Favor, J.; Deen, P.M.T.; Ohtaka-Maruyama, C.; Lu, Y.; Bragin, A.; Skach, W.R.; Chepelinsky, A.B.; Grimes, P.A.; Stambolian, D.E.

    2001-01-01

    Hfi is a dominant cataract mutation where heterozygotes show hydropic lens fibers and homozygotes show total lens opacity. The Hfi locus was mapped to the distal part of mouse chromosome 10 close to the major intrinsic protein (Mip), which is expressed only in cell membranes of lens fibers. Molecula

  9. Association of a Chromosomal Rearrangement Event with Mouse Posterior Polymorphous Corneal Dystrophy and Alterations in Csrp2bp, Dzank1, and Ovol2 Gene Expression.

    Directory of Open Access Journals (Sweden)

    Anna L Shen

    Full Text Available We have previously described a mouse model of human posterior polymorphous corneal dystrophy (PPCD and localized the causative mutation to a 6.2 Mbp region of chromosome 2, termed Ppcd1. We now show that the gene rearrangement linked to mouse Ppcd1 is a 3.9 Mbp chromosomal inversion flanked by 81 Kbp and 542 bp deletions. This recombination event leads to deletion of Csrp2bp Exons 8 through 11, Dzank1 Exons 20 and 21, and the pseudogene Znf133. In addition, we identified translocation of novel downstream sequences to positions adjacent to Csrp2bp Exon 7 and Dzank1 Exon 20. Twelve novel fusion transcripts involving Csrp2bp or Dzank1 linked to downstream sequences have been identified. Eight are expressed at detectable levels in PPCD1 but not wildtype eyes. Upregulation of two Csrp2bp fusion transcripts, as well as upregulation of the adjacent gene, Ovol2, was observed. Absence of the PPCD1 phenotype in animals haploinsufficient for Csrp2bp or both Csrp2bp and Dzank1 rules out haploinsufficiency of these genes as a cause of mouse PPCD1. Complementation experiments confirm that PPCD1 embryonic lethality is due to disruption of Csrp2bp expression. The ocular expression pattern of Csrp2bp is consistent with a role for this protein in corneal development and pathogenesis of PPCD1.

  10. 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.

  11. ATLAS DQ2 Deletion Service

    CERN Document Server

    OLEYNIK, D; The ATLAS collaboration; GARONNE, V; CAMPANA, S

    2012-01-01

    The ATLAS Distributed Data Management project DQ2 is responsible for the replication, access and bookkeeping of ATLAS data across more than 100 distributed grid sites. It also enforces data management policies decided on by the collaboration and defined in the ATLAS computing model. The DQ2 Deletion Service is one of the most important DDM services. This distributed service interacts with 3rd party grid middleware and the DQ2 catalogues to serve data deletion requests on the grid. Furthermore, it also takes care of retry strategies, check-pointing transactions, load management and fault tolerance. In this paper special attention is paid to the technical details which are used to achieve the high performance of service, accomplished without overloading either site storage, catalogues or other DQ2 components. Special attention is also paid to the deletion monitoring service that allows operators a detailed view of the working system.

  12. 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.

  13. 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.

  14. Electronic states of BP, BP +, BP -, B 2P 2, B2P2- and B2P2+

    Science.gov (United States)

    Linguerri, Roberto; Komiha, Najia; Oswald, Rainer; Mitrushchenkov, Alexander; Rosmus, Pavel

    2008-05-01

    Using augmented sextuple zeta basis sets and internally contracted multireference configuration interaction (MRCI) wavefunctions, potential energy, electric dipole and transition moments have been computed for the X 3Π, a 1Σ +, b 1Π and A 3Σ - states of BP, X 2Σ + and A 2Π states of BP - and X 4Σ - and A 4Π states of BP +. From these data spectroscopic constants, radiative transition probabilities and photoelectron spectra of BP - and BP have been evaluated. The non-vanishing spin-orbit coupling elements between the four low lying triplet and singlet states of the neutral BP have also been calculated from MRCI wavefunctions. The treatment of the corresponding perturbations in the manifold of dense rovibrational states in the three lowest states would require a precise knowledge of the electronic excitation energies. Our best singlet-triplet separations (X-a) are calculated to be 2412 cm -1 (MRCI) and 2482 cm -1 (restricted coupled cluster with perturbative triples (RCCSD(T))) with an estimated error bound of about ±200 cm -1. All three states have long radiative lifetimes with cascading among the rovibrational levels of different states. The ionization energy IE e of BP is calculated to be 9.22 eV (MRCI) and 9.48 eV (RCCSD(T)), the electron affinity EA e 2.51 eV (MRCI) and 2.74 eV (RCCSD(T)). The photoelectron spectra of BP and BP - have been obtained from the Franck-Condon factors of the MRCI potentials. For the UV spectroscopy the dipole allowed radiative transition probabilities are given for A 3Σ - ↔ X 3Π, b 1Π ↔ a 1Σ + of BP, A 2Π ↔ X 2Σ + of BP - and A 4Π ↔ X 4Σ - of BP +. The ionization energy IE e of B 2P 2 of 8.71 eV and the electron affinity EA e of 2.34 eV have been calculated by the RCCSD(T)/aVQZ approach. Also the harmonic vibrational wavenumbers for the electronic ground states of the ions B2P2+ and B2P2- are given.

  15. EGb761对NMB诱导的小鼠妊娠子宫平滑肌细胞中NF-κB活性和 IL-6表达的影响%The effects of EGb761 on the activity of NF-κBp65 and expression of IL-6 induced by NMB in pregnant primary cultured smooth muscle cells

    Institute of Scientific and Technical Information of China (English)

    张卫社; 谢志萍; 吴梅婷; 费奎琳; 梁清华

    2012-01-01

    Aim To investigate the effects of Ginkgo biloba extract 761 (EGb761) on the activity of nuclear factor κB p65 (NF-κBp65) and expression of interleu-kin-6 (IL-6) induced by Neuromedin B(NMB) in primary cultured smooth muscle cells from the term. Methods The primary cultured smooth muscle cells with positive expression of NMB receptor (NMBR) from the term were prepared. The combination of NMBR and NF-κBp65 RNA interference (RNAi), real time PCR and Phosphorylation ELISA methods were used to study the effects of EGb761 on the activity of NF-κBp65 and expression of IL-6 induced by NMB in smooth muscle cells. Results The NF-κBp65 DNA binding activity was significantly lower in EGb761 group with high concentration (100 mg · L-1) than that in control group and low dose concentration group (P<0.01). However, there were not differencescompared low or middle concentration groups with control group. The pretreated with high concentration of EGb761 could significantly reduce NF-κBp65 activity and IL-6 expression induced by NMB in pregnant smooth muscle cells (P < 0. 01), and these changes were significantly correlated (r = 0. 892, P <0. 01). Besides, the inhibiting role of EGb761 could be blocked by NMBR and NF-κB RNAi, respectively. Moreover, the blocking efficiency of two genes knockdown showed no significant difference. Conclusion EGb761 can inhibit NF-κBp65 activity and expression of IL-6 via NMBR pathway in primary cultured smooth muscle cells from the term.%目的 探讨银杏叶提取物EGb761对神经调节素B(Neuromedin B,NMB)诱导的分娩期小鼠子宫平滑肌细胞中NF-κB活性和 IL-6表达的影响.方法 应用原代培养的、NMB受体(Neuromedin B receptor,NMBR)表达阳性的分娩期小鼠子宫平滑肌细胞,联合NMBR和核因子κB (Nuclear factor kappa B,NF-κB) p65的 RNA干扰技术、real-time PCR和磷酸化ELISA等方法,确定EGb761对NMB诱导的小鼠子宫平滑肌细胞中NF-κB和 IL-6表达的影响.结果 高浓度的 EGb761

  16. 76 FR 22680 - Procurement List; Deletions

    Science.gov (United States)

    2011-04-22

    ... INFORMATION: Deletions On 2/25/2011 (76 FR 10571), the Committee for Purchase From People Who Are Blind or... PEOPLE WHO ARE BLIND OR SEVERELY DISABLED Procurement List; Deletions AGENCY: Committee for Purchase From People Who Are Blind or Severely Disabled. ACTION: Deletions from the Procurement List. SUMMARY:...

  17. Loss of full length CtBP1 expression enhances the invasive potential of human melanoma

    International Nuclear Information System (INIS)

    The C-terminal binding protein 1 (CtBP1) is a known co-repressor of gene transcription. We recently revealed that CtBP1 expression is lost in melanoma cells and melanoma inhibitory activity (MIA) expression is subsequently increased. The present study was performed to evaluate a more general role of CtBP1 in human melanoma and identify further CtBP1-regulated target genes. Sequence analysis and expression profile of CtBP1 in melanoma cell lines were done by PCR. Boyden Chamber assays and co-immunoprecipitation were performed to investigate the functional role of CtBP1. Gene expression analysis and micro array data were used to define target genes. Interestingly, we detected an alternative splice product of CtBP1 with unknown function whose expression is induced at reduction of full length CtBP1. Overexpression of full length CtBP1 in melanoma cells had no effect on cell proliferation but did influence cell migration and invasiveness. To understand the effect of CtBP1 we identified putative LEF/TCF target genes found to be strongly expressed in melanoma using DNA microarray analysis. We focused on fourteen genes not previously associated with melanoma. Detailed analysis revealed that most of these were known to be involved in tumor metastasis. Eleven genes had expression profiles associated with melanoma cell invasiveness. In summary, this study revealed that reduction of CtBP1 expression is correlated with migratory, invasive potential of melanoma cells

  18. Hepatic Mttp deletion reverses gallstone susceptibility in L-Fabp knockout mice

    OpenAIRE

    Xie, Yan; Fung, Ho Yee Joyce; Newberry, Elizabeth P.; Kennedy, Susan,; Luo, Jianyang; Crooke, Rosanne M.; Graham, Mark J.; Davidson, Nicholas O.

    2014-01-01

    Previous studies demonstrated that L-Fabp KO mice are more susceptible to lithogenic diet (LD)-induced gallstones because of altered hepatic cholesterol metabolism and increased canalicular cholesterol secretion. Other studies demonstrated that liver-specific deletion of microsomal triglyceride transfer protein (Mttp-LKO) reduced LD-induced gallstone formation by increasing biliary phospholipid secretion. Here we show that mice with combined deletion (i.e., DKO mice) are protected from LD-ind...

  19. Identification and characterization of a novel calcyclin binding protein (CacyBP) gene from Apis cerana cerana.

    Science.gov (United States)

    Yu, Xiaoli; Lu, Wenjing; Sun, Rujiang; Guo, Xingqi; Xu, Baohua

    2012-08-01

    Calcyclin binding protein (CacyBP), a homolog of Sgt1, was shown to interact with some S100 proteins, Skp1, tubulin, actin and ERK1/2 kinases. Studies have also shown that CacyBP is a neuronal protein in mammals. Limited information is available regarding the properties and functions of CacyBP in insects. Here, we cloned and characterized a novel CacyBP gene, named AccCacyBP, from honeybee (Apis cerana cerana). Bioinformatic analysis indicated that AccCacyBP was highly conserved and closely related to the CacyBP of other insects. Promoter analysis revealed a number of putative tissue, development and stress-related transcription factor-binding sites. RT-qPCR demonstrated that AccCacyBP was expressed at all of the stages of development, especially in the brains of honeybees. Moreover, immunohistochemistry analysis showed the presence of AccCacyBP in the brain. The transcript levels of AccCacyBP in the brains of honeybees were developmentally induced and upregulated by exposure to oxidative stresses, including UV-light, acetamiprid and HgCl(2). This study demonstrates that the CacyBP gene in honeybees may be a neuronal protein involved in the developmental regulation and the stress-response of the brain of honeybees. PMID:22539186

  20. 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.

  1. Spectroscopic observations of ASASSN-15bp

    Science.gov (United States)

    Williams, S. C.; Darnley, M. J.; Bode, M. F.; Copperwheat, C. M.

    2015-01-01

    We report spectroscopic observations of the optical transient ASASSN-15bp (ATel #6981) taken on 2015 January 25.31 UT using the FRODOSpec spectrograph (Barnsley et al. 2012) on the Liverpool Telescope (Steele et al. 2004).

  2. 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.

  3. 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.

  4. Neuropathological signs of inflammation correlate with mitochondrial DNA deletions in mesial temporal lobe epilepsy.

    Science.gov (United States)

    Volmering, Elisa; Niehusmann, Pitt; Peeva, Viktoriya; Grote, Alexander; Zsurka, Gábor; Altmüller, Janine; Nürnberg, Peter; Becker, Albert J; Schoch, Susanne; Elger, Christian E; Kunz, Wolfram S

    2016-08-01

    Accumulation of mitochondrial DNA (mtDNA) deletions has been proposed to be responsible for the presence of respiratory-deficient neurons in several CNS diseases. Deletions are thought to originate from double-strand breaks due to attack of reactive oxygen species (ROS) of putative inflammatory origin. In epileptogenesis, emerging evidence points to chronic inflammation as an important feature. Here we aimed to analyze the potential association of inflammation and mtDNA deletions in the hippocampal tissue of patients with mesial temporal lobe epilepsy (mTLE) and hippocampal sclerosis (HS). Hippocampal and parahippocampal tissue samples from 74 patients with drug-refractory mTLE served for mtDNA analysis by multiplex PCR as well as long-range PCR, single-molecule PCR and ultra-deep sequencing of mtDNA in selected samples. Patients were sub-classified according to neuropathological findings. Semi-quantitative assessment of neuronal cell loss was performed in the hippocampal regions CA1-CA4. Inflammatory infiltrates were quantified by cell counts in the CA1, CA3 and CA4 regions from well preserved hippocampal samples (n = 33). Samples with HS showed a significantly increased frequency of a 7436-bp mtDNA deletion (p T transversions compared to mTLE patients with different histopathology. Interestingly, the number of T-lymphocytes in the hippocampal CA1, CA3 and CA4 regions was, similar to the 7436-bp mtDNA deletion, significantly increased in samples with HS compared to other subgroups. Our findings show a coincidence of HS, increased somatic G>T transversions, the presence of a specific mtDNA deletion, and increased inflammatory infiltrates. These results support the hypothesis that chronic inflammation leads to mitochondrial dysfunction by ROS-mediated mtDNA mutagenesis which promotes epileptogenesis and neuronal cell loss in patients with mTLE and HS. PMID:26993140

  5. Dissecting the phenotypes of Dravet syndrome by gene deletion.

    Science.gov (United States)

    Rubinstein, Moran; Han, Sung; Tai, Chao; Westenbroek, Ruth E; Hunker, Avery; Scheuer, Todd; Catterall, William A

    2015-08-01

    Neurological and psychiatric syndromes often have multiple disease traits, yet it is unknown how such multi-faceted deficits arise from single mutations. Haploinsufficiency of the voltage-gated sodium channel Nav1.1 causes Dravet syndrome, an intractable childhood-onset epilepsy with hyperactivity, cognitive deficit, autistic-like behaviours, and premature death. Deletion of Nav1.1 channels selectively impairs excitability of GABAergic interneurons. We studied mice having selective deletion of Nav1.1 in parvalbumin- or somatostatin-expressing interneurons. In brain slices, these deletions cause increased threshold for action potential generation, impaired action potential firing in trains, and reduced amplification of postsynaptic potentials in those interneurons. Selective deletion of Nav1.1 in parvalbumin- or somatostatin-expressing interneurons increases susceptibility to thermally-induced seizures, which are strikingly prolonged when Nav1.1 is deleted in both interneuron types. Mice with global haploinsufficiency of Nav1.1 display autistic-like behaviours, hyperactivity and cognitive impairment. Haploinsufficiency of Nav1.1 in parvalbumin-expressing interneurons causes autistic-like behaviours, but not hyperactivity, whereas haploinsufficiency in somatostatin-expressing interneurons causes hyperactivity without autistic-like behaviours. Heterozygous deletion in both interneuron types is required to impair long-term spatial memory in context-dependent fear conditioning, without affecting short-term spatial learning or memory. Thus, the multi-faceted phenotypes of Dravet syndrome can be genetically dissected, revealing synergy in causing epilepsy, premature death and deficits in long-term spatial memory, but interneuron-specific effects on hyperactivity and autistic-like behaviours. These results show that multiple disease traits can arise from similar functional deficits in specific interneuron types. PMID:26017580

  6. 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

  7. Regulation of B cell differentiation by the ubiquitin-binding protein TAX1BP1

    Science.gov (United States)

    Matsushita, Nobuko; Suzuki, Midori; Ikebe, Emi; Nagashima, Shun; Inatome, Ryoko; Asano, Kenichi; Tanaka, Masato; Matsushita, Masayuki; Kondo, Eisaku; Iha, Hidekatsu; Yanagi, Shigeru

    2016-01-01

    Tax1-binding protein 1 (TAX1BP1) is a ubiquitin-binding protein that restricts nuclear factor-κB (NF-κB) activation and facilitates the termination of aberrant inflammation. However, its roles in B-cell activation and differentiation are poorly understood. To evaluate the function of TAX1BP1 in B cells, we established TAX1BP1-deficient DT40 B cells that are hyper-responsive to CD40-induced extracellular signal-regulated kinase (ERK) activation signaling, exhibit prolonged and exaggerated ERK phosphorylation and show enhanced B lymphocyte-induced maturation protein 1 (Blimp-1; a transcription factor inducing plasma cell differentiation) expression that is ERK-dependent. Furthermore, TAX1BP1-deficient cells exhibit significantly decreased surface IgM expression and increased IgM secretion. Moreover, TAX1BP1-deficient mice display reduced germinal center formation and antigen-specific antibody production. These findings show that TAX1BP1 restricts ERK activation and Blimp-1 expression and regulates germinal center formation. PMID:27515252

  8. 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.

  9. Complicated biallelic inactivation of Pten in radiation-induced mouse thymic lymphomas

    International Nuclear Information System (INIS)

    Inactivation of the phosphatase and tensin homolog gene (Pten) occurs via multiple tissue-dependent mechanisms including epigenetic silencing, point mutations, insertions, and deletions. Although frequent loss of heterozygosity around the Pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the proportion of lymphomas with inactivated Pten and the spectrum of causal aberrations have not been extensively characterized. Here, we assessed the mode of Pten inactivation by comprehensive analysis of the expression and alteration of Pten in 23 radiation-induced thymic lymphomas developed in B6C3F1 mice. We found no evidence for methylation-associated silencing of Pten; rather, complex structural abnormalities comprised of missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions were identified in 8 of 23 lymphomas (35%). Sequencing of deletion breakpoints suggested that aberrant V(D)J recombination and microhomology-mediated rearrangement were responsible for the focal deletions. Seven of the 8 lymphomas had biallelic alterations, and 4 of them did not express Pten protein. These Pten aberrations coincided with downstream Akt phosphorylation. In conclusion, we demonstrate that Pten inactivation is frequently biallelic and is caused by a variety of structural abnormalities (rather than by epigenetic silencing) and is involved in radiation-induced lymphomagenesis.

  10. Deletion 22q13.3 syndrome

    OpenAIRE

    Phelan Mary C

    2008-01-01

    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 syndr...

  11. Effect of 5 '-deletion of Arabi dopsis profilin2 promoter on its vascular specific expression

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Based on the published sequence of profilin2promoter of Arabidopsis thaliana, a full-length promoter ments with length of 1380, 1153, 969 and 597 bp were then fused with gus (uidA) gene respectively. Constructed plant expression vectors were individually transferred into Kalan choe laciniata and transgenic plants regenerated. GUS his tochemical assay confirmed that the full-length promoter Pfnl.7 was vascular-specific. Deletion assays showed that profilin2 promoter could be divided into three parts. Dele tion of fragment 1 ( -1667--1380 bp) resulted in constitu tive expression, suggesting that element(s) responsible for vascular-specific expression might exist in this region. Frag ment 2 located at -1153 - -597 bp strongly inhibited gus gene expression. Fragment 3 ( -597 - -1 bp) is considered as a basic domain of profilin2.

  12. 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.

  13. 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.

  14. Size unlimited markerless deletions by a transconjugative plasmid-system in Bacillus licheniformis.

    Science.gov (United States)

    Rachinger, Michael; Bauch, Melanie; Strittmatter, Axel; Bongaerts, Johannes; Evers, Stefan; Maurer, Karl-Heinz; Daniel, Rolf; Liebl, Wolfgang; Liesegang, Heiko; Ehrenreich, Armin

    2013-09-20

    Conjugative shuttle vectors of the pKVM series, based on an IncP transfer origin and the pMAD vector with a temperature sensitive replication were constructed to establish a markerless gene deletion protocol for Bacilli without natural competence such as the exoenzyme producer Bacillus licheniformis. The pKVM plasmids can be conjugated to strains of B. licheniformis and B. subtilis. For chromosomal gene deletion, regions flanking the target gene are fused and cloned in a pKVM vector prior to conjugative transfer from Escherichia coli to B. licheniformis. Appropriate markers on the vector backbone allow for the identification of the integration at the target locus and thereafter the vector excision, both events taking place via homologous recombination. The functionality of the deletion system was demonstrated with B. licheniformis by a markerless 939 bp in-frame deletion of the yqfD gene and the deletion of a 31 kbp genomic segment carrying a PBSX-like prophage. PMID:23916947

  15. 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.

  16. 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.

  17. 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.

  18. 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

  19. 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.

  20. 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.

  1. 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.

  2. 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.

  3. The exon 55 deletion in the nebulin gene--one single founder mutation with world-wide occurrence.

    Science.gov (United States)

    Lehtokari, Vilma-Lotta; Greenleaf, Rebecca S; DeChene, Elizabeth T; Kellinsalmi, Mutsumi; Pelin, Katarina; Laing, Nigel G; Beggs, Alan H; Wallgren-Pettersson, Carina

    2009-03-01

    In 2004, Anderson et al. reported a homozygous 2502 bp deletion including exon 55 of the nebulin gene in five Ashkenazi Jewish probands with nemaline myopathy. We determined the occurrence of this deletion in a world-wide series of 355 nemaline myopathy probands with no previously known mutation in other genes and found the mutation in 14 probands, two of whom represented families previously ascertained by Anderson et al. Two of the families were not of known Ashkenazi Jewish descent but they had the haplotype known to segregate with this mutation. In all but two of eight homozygous patients, the clinical picture was more severe than in typical nemaline myopathy. PMID:19232495

  4. The exon 55 deletion in the nebulin gene - one single founder mutation with world-wide occurrence

    OpenAIRE

    Lehtokari, Vilma-Lotta; Greenleaf, Rebecca S.; DeChene, Elizabeth T; Kellinsalmi, Mutsumi; Pelin, Katarina; Laing, Nigel G.; Beggs, Alan H.; Wallgren-Pettersson, Carina

    2009-01-01

    Anderson and co-workers (2004) reported a homozygous 2,502 bp deletion including exon 55 of the nebulin gene in five Ashkenazi Jewish probands with nemaline myopathy (NM) [1]. We determined the occurrence of this deletion in a world-wide series of 355 NM probands with no previously known mutation in other genes and found the mutation in 14 probands. Two of the families were not of known Ashkenazi Jewish descent but they had the haplotype known to segregate with this mutation. In all but two o...

  5. 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...

  6. 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...

  7. 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...

  8. 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

  9. 13Q DELETIONS IN LYMPHOID MALIGNANCIES

    NARCIS (Netherlands)

    HERMANSON, M; GRANDER, D; MERUP, M; WU, XS; HEYMAN, M; RASOOL, O; JULIUSSON, G; GAHRTON, G; DETLOFSSON, R; NIKIFOROVA, N; BUYS, C; SODERHALL, S; YANKOVSKY, N; ZABAROVSKY, E; EINHORN, S

    1995-01-01

    Previous studies have indicated that a candidate tumor suppressor gene resides telomeric of the RB1 gene at 13q14, a region that is commonly deleted in B-cell chronic lymphocytic leukemia (B-CLL). In this study, we have evaluated the frequency and minimal region of overlap for 13q deletions in malig

  10. 78 FR 56679 - Procurement List; Deletions

    Science.gov (United States)

    2013-09-13

    ... 8/2/2013 (78 FR 46927-46928), the Committee for Purchase From People Who Are Blind or Severely... PEOPLE WHO ARE BLIND OR SEVERELY DISABLED Procurement List; Deletions AGENCY: Committee for Purchase From People Who Are Blind or Severely Disabled. ACTION: Deletions from the Procurement List. SUMMARY:...

  11. 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...

  12. AcEST: BP917025 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000094_H07 471 Adiantum capillus-veneris mRNA. clone: YMU001_000094_H07. BP917025 - Show BP917025...is mRNA. clone: YMU001_000094_H07. Accession BP917025 Tissue type prothallium Developmental stage - Contig I... programs, Nucleic Acids Res. 25:3389-3402. Query= BP917025|Adiantum capillus-ven...ation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917025

  13. AcEST: BP917781 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_D04 511 Adiantum capillus-veneris mRNA. clone: YMU001_000105_D04. BP917781 - Show BP9177...is mRNA. clone: YMU001_000105_D04. Accession BP917781 Tissue type prothallium Developmental stage - Contig I... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177... programs, Nucleic Acids Res. 25:3389-3402. Query= BP917781|Adiantum capillus-ven

  14. 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

  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: BP914066 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_E02 515 Adiantum capillus-veneris mRNA. clone: YMU001_000039_E02. BP914066 - Show BP91406...is mRNA. clone: YMU001_000039_E02. Accession BP914066 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91406...h programs, Nucleic Acids Res. 25:3389-3402. Query= BP914066|Adiantum capillus-ve

  17. AcEST: BP918406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_B06 468 Adiantum capillus-veneris mRNA. clone: YMU001_000113_B06. BP918406 - Show BP918406...is mRNA. clone: YMU001_000113_B06. Accession BP918406 Tissue type prothallium Developmental stage - Contig I...programs, Nucleic Acids Res. 25:3389-3402. Query= BP918406|Adiantum capillus-vene...ams, Nucleic Acids Res. 25:3389-3402. Query= BP918406|Adiantum capillus-veneris m

  18. 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

  19. AcEST: BP914473 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_C10 217 Adiantum capillus-veneris mRNA. clone: YMU001_000059_C10. BP914473 - Show BP9144...is mRNA. clone: YMU001_000059_C10. Accession BP914473 Tissue type prothallium Developmental stage - Contig I...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914473|Adiantum capil

  20. 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-

  1. 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.

  2. 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.

  3. 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

    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...

  4. A 19-base pair deletion polymorphism in dihydrofolate reductase is associated with increased unmetabolized folic acid in plasma and decreased red blood cell folate

    Science.gov (United States)

    Dihydrofolate reductase (DHFR) catalyzes the reduction of folic acid to tetrahydrofolate (THF). A 19-bp noncoding deletion allele maps to intron 1, beginning 60 bases from the splice donor site, and has been implicated in neural tube defects and cancer, presumably by influencing folate metabolism. T...

  5. 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...

  6. N-myc 下游调节基因-2在大鼠肠缺血再灌注肺损伤中的表达及其与 NF-κBp65的相关研究%N-myc down stream regulated gene 2 expression in lung tissue of rat with acute lung injury induced by intestinal ischemia-reperfusion injury and relationship with nuclear transcription factor-kappaBp65

    Institute of Scientific and Technical Information of China (English)

    杨波; 张志培; 姜鹏; 葛鹏; 姜涛

    2012-01-01

      目的通过建立大鼠肠缺血再灌注肺损伤(IIRI)模型,观察大鼠肠缺血再灌注肺损伤,肺组织中N-myc下游调节基因-2(NDRG2)表达水平的变化.方法50只健康成年雄性SD大鼠随机分成对照组(control)、缺血再灌注组(I/R)(其中根据缺血再灌注时间又分4个亚组),每组10只.缺血再灌注4个亚组选择缺血60min后分别再灌注30、60、120和180min,获取样本肺组织.术后样本行病理(HE)、湿干重比例(W/D)检测,免疫组化、Western-blot对NDRG2、核转录因子-κBp65(NF-κBp65)检测,RT-PCR方法对NDRG2在mRNA水平含量进行检测,TUNEL法对凋亡细胞进行检测.结果缺血再灌注组与对照组比较,缺血再灌注组肺泡壁增宽,肺泡腔内可见出血等炎症表现,W/D比值显著性升高(P<0.05),免疫组化显示NF-κBp65发生核转位现象,NF-κBp65蛋白水平表达明显升高(P<0.05),肺组织NDRG2在mRNA水平和蛋白水平的表达明显降低(P<0.05).结论缺血再灌注损伤可下调肺组织中NDRG2的表达,NDRG2可能通过对NF-κB通路进行调控,是导致缺血再灌注后肺损伤的靶向调控位点,对肠缺血再灌注肺损伤的大鼠起保护作用.

  7. Multivalent display of the antimicrobial peptides BP100 and BP143

    OpenAIRE

    Imma Güell; Rafael Ferre; Kasper K. Sørensen; Esther Badosa; Iteng Ng-Choi; Emilio Montesinos; Eduard Bardají; Lidia Feliu; Jensen, Knud J; Marta Planas

    2012-01-01

    Carbohydrates are considered as promising templates for the display of multiple copies of antimicrobial peptides. Herein, we describe the design and synthesis of chimeric structures containing two or four copies of the antimicrobial peptides KKLFKKILKYL-NH2 (BP100) and KKLfKKILKYL-NH2 (BP143) attached to the carbohydrate template cyclodithioerythritol (cDTE) or α-D-galactopyranoside (Galp). The synthesis involved the preparation of the corresponding peptide aldehyde followed by coupling ...

  8. BP Oil Company's approach to risk management

    International Nuclear Information System (INIS)

    The oil and chemical industries face major challenges in deciding how to handle the numerous recommendations coming from various audits, reviews and studies conducted in the functional areas of personnel health and safety, loss prevention, and environmental protection. And, the number of recommendations continues to grow with time, as regulations and normal business requirements are met. BP Oil has developed a methodology for risk ranking the events leading to specific recommendations and then determining the cost-effectiveness of the recommendations in reducing the risk. The author completed successful pilot tests of this methodology at two of BP Oil's petroleum refineries, examining the recommendations from process hazards analyses and studies completed over the past few years. The methodology has since been implemented throughout their petroleum refining, distribution, transportation, and retail business streams

  9. Translation control during prolonged mTORC1 inhibition mediated by 4E-BP3

    Science.gov (United States)

    Tsukumo, Yoshinori; Alain, Tommy; Fonseca, Bruno D.; Nadon, Robert; Sonenberg, Nahum

    2016-01-01

    Targeting mTORC1 is a highly promising strategy in cancer therapy. Suppression of mTORC1 activity leads to rapid dephosphorylation of eIF4E-binding proteins (4E-BP1–3) and subsequent inhibition of mRNA translation. However, how the different 4E-BPs affect translation during prolonged use of mTOR inhibitors is not known. Here we show that the expression of 4E-BP3, but not that of 4E-BP1 or 4E-BP2, is transcriptionally induced during prolonged mTORC1 inhibition in vitro and in vivo. Mechanistically, our data reveal that 4E-BP3 expression is controlled by the transcription factor TFE3 through a cis-regulatory element in the EIF4EBP3 gene promoter. CRISPR/Cas9-mediated EIF4EBP3 gene disruption in human cancer cells mitigated the inhibition of translation and proliferation caused by prolonged treatment with mTOR inhibitors. Our findings show that 4E-BP3 is an important effector of mTORC1 and a robust predictive biomarker of therapeutic response to prolonged treatment with mTOR-targeting drugs in cancer. PMID:27319316

  10. 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

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

    International Nuclear Information System (INIS)

    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 Tyr174, Tyr183 and Tyr446 in mouse 3BP2 are predominantly phosphorylated by Syk, and the phosphorylation of Tyr183 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 Tyr174, Tyr183 and Tyr426 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 Tyr426 is required for the inducible interaction with the SH2 domain of Vav3. Moreover, the expression of the mutant form of 3BP2 in which Tyr426 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 Tyr426 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

  12. 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.

  13. 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.

  14. Role of 53BP1 in the regulation of DNA double-strand break repair pathway choice.

    Science.gov (United States)

    Gupta, Arun; Hunt, Clayton R; Chakraborty, Sharmistha; Pandita, Raj K; Yordy, John; Ramnarain, Deepti B; Horikoshi, Nobuo; Pandita, Tej K

    2014-01-01

    The p53-binding protein 1 (53BP1) is a well-known DNA damage response (DDR) factor, which is recruited to nuclear structures at the site of DNA damage and forms readily visualized ionizing radiation (IR) induced foci. Depletion of 53BP1 results in cell cycle arrest in G2/M phase as well as genomic instability in human as well as mouse cells. Within the DNA damage response mechanism, 53BP1 is classified as an adaptor/mediator, required for processing of the DNA damage response signal and as a platform for recruitment of other repair factors. More recently, specific 53BP1 contributions to DSB repair pathway choice have been recognized and are being characterized. In this review, we have summarized recent advances in understanding the role of 53BP1 in regulating DNA DSBs repair pathway choice, variable diversity joining [V(D)J] recombination and class-switch recombination (CSR). PMID:24320053

  15. 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.

  16. The Value of a BP Determination Method Using a Novel Non-Invasive BP Device against the Invasive Catheter Measurement

    OpenAIRE

    Jinsong Xu; Yanqing Wu; Hai Su; Weitong Hu; Juxiang Li; Wenying Wang; Xin Liu; Xiaoshu Cheng

    2014-01-01

    OBJECTIVE: The aim of this study was to evaluate the accuracy of a new blood pressure (BP) measurement method (Pulse method). METHODS: This study enrolled 45 patients for selective percutaneous coronary intervention (PCI) via right radial artery. A BP device using either oscillometric (Microlife 3AC1-1) or Pulse method(RG-BP11)was used. At the beginning of each PCI, intra-radial BP was measured before Microlife BP or Pulse BP measurement as its own reference, respectively. At the end of PCI, ...

  17. 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.

  18. 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...

  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. A chloroplast DNA deletion located in RNA polymerase gene rpoC2 in CMS lines of sorghum.

    Science.gov (United States)

    Chen, Z; Muthukrishnan, S; Liang, G H; Schertz, K F; Hart, G E

    1993-01-01

    Fertile lines of sorghum (Sorghum bicolor) were shown to differ from cytoplasmic male sterile (CMS) lines by the presence of a 3.8 kb HindIII chloroplast DNA fragment in the former and a smaller (3.7 kb) fragment in the latter. DNA/DNA hybridization studies showed that these two fragments are homologous. Fertile plants from S. versicolor, S. almum, S. halepense, and Sorghastrum nutans (Yellow Indiangrass) also have the 3.8 kb fragment, and CMS lines studied containing A1, A2 and A3 cytoplasms have the 3.7 kb fragment. The size difference between the two fragments was localized to a 1.0 kb SacI-HindIII fragment by restriction mapping. A 165 bp deletion, which is flanked by a 51 bp tandem repeat, was identified in the CMS lines by sequencing the clones. Comparison of the two sequences with those from maize, rice, tobacco, spinach, pea, and liverwort revealed that the deleted sequence is located in the middle of the RNA polymerase beta" subunit encoded by the gene rpoC2. The amino acid sequence deleted in the CMS lines is in a monocot-specific region which contains two protein motifs that are characteristic of several transcriptional activation factors, namely, a leucine zipper motif and an acidic domain capable of forming an amphipathic alpha-helix. Further studies designed to determine whether or not the deletion is involved in CMS of sorghum are underway.

  2. A chloroplast DNA deletion located in RNA polymerase gene rpoC2 in CMS lines of sorghum.

    Science.gov (United States)

    Chen, Z; Muthukrishnan, S; Liang, G H; Schertz, K F; Hart, G E

    1993-01-01

    Fertile lines of sorghum (Sorghum bicolor) were shown to differ from cytoplasmic male sterile (CMS) lines by the presence of a 3.8 kb HindIII chloroplast DNA fragment in the former and a smaller (3.7 kb) fragment in the latter. DNA/DNA hybridization studies showed that these two fragments are homologous. Fertile plants from S. versicolor, S. almum, S. halepense, and Sorghastrum nutans (Yellow Indiangrass) also have the 3.8 kb fragment, and CMS lines studied containing A1, A2 and A3 cytoplasms have the 3.7 kb fragment. The size difference between the two fragments was localized to a 1.0 kb SacI-HindIII fragment by restriction mapping. A 165 bp deletion, which is flanked by a 51 bp tandem repeat, was identified in the CMS lines by sequencing the clones. Comparison of the two sequences with those from maize, rice, tobacco, spinach, pea, and liverwort revealed that the deleted sequence is located in the middle of the RNA polymerase beta" subunit encoded by the gene rpoC2. The amino acid sequence deleted in the CMS lines is in a monocot-specific region which contains two protein motifs that are characteristic of several transcriptional activation factors, namely, a leucine zipper motif and an acidic domain capable of forming an amphipathic alpha-helix. Further studies designed to determine whether or not the deletion is involved in CMS of sorghum are underway. PMID:8437572

  3. 电离辐射致人外周血有核细胞mtDNA4977bp缺失水平分析%Analysis of mtDNA 4977bp Deletion Induced by Ionizing Radiation in Human Peripheral Blood Nucleated Cells Using Real-time PCR

    Institute of Scientific and Technical Information of China (English)

    范天黎; 王平; 刘玉龙; 韩林; 吕玉民

    2010-01-01

    采集6名正常人外周血,体外进行~(60)Co γ射线单次照射,剂量分别为0、1、2、3、4和5 Gy.照射后2小时采用实时定量PCR方法检测~(60)Co γ射线诱发的人外周血有核细胞mtDNA 4977bp缺失(△mtDNA~(4977))和mtDNA总拷贝数(mtDNA~(total)),探讨用△mtDNA4977为指标进行辐射事故生物剂量估算的可能性.结果表明,在0~5 Gy照射剂量范围内,6名健康人mtDNA样品中的mtDNA~(total)拷贝数、△mtDNA~(4977)拷贝数和△mtDNA~(4977)缺失率在照射后明显高于未照射(0 Gy)的mtDNA样品(p<0.05),但各照射剂量组间未见明显差异(p>0.05).提示电离辐射能够诱发人外周血mtDNA样品中4977bp缺失的累积和mtDNA总拷贝数的增加,但△mtDNA~(4977)水平与受照剂量间未见明显的剂量-效应关系.

  4. 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

  5. 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

  6. 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

  7. AcEST: BP917767 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_B11 76 Adiantum capillus-veneris mRNA. clone: YMU001_000105_B11. BP917767 - Show BP9177... mRNA. clone: YMU001_000105_B11. Accession BP917767 Tissue type prothallium Developmental stage - Contig ID

  8. 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

  9. AcEST: BP916367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000086_H07 86 Adiantum capillus-veneris mRNA. clone: YMU001_000086_H07. BP916367 - Show BP916367... mRNA. clone: YMU001_000086_H07. Accession BP916367 Tissue type prothallium Developmental stage - Contig ID

  10. AcEST: BP914480 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_D05 74 Adiantum capillus-veneris mRNA. clone: YMU001_000059_D05. BP914480 - Show BP9144... mRNA. clone: YMU001_000059_D05. Accession BP914480 Tissue type prothallium Developmental stage - Contig ID

  11. 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

  12. 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.

  13. Roles of the RecJ and RecQ proteins in spontaneous formation of deletion mutations in the Escherichia coli K12 endogenous tonB gene.

    Science.gov (United States)

    Mashimo, Kazumi; Kawata, Masakado; Yamamoto, Kazuo

    2003-07-01

    The endogenous tonB gene of Escherichia coli was used as a target for spontaneous deletion mutations which were isolated from recJ(-) and recQ(-) cells. Large deletions, due to simultaneous mutations of the trp operon, were also isolated. The rates of tonB mutation were 2.77 x 10(-8), 4.13 x 10(-8) and 5.00 x 10(-8) for rec(+), recJ(-) and recQ(-) cells, respectively. We analyzed 94 and 99 tonB mutants from the recJ(-) and recQ(-) cells, respectively, by sequencing. We found that IS insertion dominated, followed by base substitutions, frameshifts and deletions in both recJ(-) and recQ(-) strains. We then analyzed 55 tonB-trp deletions, ranging in size from 5907 to 20,832 bp, from the recJ(-) strains and 47 tonB-trp deletions, ranging in size from 4,959 to 16,390 bp from the recQ(-) strains. About one-third of tonB-trp deletions from both the recJ(-) and the recQ(-) cells were found to have occurred between short sequence repeats at the deletion termini. About one-third of tonB-trp deletions from both mutants showed 2-4 bp repeats in the immediate vicinity of the endpoints, which appeared to indicate no clear association with deletion. The remaining one-third of tonB-trp deletions had no homology at the endpoint. These results were similar to those for the rec(+) cells. Hanada and colleagues demonstrated that structually similar rearrangements arising during lambda bio phage formation (illegitimate recombination) increased in the recQ(-) strain. To explain this discrepancy, we interpreted as distinctive the mechanism for rearrangement during transducing phage formation which is recQ-dependent and that for deletions formed in chromosomes which is recQ-independent. PMID:12840109

  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. 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

  16. AcEST: BP912003 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_H07 455 Adiantum capillus-veneris mRNA. clone: YMU001_000011_H07. BP9120...03 CL3942Contig1 Show BP912003 Clone id YMU001_000011_H07 Library YMU01 Length 455 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000011_H07. Accession BP912003 Tissue type prothallium Developmental stag..., Nucleic Acids Res. 25:3389-3402. Query= BP912003|Adiantum capillus-veneris mRNA...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  17. 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

  18. 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

  19. 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

  20. 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

  1. AcEST: BP912065 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_F05 374 Adiantum capillus-veneris mRNA. clone: YMU001_000012_F05. BP912065 - Show BP912065 Clone id YMU001_000012_F05 Library YMU01 Length 374 Definition Adiantum capillus-veneris mRNA. clone: YMU001_000012_F05. Accession BP912065 ...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912065|Adiantum capillus-veneris mRNA, clone: YMU...programs, Nucleic Acids Res. 25:3389-3402. Query= BP912065|Adiantum capillus-vene

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. AcEST: BP912007 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_A01 574 Adiantum capillus-veneris mRNA. clone: YMU001_000012_A01. BP912007 - Show BP9120...is mRNA. clone: YMU001_000012_A01. Accession BP912007 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP912007|Adiantum capillus-veneris mRNA, clone: YMU001_000012_A...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912007|Adiantum capillus-veneris

  8. 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

  9. 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

  10. 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

  11. AcEST: BP912074 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_G05 524 Adiantum capillus-veneris mRNA. clone: YMU001_000012_G05. BP912074 - Show BP9120...is mRNA. clone: YMU001_000012_G05. Accession BP912074 Tissue type prothallium Developmental stage - Contig I...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120...nd PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120...ength = 1129 Score = 48.9 bits (115), Expect = 2e-04 Identities = 28/120 (23%), Positives = 64/120 (53%) Fra

  12. AcEST: BP912012 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_A06 542 Adiantum capillus-veneris mRNA. clone: YMU001_000012_A06. BP9120...12 CL2421Contig1 Show BP912012 Clone id YMU001_000012_A06 Library YMU01 Length 542 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000012_A06. Accession BP912012 Tissue type prothallium Developmental stag...rams, Nucleic Acids Res. 25:3389-3402. Query= BP912012|Adiantum capillus-veneris ...d BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9120

  13. AcEST: BP917117 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000096_B11 125 Adiantum capillus-veneris mRNA. clone: YMU001_000096_B11. BP917117... CL2704Contig1 Show BP917117 Clone id YMU001_000096_B11 Library YMU01 Length 125 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000096_B11. Accession BP917117 Tissue type prothallium Developmental stag...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917117...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917117

  14. AcEST: BP917177 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000097_C05 471 Adiantum capillus-veneris mRNA. clone: YMU001_000097_C05. BP917177 - Show BP91717...is mRNA. clone: YMU001_000097_C05. Accession BP917177 Tissue type prothallium Developmental stage - Contig I...search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917177|Adiantum capillus-veneris mRNA, clone: YMU...97), Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917

  15. AcEST: BP920166 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G12 149 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G12. BP920166 - Show BP92016...is mRNA. clone: YMU001_000133_G12. Accession BP920166 Tissue type prothallium Developmental stage - Contig I...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92016...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920166|Adiantum capillus-veneris

  16. AcEST: BP920169 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H03 505 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H03. BP920169 - Show BP92016...is mRNA. clone: YMU001_000133_H03. Accession BP920169 Tissue type prothallium Developmental stage - Contig I...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92016...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920169|Adiantum cap

  17. AcEST: BP920164 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G09 447 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G09. BP920164 - Show BP92016...is mRNA. clone: YMU001_000133_G09. Accession BP920164 Tissue type prothallium Developmental stage - Contig I...ST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920164|A...se search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920164|Adiantum cap

  18. AcEST: BP920163 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G08 372 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G08. BP92016...3 CL2472Contig1 Show BP920163 Clone id YMU001_000133_G08 Library YMU01 Length 372 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000133_G08. Accession BP920163 Tissue type prothallium Developmental stag...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920163|Adiantum cap... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920163|Adiantum capillus-veneris mRNA, clone: YM

  19. AcEST: BP920161 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G06 542 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G06. BP920161 - Show BP92016...is mRNA. clone: YMU001_000133_G06. Accession BP920161 Tissue type prothallium Developmental stage - Contig I...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9201...ped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92016

  20. AcEST: BP912016 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000012_A10 262 Adiantum capillus-veneris mRNA. clone: YMU001_000012_A10. BP912016 - Show BP912016...is mRNA. clone: YMU001_000012_A10. Accession BP912016 Tissue type prothallium Developmental stage - Contig I...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912016|Adiantum capillus-veneris mRNA, clone:.... 25:3389-3402. Query= BP912016|Adiantum capillus-veneris mRNA, clone: YMU001_000012_A10. (262 letters) Data

  1. AcEST: BP920165 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G11 301 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G11. BP920165 - Show BP92016...is mRNA. clone: YMU001_000133_G11. Accession BP920165 Tissue type prothallium Developmental stage - Contig I...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920165...and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92016

  2. AcEST: BP920168 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H02 390 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H02. BP920168 - Show BP92016...is mRNA. clone: YMU001_000133_H02. Accession BP920168 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920168|Adiantum capillus-veneris mRNA,...c Acids Res. 25:3389-3402. Query= BP920168|Adiantum capillus-veneris mRNA, clone: YMU001_000133_H02. (390 le

  3. AcEST: BP920167 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_H01 152 Adiantum capillus-veneris mRNA. clone: YMU001_000133_H01. BP920167 - Show BP92016...is mRNA. clone: YMU001_000133_H01. Accession BP920167 Tissue type prothallium Developmental stage - Contig I...ids Res. 25:3389-3402. Query= BP920167|Adiantum capillus-veneris mRNA, clone: YMU...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920167

  4. AcEST: BP919001 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000120_A02 410 Adiantum capillus-veneris mRNA. clone: YMU001_000120_A02. BP919001... CL1112Contig1 Show BP919001 Clone id YMU001_000120_A02 Library YMU01 Length 410 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000120_A02. Accession BP919001 Tissue type prothallium Developmental stag...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919001|Adiantum capillus...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP919001|Adiantum capillus-veneris mRNA, clone: YMU00

  5. AcEST: BP919941 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_H09 463 Adiantum capillus-veneris mRNA. clone: YMU001_000130_H09. BP91994...1 CL396Contig1 Show BP919941 Clone id YMU001_000130_H09 Library YMU01 Length 463 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000130_H09. Accession BP919941 Tissue type prothallium Developmental stage...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919941|Adiantum capi...d PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91994

  6. AcEST: BP919946 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_A10 457 Adiantum capillus-veneris mRNA. clone: YMU001_000131_A10. BP919946 - Show BP91994...is mRNA. clone: YMU001_000131_A10. Accession BP919946 Tissue type prothallium Developmental stage - Contig I...s Res. 25:3389-3402. Query= BP919946|Adiantum capillus-veneris mRNA, clone: YMU00...ST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919946|A

  7. AcEST: BP911994 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_G08 559 Adiantum capillus-veneris mRNA. clone: YMU001_000011_G08. BP911994... CL4209Contig1 Show BP911994 Clone id YMU001_000011_G08 Library YMU01 Length 559 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000011_G08. Accession BP911994 Tissue type prothallium Developmental stag...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911994|Adiantum ... programs, Nucleic Acids Res. 25:3389-3402. Query= BP911994|Adiantum capillus-veneris mRNA, clone: YMU001_00

  8. AcEST: BP919948 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_A12 489 Adiantum capillus-veneris mRNA. clone: YMU001_000131_A12. BP919948 - Show BP91994...is mRNA. clone: YMU001_000131_A12. Accession BP919948 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919948|Adia...leic Acids Res. 25:3389-3402. Query= BP919948|Adiantum capillus-veneris mRNA, clone: YMU001_000131_A12. (489

  9. AcEST: BP919943 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000130_H11 517 Adiantum capillus-veneris mRNA. clone: YMU001_000130_H11. BP919943 - Show BP91994...is mRNA. clone: YMU001_000130_H11. Accession BP919943 Tissue type prothallium Developmental stage - Contig I...c Acids Res. 25:3389-3402. Query= BP919943|Adiantum capillus-veneris mRNA, clone: YMU001_000130_H11. (493 le... Res. 25:3389-3402. Query= BP919943|Adiantum capillus-veneris mRNA, clone: YMU001

  10. AcEST: BP919949 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000131_B01 318 Adiantum capillus-veneris mRNA. clone: YMU001_000131_B01. BP91994...9 CL2311Contig1 Show BP919949 Clone id YMU001_000131_B01 Library YMU01 Length 318 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000131_B01. Accession BP919949 Tissue type prothallium Developmental stag...I-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91994...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91994

  11. AcEST: BP914147 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000042_D12 534 Adiantum capillus-veneris mRNA. clone: YMU001_000042_D12. BP914147 - Show BP91414...is mRNA. clone: YMU001_000042_D12. Accession BP914147 Tissue type prothallium Developmental stage - Contig I...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91414...niprot_sprot.fasta 412,525 sequences; 148,809,765 total letters Searching......................................ids Res. 25:3389-3402. Query= BP914147|Adiantum capillus-veneris mRNA, clone: YMU001_000042_D12. (534 letter

  12. AcEST: BP917711 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_E02 534 Adiantum capillus-veneris mRNA. clone: YMU001_000104_E02. BP917711 - Show BP9177...is mRNA. clone: YMU001_000104_E02. Accession BP917711 Tissue type prothallium Developmental stage - Contig I...s. 25:3389-3402. Query= BP917711|Adiantum capillus-veneris mRNA, clone: YMU001_000104_E02. (534 letters) Dat...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917711|Adiantum capillus-ve

  13. AcEST: BP917703 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_D05 340 Adiantum capillus-veneris mRNA. clone: YMU001_000104_D05. BP9177...03 CL1948Contig1 Show BP917703 Clone id YMU001_000104_D05 Library YMU01 Length 340 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000104_D05. Accession BP917703 Tissue type prothallium Developmental stag...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917703|Adiantum capillus-veneris mRNA, clone: YMU00...ic Acids Res. 25:3389-3402. Query= BP917703|Adiantum capillus-veneris mRNA, clone

  14. AcEST: BP917787 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_D11 582 Adiantum capillus-veneris mRNA. clone: YMU001_000105_D11. BP917787 - Show BP9177...is mRNA. clone: YMU001_000105_D11. Accession BP917787 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917787|Adiantum capillus-veneris mRNA,...apped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  15. AcEST: BP917732 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_G02 305 Adiantum capillus-veneris mRNA. clone: YMU001_000104_G02. BP917732 - Show BP9177...is mRNA. clone: YMU001_000104_G02. Accession BP917732 Tissue type prothallium Developmental stage - Contig I...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917732|Adiantum capillus-veneris mRNA...ds Res. 25:3389-3402. Query= BP917732|Adiantum capillus-veneris mRNA, clone: YMU001_000104_G02. (305 letters

  16. AcEST: BP917756 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A08 493 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A08. BP917756 - Show BP9177...is mRNA. clone: YMU001_000105_A08. Accession BP917756 Tissue type prothallium Developmental stage - Contig I...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917756|Adi...ograms, Nucleic Acids Res. 25:3389-3402. Query= BP917756|Adiantum capillus-veneris mRNA, clone: YMU001_00010

  17. AcEST: BP917783 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_D07 525 Adiantum capillus-veneris mRNA. clone: YMU001_000105_D07. BP917783 - Show BP9177...is mRNA. clone: YMU001_000105_D07. Accession BP917783 Tissue type prothallium Developmental stage - Contig I...ids Res. 25:3389-3402. Query= BP917783|Adiantum capillus-veneris mRNA, clone: YMU001_000105_D07. (525 letter...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  18. AcEST: BP917763 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_B06 159 Adiantum capillus-veneris mRNA. clone: YMU001_000105_B06. BP917763 - Show BP9177...is mRNA. clone: YMU001_000105_B06. Accession BP917763 Tissue type prothallium Developmental stage - Contig I...leic Acids Res. 25:3389-3402. Query= BP917763|Adiantum capillus-veneris mRNA, clo...d PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  19. AcEST: BP917796 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_E10 461 Adiantum capillus-veneris mRNA. clone: YMU001_000105_E10. BP9177...96 CL2065Contig1 Show BP917796 Clone id YMU001_000105_E10 Library YMU01 Length 461 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000105_E10. Accession BP917796 Tissue type prothallium Developmental stag...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917796|Adiantum capillus-...ids Res. 25:3389-3402. Query= BP917796|Adiantum capillus-veneris mRNA, clone: YMU

  20. AcEST: BP911772 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_A06 326 Adiantum capillus-veneris mRNA. clone: YMU001_000009_A06. BP911772 - Show BP91177...is mRNA. clone: YMU001_000009_A06. Accession BP911772 Tissue type prothallium Developmental stage - Contig I...-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91177...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91177

  1. AcEST: BP917735 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_G07 461 Adiantum capillus-veneris mRNA. clone: YMU001_000104_G07. BP917735 - Show BP9177...is mRNA. clone: YMU001_000104_G07. Accession BP917735 Tissue type prothallium Developmental stage - Contig I...eic Acids Res. 25:3389-3402. Query= BP917735|Adiantum capillus-veneris mRNA, clon...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917735|Adiantum cap

  2. AcEST: BP911771 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_A05 478 Adiantum capillus-veneris mRNA. clone: YMU001_000009_A05. BP911771 - Show BP91177...is mRNA. clone: YMU001_000009_A05. Accession BP911771 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP911771|Adiantum capillus-veneris mRNA, clone... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911771|Adiantum capillus-veneri

  3. AcEST: BP917727 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_F09 528 Adiantum capillus-veneris mRNA. clone: YMU001_000104_F09. BP917727 - Show BP9177...is mRNA. clone: YMU001_000104_F09. Accession BP917727 Tissue type prothallium Developmental stage - Contig I...Res. 25:3389-3402. Query= BP917727|Adiantum capillus-veneris mRNA, clone: YMU001_000104_F09. (528 letters) D...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  4. AcEST: BP917741 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_H02 445 Adiantum capillus-veneris mRNA. clone: YMU001_000104_H02. BP917741 - Show BP9177...is mRNA. clone: YMU001_000104_H02. Accession BP917741 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= BP9177...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  5. AcEST: BP917752 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A04 422 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A04. BP917752 - Show BP9177...is mRNA. clone: YMU001_000105_A04. Accession BP917752 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= BP9177...rch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917752|Adiantum capillus-...ncharacterized protein OS=Vitis vinifera GN=VITISV_008296 PE=4 SV=1 Length = 1027 Score = 72.8 bits (177

  6. AcEST: BP917740 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_G12 396 Adiantum capillus-veneris mRNA. clone: YMU001_000104_G12. BP917740 - Show BP9177...is mRNA. clone: YMU001_000104_G12. Accession BP917740 Tissue type prothallium Developmental stage - Contig I...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917740|Adiantum capillus-veneris mR...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917740|Adiantum ...: 4 DLLKAYVTEVDQRDQWKNHSPLVEYVYNYSTHTSTRKTLFKVTEERLKIRLIVKTLG--K 177 D+L+A V +D +

  7. AcEST: BP917700 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_D02 544 Adiantum capillus-veneris mRNA. clone: YMU001_000104_D02. BP9177...00 CL272Contig1 Show BP917700 Clone id YMU001_000104_D02 Library YMU01 Length 544 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000104_D02. Accession BP917700 Tissue type prothallium Developmental stage... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917700|Adiantum capillus-ven...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917700|Adiantum capillus-vener

  8. AcEST: BP917712 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_E03 514 Adiantum capillus-veneris mRNA. clone: YMU001_000104_E03. BP917712 - Show BP9177...is mRNA. clone: YMU001_000104_E03. Accession BP917712 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917712|Adia...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917712|Adiantu...073 PE=4 SV=1 Length = 146 Score = 34.7 bits (78), Expect = 2.5 Identities = 22/91 (24%), Positives = 38/91

  9. AcEST: BP917747 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_H10 483 Adiantum capillus-veneris mRNA. clone: YMU001_000104_H10. BP917747 - Show BP9177...is mRNA. clone: YMU001_000104_H10. Accession BP917747 Tissue type prothallium Developmental stage - Contig I...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177...s. 25:3389-3402. Query= BP917747|Adiantum capillus-veneris mRNA, clone: YMU001_000104_H10. (483 letters) Dat

  10. AcEST: BP917743 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_H04 524 Adiantum capillus-veneris mRNA. clone: YMU001_000104_H04. BP917743 - Show BP9177...is mRNA. clone: YMU001_000104_H04. Accession BP917743 Tissue type prothallium Developmental stage - Contig I...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917743|Adiantum capi...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917743|Adiantum capillus-veneris mRNA, clo

  11. AcEST: BP917775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_C08 544 Adiantum capillus-veneris mRNA. clone: YMU001_000105_C08. BP917775 - Show BP9177...is mRNA. clone: YMU001_000105_C08. Accession BP917775 Tissue type prothallium Developmental stage - Contig I...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917775|Adiantum capill

  12. AcEST: BP917780 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_D03 505 Adiantum capillus-veneris mRNA. clone: YMU001_000105_D03. BP917780 - Show BP9177...is mRNA. clone: YMU001_000105_D03. Accession BP917780 Tissue type prothallium Developmental stage - Contig I...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177...ein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917780|Ad...) Frame = +1 Query: 229 TLGN*FDLFGPPIRRLPF-WIVLWSILGLA*GGAC 330 TLG D+F P ++LP W+ LWS LG GG C Sbjct: 177

  13. AcEST: BP911775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000009_A09 285 Adiantum capillus-veneris mRNA. clone: YMU001_000009_A09. BP91177...5 CL2064Contig1 Show BP911775 Clone id YMU001_000009_A09 Library YMU01 Length 285 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000009_A09. Accession BP911775 Tissue type prothallium Developmental stag...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911775...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911775|Adiantum capillus

  14. AcEST: BP917799 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_F02 443 Adiantum capillus-veneris mRNA. clone: YMU001_000105_F02. BP917799 - Show BP9177...is mRNA. clone: YMU001_000105_F02. Accession BP917799 Tissue type prothallium Developmental stage - Contig I...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91779...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917799|Adiantum capillus

  15. AcEST: BP917718 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_E11 470 Adiantum capillus-veneris mRNA. clone: YMU001_000104_E11. BP917718 - Show BP9177...is mRNA. clone: YMU001_000104_E11. Accession BP917718 Tissue type prothallium Developmental stage - Contig I...earch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917718|Adiantum capillus-veneris mRNA, clone: YMU0...es. 25:3389-3402. Query= BP917718|Adiantum capillus-veneris mRNA, clone: YMU001_000104_E11. (470 letters) Da

  16. AcEST: BP917785 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_D09 516 Adiantum capillus-veneris mRNA. clone: YMU001_000105_D09. BP917785 - Show BP9177...is mRNA. clone: YMU001_000105_D09. Accession BP917785 Tissue type prothallium Developmental stage - Contig I...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917785|Adiantum capillus-veneris mRNA,

  17. AcEST: BP917736 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_G08 378 Adiantum capillus-veneris mRNA. clone: YMU001_000104_G08. BP917736 - Show BP9177...is mRNA. clone: YMU001_000104_G08. Accession BP917736 Tissue type prothallium Developmental stage - Contig I...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917736|Adiantum capillus-veneris... programs, Nucleic Acids Res. 25:3389-3402. Query= BP917736|Adiantum capillus-veneris mRNA, clone: YMU001_00

  18. AcEST: BP917708 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_D11 459 Adiantum capillus-veneris mRNA. clone: YMU001_000104_D11. BP9177...08 CL668Contig1 Show BP917708 Clone id YMU001_000104_D11 Library YMU01 Length 459 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000104_D11. Accession BP917708 Tissue type prothallium Developmental stage...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP917708|Adiantum capillus-vener...cids Res. 25:3389-3402. Query= BP917708|Adiantum capillus-veneris mRNA, clone: YMU001_000104_D11. (459 lette

  19. AcEST: BP916177 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000084_C01 435 Adiantum capillus-veneris mRNA. clone: YMU001_000084_C01. BP916177 - Show BP916177...is mRNA. clone: YMU001_000084_C01. Accession BP916177 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= BP916177...d PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916177

  20. AcEST: BP917716 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000104_E09 452 Adiantum capillus-veneris mRNA. clone: YMU001_000104_E09. BP9177...16 CL2904Contig1 Show BP917716 Clone id YMU001_000104_E09 Library YMU01 Length 452 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000104_E09. Accession BP917716 Tissue type prothallium Developmental stag...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917716|Adiant...T and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  1. AcEST: BP917771 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_C03 433 Adiantum capillus-veneris mRNA. clone: YMU001_000105_C03. BP917771 - Show BP9177...is mRNA. clone: YMU001_000105_C03. Accession BP917771 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= BP9177...of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  2. AcEST: BP921773 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_A04 367 Adiantum capillus-veneris mRNA. clone: YMU001_000154_A04. BP921773 - Show BP92177...is mRNA. clone: YMU001_000154_A04. Accession BP921773 Tissue type prothallium Developmental stage - Contig I... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921773|Adiantum capillus-ven...ograms, Nucleic Acids Res. 25:3389-3402. Query= BP921773|Adiantum capillus-veneris mRNA, clone: YMU001_00015

  3. AcEST: BP921177 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000146_F04 542 Adiantum capillus-veneris mRNA. clone: YMU001_000146_F04. BP921177 - Show BP921177...is mRNA. clone: YMU001_000146_F04. Accession BP921177 Tissue type prothallium Developmental stage - Contig I..., Nucleic Acids Res. 25:3389-3402. Query= BP921177|Adiantum capillus-veneris mRNA, clone: YMU001_000146_F04....T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921177|Ad

  4. AcEST: BP921778 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000154_A09 262 Adiantum capillus-veneris mRNA. clone: YMU001_000154_A09. BP921778 - Show BP92177...is mRNA. clone: YMU001_000154_A09. Accession BP921778 Tissue type prothallium Developmental stage - Contig I...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP92177...s, Nucleic Acids Res. 25:3389-3402. Query= BP921778|Adiantum capillus-veneris mRNA, clone: YMU001_000154_A09

  5. AcEST: BP917751 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A03 466 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A03. BP9177...51 CL2236Contig1 Show BP917751 Clone id YMU001_000105_A03 Library YMU01 Length 466 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000105_A03. Accession BP917751 Tissue type prothallium Developmental stag...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917751|Adiantum..., Nucleic Acids Res. 25:3389-3402. Query= BP917751|Adiantum capillus-veneris mRNA, clone: YMU001_000105_A03.

  6. AcEST: BP917768 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_B12 509 Adiantum capillus-veneris mRNA. clone: YMU001_000105_B12. BP917768 - Show BP9177...is mRNA. clone: YMU001_000105_B12. Accession BP917768 Tissue type prothallium Developmental stage - Contig I...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177...Res. 25:3389-3402. Query= BP917768|Adiantum capillus-veneris mRNA, clone: YMU001_000105_B12. (509 letters) D

  7. AcEST: BP917792 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_E06 308 Adiantum capillus-veneris mRNA. clone: YMU001_000105_E06. BP917792 - Show BP9177...is mRNA. clone: YMU001_000105_E06. Accession BP917792 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP917792|Adiantum capillus-veneris mRNA, clone: YMU001_000105_E06. (308 l...Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9177

  8. 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

  9. 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|

  10. 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

  11. 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

  12. AcEST: BP920121 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_C06 542 Adiantum capillus-veneris mRNA. clone: YMU001_000133_C06. BP920121 - Show BP92012...is mRNA. clone: YMU001_000133_C06. Accession BP920121 Tissue type prothallium Developmental stage - Contig I...ds Res. 25:3389-3402. Query= BP920121|Adiantum capillus-veneris mRNA, clone: YMU001_000133_C06. (542 letters...Res. 25:3389-3402. Query= BP920121|Adiantum capillus-veneris mRNA, clone: YMU001_000133_C06. (542 letters) D

  13. 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

  14. AcEST: BP920158 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000133_G02 530 Adiantum capillus-veneris mRNA. clone: YMU001_000133_G02. BP92015...8 CL188Contig1 Show BP920158 Clone id YMU001_000133_G02 Library YMU01 Length 530 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000133_G02. Accession BP920158 Tissue type prothallium Developmental stage.... 25:3389-3402. Query= BP920158|Adiantum capillus-veneris mRNA, clone: YMU001_000133_G02. (530 letters) Data... programs, Nucleic Acids Res. 25:3389-3402. Query= BP920158|Adiantum capillus-ven

  15. 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_

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. AcEST: BP918100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000109_F01 496 Adiantum capillus-veneris mRNA. clone: YMU001_000109_F01. BP918100... CL8Contig1 Show BP918100 Clone id YMU001_000109_F01 Library YMU01 Length 496 Definition Adiantum capil...lus-veneris mRNA. clone: YMU001_000109_F01. Accession BP918100 Tissue type prothallium Developmental stage -...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918100... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918100|Adia

  8. AcEST: BP914100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_H03 542 Adiantum capillus-veneris mRNA. clone: YMU001_000039_H03. BP914100 - Show BP914100...is mRNA. clone: YMU001_000039_H03. Accession BP914100 Tissue type prothallium Developmental stage - Contig I...ams, Nucleic Acids Res. 25:3389-3402. Query= BP914100|Adiantum capillus-veneris mRNA, clone: YMU001_000039_H...ped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914100

  9. AcEST: BP912100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000015_B06 447 Adiantum capillus-veneris mRNA. clone: YMU001_000015_B06. BP912100 - Show BP912100...is mRNA. clone: YMU001_000015_B06. Accession BP912100 Tissue type prothallium Developmental stage - Contig I...s. 25:3389-3402. Query= BP912100|Adiantum capillus-veneris mRNA, clone: YMU001_00...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912100|Adiantum capi

  10. AcEST: BP916100 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000083_B04 427 Adiantum capillus-veneris mRNA. clone: YMU001_000083_B04. BP916100... CL115Contig1 Show BP916100 Clone id YMU001_000083_B04 Library YMU01 Length 427 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000083_B04. Accession BP916100 Tissue type prothallium Developmental stage...s, Nucleic Acids Res. 25:3389-3402. Query= BP916100|Adiantum capillus-veneris mRN... PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916100

  11. AcEST: BP921008 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_E02 477 Adiantum capillus-veneris mRNA. clone: YMU001_000144_E02. BP921008 - Show BP92100...is mRNA. clone: YMU001_000144_E02. Accession BP921008 Tissue type prothallium Developmental stage - Contig I...c Acids Res. 25:3389-3402. Query= BP921008|Adiantum capillus-veneris mRNA, clone:...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921008|Adiantum capillus-

  12. AcEST: BP914062 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_D10 340 Adiantum capillus-veneris mRNA. clone: YMU001_000039_D10. BP914062 - Show BP91406...is mRNA. clone: YMU001_000039_D10. Accession BP914062 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= BP91406...ST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91406

  13. AcEST: BP914064 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_D12 560 Adiantum capillus-veneris mRNA. clone: YMU001_000039_D12. BP91406...4 CL532Contig1 Show BP914064 Clone id YMU001_000039_D12 Library YMU01 Length 560 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000039_D12. Accession BP914064 Tissue type prothallium Developmental stage...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914064|Adiantum capillus-vener...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914064|Adi

  14. AcEST: BP921406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000149_E02 542 Adiantum capillus-veneris mRNA. clone: YMU001_000149_E02. BP921406... CL4001Contig1 Show BP921406 Clone id YMU001_000149_E02 Library YMU01 Length 542 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000149_E02. Accession BP921406 Tissue type prothallium Developmental stag...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921406|Adiantum capillus-veneris mRNA, cl...s Res. 25:3389-3402. Query= BP921406|Adiantum capillus-veneris mRNA, clone: YMU00

  15. AcEST: BP912406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_F09 348 Adiantum capillus-veneris mRNA. clone: YMU001_000018_F09. BP912406... CL1894Contig1 Show BP912406 Clone id YMU001_000018_F09 Library YMU01 Length 348 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000018_F09. Accession BP912406 Tissue type prothallium Developmental stag...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912406|Adiantum capillus-veneris mRNA...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912406

  16. AcEST: BP914067 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_E03 508 Adiantum capillus-veneris mRNA. clone: YMU001_000039_E03. BP91406...7 CL855Contig1 Show BP914067 Clone id YMU001_000039_E03 Library YMU01 Length 508 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000039_E03. Accession BP914067 Tissue type prothallium Developmental stage...neration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91406...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914067|Adiantum capillus-veneris mRNA, c

  17. AcEST: BP914061 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_D09 599 Adiantum capillus-veneris mRNA. clone: YMU001_000039_D09. BP91406...1 CL1730Contig1 Show BP914061 Clone id YMU001_000039_D09 Library YMU01 Length 599 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000039_D09. Accession BP914061 Tissue type prothallium Developmental stag... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914061|Adia...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914061|Adiantum capillus-veneris mRNA, c

  18. AcEST: BP914406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_E09 562 Adiantum capillus-veneris mRNA. clone: YMU001_000058_E09. BP914406... CL513Contig1 Show BP914406 Clone id YMU001_000058_E09 Library YMU01 Length 562 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000058_E09. Accession BP914406 Tissue type prothallium Developmental stage...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914406|Adiantum capillus...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914406

  19. AcEST: BP920406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000136_G02 527 Adiantum capillus-veneris mRNA. clone: YMU001_000136_G02. BP920406 - Show BP920406...is mRNA. clone: YMU001_000136_G02. Accession BP920406 Tissue type prothallium Developmental stage - Contig I...base search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920406|Adiantum capillus-veneris mRNA, clone...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920406|Adiantum capillus-veneris mRNA, c

  20. AcEST: BP914063 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_D11 515 Adiantum capillus-veneris mRNA. clone: YMU001_000039_D11. BP914063 - Show BP91406...is mRNA. clone: YMU001_000039_D11. Accession BP914063 Tissue type prothallium Developmental stage - Contig I...es. 25:3389-3402. Query= BP914063|Adiantum capillus-veneris mRNA, clone: YMU001_000039_D11. (515 letters) Da...ein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914063|Adiantum capillus-veneris mRN

  1. AcEST: BP916406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000087_D01 556 Adiantum capillus-veneris mRNA. clone: YMU001_000087_D01. BP916406... CL1913Contig1 Show BP916406 Clone id YMU001_000087_D01 Library YMU01 Length 556 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000087_D01. Accession BP916406 Tissue type prothallium Developmental stag...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916406|Adiantum capill...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916406|Adiantum capillus-veneris mRNA, c

  2. AcEST: BP914068 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000039_E04 420 Adiantum capillus-veneris mRNA. clone: YMU001_000039_E04. BP914068 - Show BP91406...is mRNA. clone: YMU001_000039_E04. Accession BP914068 Tissue type prothallium Developmental stage - Contig I...PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91406...se search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914068|Adiantum capillus-veneris mRNA, clone:

  3. AcEST: BP913406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000029_H06 570 Adiantum capillus-veneris mRNA. clone: YMU001_000029_H06. BP913406 - Show BP913406...is mRNA. clone: YMU001_000029_H06. Accession BP913406 Tissue type prothallium Developmental stage - Contig I...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP913406|Adiantum capillus-veneris mRNA, clone: YMU00...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913406|Adiantum capil...LDVTRGLVNGARGVVVAFES--GKHG---------------LPH 406 Query: 387 VRFACNRAEIVIGPDRQTVESGGMQVARRIQVPLILAWALSVHKCQGM

  4. AcEST: BP915406 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000071_B11 433 Adiantum capillus-veneris mRNA. clone: YMU001_000071_B11. BP915406 - Show BP915406...is mRNA. clone: YMU001_000071_B11. Accession BP915406 Tissue type prothallium Developmental stage - Contig I...Acids Res. 25:3389-3402. Query= BP915406|Adiantum capillus-veneris mRNA, clone: Y...leic Acids Res. 25:3389-3402. Query= BP915406|Adiantum capillus-veneris mRNA, clone: YMU001_000071_B11. (433

  5. AcEST: BP912343 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A05 305 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A05. BP912343 - Show BP91234...is mRNA. clone: YMU001_000018_A05. Accession BP912343 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= BP91234...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912343|Adiantum capill

  6. AcEST: BP912346 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A08 453 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A08. BP912346 - Show BP91234...is mRNA. clone: YMU001_000018_A08. Accession BP912346 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP912346|Adiantum capillus-veneris mRNA, clone...nd PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91234

  7. AcEST: BP912344 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A06 486 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A06. BP91234...4 CL599Contig1 Show BP912344 Clone id YMU001_000018_A06 Library YMU01 Length 486 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000018_A06. Accession BP912344 Tissue type prothallium Developmental stage... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912344|Adiantum capil...leic Acids Res. 25:3389-3402. Query= BP912344|Adiantum capillus-veneris mRNA, clone: YMU001_000018_A06. (468

  8. AcEST: BP912340 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A02 465 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A02. BP91234...0 CL1330Contig1 Show BP912340 Clone id YMU001_000018_A02 Library YMU01 Length 465 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000018_A02. Accession BP912340 Tissue type prothallium Developmental stag...Nucleic Acids Res. 25:3389-3402. Query= BP912340|Adiantum capillus-veneris mRNA, ...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91234

  9. AcEST: BP912349 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A11 539 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A11. BP912349 - Show BP91234...is mRNA. clone: YMU001_000018_A11. Accession BP912349 Tissue type prothallium Developmental stage - Contig I... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91234...ucleic Acids Res. 25:3389-3402. Query= BP912349|Adiantum capillus-veneris mRNA, clone: YMU001_000018_A11. (5

  10. AcEST: BP912342 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000018_A04 553 Adiantum capillus-veneris mRNA. clone: YMU001_000018_A04. BP91234...2 CL2124Contig1 Show BP912342 Clone id YMU001_000018_A04 Library YMU01 Length 553 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000018_A04. Accession BP912342 Tissue type prothallium Developmental stag...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912342|Adiantum capillus-veneris mRNA, clone:...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912342|Adiantum capillus-

  11. AcEST: BP919367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000124_C07 523 Adiantum capillus-veneris mRNA. clone: YMU001_000124_C07. BP919367... CL601Contig1 Show BP919367 Clone id YMU001_000124_C07 Library YMU01 Length 523 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000124_C07. Accession BP919367 Tissue type prothallium Developmental stage...es. 25:3389-3402. Query= BP919367|Adiantum capillus-veneris mRNA, clone: YMU001_000124_C07. (523 letters) Da...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919367|Adiantum ca

  12. AcEST: BP914367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_B03 578 Adiantum capillus-veneris mRNA. clone: YMU001_000058_B03. BP914367 - Show BP914367...is mRNA. clone: YMU001_000058_B03. Accession BP914367 Tissue type prothallium Developmental stage - Contig I...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914367|Adiantum ...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914367|

  13. AcEST: BP913671 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A02 620 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A02. BP913671 - Show BP91367...is mRNA. clone: YMU001_000033_A02. Accession BP913671 Tissue type prothallium Developmental stage - Contig I... Nucleic Acids Res. 25:3389-3402. Query= BP913671|Adiantum capillus-veneris mRNA, clone: YMU001_000033_A02. ...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913671|Adiantum capillus-veneris mRNA, c

  14. AcEST: BP913676 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A07 497 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A07. BP913676 - Show BP91367...is mRNA. clone: YMU001_000033_A07. Accession BP913676 Tissue type prothallium Developmental stage - Contig I... programs, Nucleic Acids Res. 25:3389-3402. Query= BP913676|Adiantum capillus-ven...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913676|Adiantum capillus-veneris mRNA, clone:

  15. AcEST: BP913367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000029_E01 457 Adiantum capillus-veneris mRNA. clone: YMU001_000029_E01. BP913367 - Show BP913367...is mRNA. clone: YMU001_000029_E01. Accession BP913367 Tissue type prothallium Developmental stage - Contig I...leic Acids Res. 25:3389-3402. Query= BP913367|Adiantum capillus-veneris mRNA, clo...AST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913367

  16. AcEST: BP913675 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A06 440 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A06. BP913675 - Show BP91367...is mRNA. clone: YMU001_000033_A06. Accession BP913675 Tissue type prothallium Developmental stage - Contig I... Nucleic Acids Res. 25:3389-3402. Query= BP913675|Adiantum capillus-veneris mRNA,...ST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91367

  17. AcEST: BP913677 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A08 517 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A08. BP913677 - Show BP91367...is mRNA. clone: YMU001_000033_A08. Accession BP913677 Tissue type prothallium Developmental stage - Contig I...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91367...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91367

  18. AcEST: BP913679 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A11 505 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A11. BP91367...9 CL11Contig1 Show BP913679 Clone id YMU001_000033_A11 Library YMU01 Length 505 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000033_A11. Accession BP913679 Tissue type prothallium Developmental stage ...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91367...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913679|Adiantum cap

  19. AcEST: BP920367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000136_C07 537 Adiantum capillus-veneris mRNA. clone: YMU001_000136_C07. BP920367 - Show BP920367...is mRNA. clone: YMU001_000136_C07. Accession BP920367 Tissue type prothallium Developmental stage - Contig I...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920367...grams, Nucleic Acids Res. 25:3389-3402. Query= BP920367|Adiantum capillus-veneris mRNA, clone: YMU001_000136

  20. AcEST: BP913674 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A05 472 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A05. BP913674 - Show BP91367...is mRNA. clone: YMU001_000033_A05. Accession BP913674 Tissue type prothallium Developmental stage - Contig I...cleic Acids Res. 25:3389-3402. Query= BP913674|Adiantum capillus-veneris mRNA, cl...rams, Nucleic Acids Res. 25:3389-3402. Query= BP913674|Adiantum capillus-veneris mRNA, clone: YMU001_000033_

  1. AcEST: BP913672 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A03 488 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A03. BP913672 - Show BP91367...is mRNA. clone: YMU001_000033_A03. Accession BP913672 Tissue type prothallium Developmental stage - Contig I...se search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913672|Adiantum cap...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913672|Adiantum capillus-

  2. AcEST: BP913678 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000033_A10 511 Adiantum capillus-veneris mRNA. clone: YMU001_000033_A10. BP913678 - Show BP91367...is mRNA. clone: YMU001_000033_A10. Accession BP913678 Tissue type prothallium Developmental stage - Contig I...ic Acids Res. 25:3389-3402. Query= BP913678|Adiantum capillus-veneris mRNA, clone: YMU001_000033_A10. (511 l...s Res. 25:3389-3402. Query= BP913678|Adiantum capillus-veneris mRNA, clone: YMU001_000033_A10. (511 letters)

  3. AcEST: BP918367 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000112_F09 563 Adiantum capillus-veneris mRNA. clone: YMU001_000112_F09. BP918367 - Show BP918367...is mRNA. clone: YMU001_000112_F09. Accession BP918367 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP918367|Adiantum capillus-veneris mRNA, clone: YMU001_000112_F09. (5...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918367|Adiantum capillus-veneris

  4. AcEST: BP919775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_A08 507 Adiantum capillus-veneris mRNA. clone: YMU001_000129_A08. BP919775 - Show BP919775...is mRNA. clone: YMU001_000129_A08. Accession BP919775 Tissue type prothallium Developmental stage - Contig I...h programs, Nucleic Acids Res. 25:3389-3402. Query= BP919775|Adiantum capillus-ve... database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919775|Adiantum capillus-veneris mRNA,

  5. AcEST: BP916775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000091_D11 369 Adiantum capillus-veneris mRNA. clone: YMU001_000091_D11. BP916775 - Show BP916775...is mRNA. clone: YMU001_000091_D11. Accession BP916775 Tissue type prothallium Developmental stage - Contig I...rams, Nucleic Acids Res. 25:3389-3402. Query= BP916775|Adiantum capillus-veneris mRNA, clone: YMU001_000091_...programs, Nucleic Acids Res. 25:3389-3402. Query= BP916775|Adiantum capillus-veneris mRNA, clone: YMU001_000

  6. AcEST: BP917753 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A05 482 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A05. BP91775...3 CL2810Contig1 Show BP917753 Clone id YMU001_000105_A05 Library YMU01 Length 482 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000105_A05. Accession BP917753 Tissue type prothallium Developmental stag... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917753|Adiant...arch programs, Nucleic Acids Res. 25:3389-3402. Query= BP917753|Adiantum capillus

  7. AcEST: BP914775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000062_G03 488 Adiantum capillus-veneris mRNA. clone: YMU001_000062_G03. BP914775... CL4173Contig1 Show BP914775 Clone id YMU001_000062_G03 Library YMU01 Length 488 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000062_G03. Accession BP914775 Tissue type prothallium Developmental stag...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914775...leic Acids Res. 25:3389-3402. Query= BP914775|Adiantum capillus-veneris mRNA, clo

  8. AcEST: BP920775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000141_D06 589 Adiantum capillus-veneris mRNA. clone: YMU001_000141_D06. BP920775 - Show BP920775...is mRNA. clone: YMU001_000141_D06. Accession BP920775 Tissue type prothallium Developmental stage - Contig I...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP920775|Adi...ms, Nucleic Acids Res. 25:3389-3402. Query= BP920775|Adiantum capillus-veneris mRNA, clone: YMU001_000141_D0

  9. AcEST: BP917750 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A02 462 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A02. BP91775...0 CL3417Contig1 Show BP917750 Clone id YMU001_000105_A02 Library YMU01 Length 462 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000105_A02. Accession BP917750 Tissue type prothallium Developmental stag...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917750|Adiantu...base search programs, Nucleic Acids Res. 25:3389-3402. Query= BP917750|Adiantum capillus-veneris mRNA, clone

  10. AcEST: BP915775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000076_F10 565 Adiantum capillus-veneris mRNA. clone: YMU001_000076_F10. BP915775 - Show BP915775...is mRNA. clone: YMU001_000076_F10. Accession BP915775 Tissue type prothallium Developmental stage - Contig I...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915775|Adiantum capillus-veneris mRNA,...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915775|Adiantum capi

  11. AcEST: BP913775 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000035_B05 311 Adiantum capillus-veneris mRNA. clone: YMU001_000035_B05. BP913775 - Show BP913775...is mRNA. clone: YMU001_000035_B05. Accession BP913775 Tissue type prothallium Developmental stage - Contig I...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913775|Adiantum capillus...d PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913775

  12. AcEST: BP917758 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000105_A12 315 Adiantum capillus-veneris mRNA. clone: YMU001_000105_A12. BP91775...8 CL2869Contig1 Show BP917758 Clone id YMU001_000105_A12 Library YMU01 Length 315 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000105_A12. Accession BP917758 Tissue type prothallium Developmental stag... Gapped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91775...rograms, Nucleic Acids Res. 25:3389-3402. Query= BP917758|Adiantum capillus-vener

  13. AcEST: BP919802 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_C12 487 Adiantum capillus-veneris mRNA. clone: YMU001_000129_C12. BP919802 - Show BP91980...is mRNA. clone: YMU001_000129_C12. Accession BP919802 Tissue type prothallium Developmental stage - Contig I...h programs, Nucleic Acids Res. 25:3389-3402. Query= BP919802|Adiantum capillus-ve...SI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91980

  14. AcEST: BP919804 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D02 242 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D02. BP91980...4 CL1786Contig1 Show BP919804 Clone id YMU001_000129_D02 Library YMU01 Length 242 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000129_D02. Accession BP919804 Tissue type prothallium Developmental stag...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919804|Adiantum capillus-veneris m...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919804|Adiantum capillus-veneris m

  15. AcEST: BP919807 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D05 485 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D05. BP91980...7 CL2558Contig1 Show BP919807 Clone id YMU001_000129_D05 Library YMU01 Length 485 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000129_D05. Accession BP919807 Tissue type prothallium Developmental stag...of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91980...tabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919807|Adiantum

  16. AcEST: BP919805 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D03 530 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D03. BP919805 - Show BP91980...is mRNA. clone: YMU001_000129_D03. Accession BP919805 Tissue type prothallium Developmental stage - Contig I...s Res. 25:3389-3402. Query= BP919805|Adiantum capillus-veneris mRNA, clone: YMU001_000129_D03. (530 letters)...in database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919805|Adi

  17. AcEST: BP919803 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D01 477 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D01. BP91980...3 CL2549Contig1 Show BP919803 Clone id YMU001_000129_D01 Library YMU01 Length 477 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000129_D01. Accession BP919803 Tissue type prothallium Developmental stag...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91980...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91980

  18. AcEST: BP919808 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D06 483 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D06. BP919808 - Show BP91980...is mRNA. clone: YMU001_000129_D06. Accession BP919808 Tissue type prothallium Developmental stage - Contig I...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919808|Adiantum capi...-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91980

  19. AcEST: BP919809 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D07 283 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D07. BP919809 - Show BP91980...is mRNA. clone: YMU001_000129_D07. Accession BP919809 Tissue type prothallium Developmental stage - Contig I...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919809|Adiantum capillus...rams, Nucleic Acids Res. 25:3389-3402. Query= BP919809|Adiantum capillus-veneris mRNA, clone: YMU001_000129_

  20. AcEST: BP919806 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_D04 576 Adiantum capillus-veneris mRNA. clone: YMU001_000129_D04. BP919806 - Show BP91980...is mRNA. clone: YMU001_000129_D04. Accession BP919806 Tissue type prothallium Developmental stage - Contig I..., Nucleic Acids Res. 25:3389-3402. Query= BP919806|Adiantum capillus-veneris mRNA, clone: YMU001_000129_D04....ms, Nucleic Acids Res. 25:3389-3402. Query= BP919806|Adiantum capillus-veneris mR

  1. AcEST: BP919800 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000129_C10 406 Adiantum capillus-veneris mRNA. clone: YMU001_000129_C10. BP919800 - Show BP91980...is mRNA. clone: YMU001_000129_C10. Accession BP919800 Tissue type prothallium Developmental stage - Contig I... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919800|Adiantum capillus-veneri...abase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919800|Adiantum capillus-veneris mRNA, clon

  2. 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

  3. AcEST: BP913000 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000025_C05 322 Adiantum capillus-veneris mRNA. clone: YMU001_000025_C05. BP913000... CL1177Contig1 Show BP913000 Clone id YMU001_000025_C05 Library YMU01 Length 322 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000025_C05. Accession BP913000 Tissue type prothallium Developmental stag.... 25:3389-3402. Query= BP913000|Adiantum capillus-veneris mRNA, clone: YMU001_000025_C05. (322 letters) Data...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP913000|Adiantum capill

  4. AcEST: BP921016 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000144_E10 528 Adiantum capillus-veneris mRNA. clone: YMU001_000144_E10. BP92101...6 CL35Contig1 Show BP921016 Clone id YMU001_000144_E10 Library YMU01 Length 528 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000144_E10. Accession BP921016 Tissue type prothallium Developmental stage ... Res. 25:3389-3402. Query= BP921016|Adiantum capillus-veneris mRNA, clone: YMU001... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921016|Adia

  5. AcEST: BP919713 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000128_C09 384 Adiantum capillus-veneris mRNA. clone: YMU001_000128_C09. BP919713 - Show BP91971...is mRNA. clone: YMU001_000128_C09. Accession BP919713 Tissue type prothallium Developmental stage - Contig I...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919713|Adiantum capillus-veneris mRNA, c...rams, Nucleic Acids Res. 25:3389-3402. Query= BP919713|Adiantum capillus-veneris

  6. AcEST: BP911971 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000011_E04 469 Adiantum capillus-veneris mRNA. clone: YMU001_000011_E04. BP911971... CL204Contig1 Show BP911971 Clone id YMU001_000011_E04 Library YMU01 Length 469 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000011_E04. Accession BP911971 Tissue type prothallium Developmental stage..., Nucleic Acids Res. 25:3389-3402. Query= BP911971|Adiantum capillus-veneris mRNA...n database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911971|Adiantum capillus-veneris mRNA,

  7. AcEST: BP919715 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000128_C11 494 Adiantum capillus-veneris mRNA. clone: YMU001_000128_C11. BP91971...5 CL3828Contig1 Show BP919715 Clone id YMU001_000128_C11 Library YMU01 Length 494 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000128_C11. Accession BP919715 Tissue type prothallium Developmental stag...ion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91971... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919715|Adia

  8. AcEST: BP919717 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000128_D01 387 Adiantum capillus-veneris mRNA. clone: YMU001_000128_D01. BP919717 - Show BP91971...is mRNA. clone: YMU001_000128_D01. Accession BP919717 Tissue type prothallium Developmental stage - Contig I...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919717|Adiantum capill... programs, Nucleic Acids Res. 25:3389-3402. Query= BP919717|Adiantum capillus-veneris mRNA, clone: YMU001_00

  9. AcEST: BP919711 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000128_C07 523 Adiantum capillus-veneris mRNA. clone: YMU001_000128_C07. BP919711 - Show BP91971...is mRNA. clone: YMU001_000128_C07. Accession BP919711 Tissue type prothallium Developmental stage - Contig I...eic Acids Res. 25:3389-3402. Query= BP919711|Adiantum capillus-veneris mRNA, clone: YMU001_000128_C07. (523 ... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919711|Adiantum capillus-ven

  10. AcEST: BP914460 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B08 541 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B08. BP914460 - Show BP9144...is mRNA. clone: YMU001_000059_B08. Accession BP914460 Tissue type prothallium Developmental stage - Contig I...ST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914460|Adiantum capil...VVFASKVPNDRMSLFSIECKEQGNLHQRDEFFLKSDDANC 143 Query: 383 LLLFPMRTSHLASPFQETTSCS 448 L H P+ +CS Sbjct: 144 YLY

  11. AcEST: BP914403 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_E06 616 Adiantum capillus-veneris mRNA. clone: YMU001_000058_E06. BP914403 - Show BP9144...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= BP91440... search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914403|Adiantum capillus-veneris mRNA, clone: YM

  12. AcEST: BP914472 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_C09 554 Adiantum capillus-veneris mRNA. clone: YMU001_000059_C09. BP9144...72 CL1425Contig1 Show BP914472 Clone id YMU001_000059_C09 Library YMU01 Length 554 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_C09. Accession BP914472 Tissue type prothallium Developmental stag...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914472|Adiantum capillus-ve...a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  13. AcEST: BP914492 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_E05 529 Adiantum capillus-veneris mRNA. clone: YMU001_000059_E05. BP914492 - Show BP9144...is mRNA. clone: YMU001_000059_E05. Accession BP914492 Tissue type prothallium Developmental stage - Contig I...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914492|Adiantum capillus-ven

  14. AcEST: BP914495 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_E08 565 Adiantum capillus-veneris mRNA. clone: YMU001_000059_E08. BP914495 - Show BP9144...is mRNA. clone: YMU001_000059_E08. Accession BP914495 Tissue type prothallium Developmental stage - Contig I...ch programs, Nucleic Acids Res. 25:3389-3402. Query= BP914495|Adiantum capillus-veneris mRNA, clone: YMU001_...VAAEAKDDELKANIQDVE-------KDEDGKEHKDT 144 Query: 394 SFRLYDGKSEPESLQSSDQDSFKKPTEIS...n of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914495|Adiantum capillus-ve

  15. AcEST: BP914410 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_F01 608 Adiantum capillus-veneris mRNA. clone: YMU001_000058_F01. BP914410 - Show BP9144...is mRNA. clone: YMU001_000058_F01. Accession BP914410 Tissue type prothallium Developmental stage - Contig I...I-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144... BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  16. AcEST: BP918144 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000110_A12 555 Adiantum capillus-veneris mRNA. clone: YMU001_000110_A12. BP918144 - Show BP918144...is mRNA. clone: YMU001_000110_A12. Accession BP918144 Tissue type prothallium Developmental stage - Contig I...rams, Nucleic Acids Res. 25:3389-3402. Query= BP918144|Adiantum capillus-veneris mRNA, clone: YMU001_000110_... Nucleic Acids Res. 25:3389-3402. Query= BP918144|Adiantum capillus-veneris mRNA, clone: YMU001_000110_A12.

  17. AcEST: BP914423 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_G03 431 Adiantum capillus-veneris mRNA. clone: YMU001_000058_G03. BP914423 - Show BP9144...is mRNA. clone: YMU001_000058_G03. Accession BP914423 Tissue type prothallium Developmental stage - Contig I...cids Res. 25:3389-3402. Query= BP914423|Adiantum capillus-veneris mRNA, clone: YM... database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914423|Adiantum capillus-veneris mRNA,

  18. AcEST: BP921144 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000146_C05 517 Adiantum capillus-veneris mRNA. clone: YMU001_000146_C05. BP921144 - Show BP921144...is mRNA. clone: YMU001_000146_C05. Accession BP921144 Tissue type prothallium Developmental stage - Contig I...on of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921144... new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921144|Adiant

  19. AcEST: BP914464 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B12 450 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B12. BP914464 - Show BP9144...is mRNA. clone: YMU001_000059_B12. Accession BP914464 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= BP9144...Nucleic Acids Res. 25:3389-3402. Query= BP914464|Adiantum capillus-veneris mRNA, clone: YMU001_000059_B12. (

  20. AcEST: BP914427 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000058_G07 481 Adiantum capillus-veneris mRNA. clone: YMU001_000058_G07. BP914427 - Show BP9144...is mRNA. clone: YMU001_000058_G07. Accession BP914427 Tissue type prothallium Developmental stage - Contig I...AST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...CVPADI 473 Query: 284 AEPGKLDEMFERMDTNNDGRVSFEEFKDAMQLDQSLRKAVLSPLERV 144 EPGKLDE+F++MD N+DG V+F+EFK AMQ D S...ase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914427|Adiantum ca

  1. AcEST: BP914463 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B11 587 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B11. BP9144...63 CL3104Contig1 Show BP914463 Clone id YMU001_000059_B11 Library YMU01 Length 587 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_B11. Accession BP914463 Tissue type prothallium Developmental stag...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914463|Adiantu...protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914463|Adiantum capillus-veneris

  2. AcEST: BP914450 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_A10 499 Adiantum capillus-veneris mRNA. clone: YMU001_000059_A10. BP9144...50 CL3143Contig1 Show BP914450 Clone id YMU001_000059_A10 Library YMU01 Length 499 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_A10. Accession BP914450 Tissue type prothallium Developmental stag...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  3. AcEST: BP914476 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_D01 391 Adiantum capillus-veneris mRNA. clone: YMU001_000059_D01. BP9144...76 CL2162Contig1 Show BP914476 Clone id YMU001_000059_D01 Library YMU01 Length 391 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_D01. Accession BP914476 Tissue type prothallium Developmental stag...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914476|Adiantu...LAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914476

  4. AcEST: BP916144 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000083_F08 124 Adiantum capillus-veneris mRNA. clone: YMU001_000083_F08. BP916144... CL2703Contig1 Show BP916144 Clone id YMU001_000083_F08 Library YMU01 Length 124 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000083_F08. Accession BP916144 Tissue type prothallium Developmental stag...Res. 25:3389-3402. Query= BP916144|Adiantum capillus-veneris mRNA, clone: YMU001_...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP916144|Adi

  5. AcEST: BP915144 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000067_A07 184 Adiantum capillus-veneris mRNA. clone: YMU001_000067_A07. BP915144... CL2423Contig1 Show BP915144 Clone id YMU001_000067_A07 Library YMU01 Length 184 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000067_A07. Accession BP915144 Tissue type prothallium Developmental stag...AST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915144...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915144|Adiantum capillus

  6. AcEST: BP914486 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_D11 638 Adiantum capillus-veneris mRNA. clone: YMU001_000059_D11. BP914486 - Show BP9144...is mRNA. clone: YMU001_000059_D11. Accession BP914486 Tissue type prothallium Developmental stage - Contig I...leic Acids Res. 25:3389-3402. Query= BP914486|Adiantum capillus-veneris mRNA, clone: YMU001_000059_D11. (613...ms, Nucleic Acids Res. 25:3389-3402. Query= BP914486|Adiantum capillus-veneris mRNA, clone: YMU001_000059_D1

  7. AcEST: BP914467 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_C03 510 Adiantum capillus-veneris mRNA. clone: YMU001_000059_C03. BP914467 - Show BP9144...is mRNA. clone: YMU001_000059_C03. Accession BP914467 Tissue type prothallium Developmental stage - Contig I... a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...Res. 25:3389-3402. Query= BP914467|Adiantum capillus-veneris mRNA, clone: YMU001_

  8. AcEST: BP911440 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000005_A06 228 Adiantum capillus-veneris mRNA. clone: YMU001_000005_A06. BP911440 - Show BP91144...is mRNA. clone: YMU001_000005_A06. Accession BP911440 Tissue type prothallium Developmental stage - Contig I...ed BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91144...LAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91144

  9. AcEST: BP914466 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_C02 620 Adiantum capillus-veneris mRNA. clone: YMU001_000059_C02. BP914466 - Show BP9144...is mRNA. clone: YMU001_000059_C02. Accession BP914466 Tissue type prothallium Developmental stage - Contig I...f protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914466|Adiantum capillus-vener... Acids Res. 25:3389-3402. Query= BP914466|Adiantum capillus-veneris mRNA, clone:

  10. AcEST: BP914462 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B10 524 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B10. BP914462 - Show BP9144...is mRNA. clone: YMU001_000059_B10. Accession BP914462 Tissue type prothallium Developmental stage - Contig I...w generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  11. AcEST: BP914474 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_C11 492 Adiantum capillus-veneris mRNA. clone: YMU001_000059_C11. BP9144...74 CL2234Contig1 Show BP914474 Clone id YMU001_000059_C11 Library YMU01 Length 492 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_C11. Accession BP914474 Tissue type prothallium Developmental stag...ration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914474|Adiantum capillus-veneris mRNA, cl

  12. AcEST: BP914456 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B04 299 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B04. BP9144...56 CL787Contig1 Show BP914456 Clone id YMU001_000059_B04 Library YMU01 Length 299 Definition Adiantum cap...illus-veneris mRNA. clone: YMU001_000059_B04. Accession BP914456 Tissue type prothallium Developmental stage... PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914456|Adiantum capillus-ven

  13. AcEST: BP914452 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_A12 535 Adiantum capillus-veneris mRNA. clone: YMU001_000059_A12. BP914452 - Show BP9144...is mRNA. clone: YMU001_000059_A12. Accession BP914452 Tissue type prothallium Developmental stage - Contig I...leic Acids Res. 25:3389-3402. Query= BP914452|Adiantum capillus-veneris mRNA, clone: YMU001_000059_A12. (535...generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914452|Adiantum ca

  14. AcEST: BP914444 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_A03 493 Adiantum capillus-veneris mRNA. clone: YMU001_000059_A03. BP9144...44 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= BP9144... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914444|Adiantum capillus-veneri

  15. AcEST: BP914454 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_B02 618 Adiantum capillus-veneris mRNA. clone: YMU001_000059_B02. BP914454 - Show BP9144...is mRNA. clone: YMU001_000059_B02. Accession BP914454 Tissue type prothallium Developmental stage - Contig I...d BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...ms, Nucleic Acids Res. 25:3389-3402. Query= BP914454|Adiantum capillus-veneris mR

  16. AcEST: BP914488 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_E01 492 Adiantum capillus-veneris mRNA. clone: YMU001_000059_E01. BP9144...88 CL2008Contig1 Show BP914488 Clone id YMU001_000059_E01 Library YMU01 Length 492 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_E01. Accession BP914488 Tissue type prothallium Developmental stag... protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...T: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914488|Ad

  17. AcEST: BP914487 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_D12 521 Adiantum capillus-veneris mRNA. clone: YMU001_000059_D12. BP914487 - Show BP9144...is mRNA. clone: YMU001_000059_D12. Accession BP914487 Tissue type prothallium Developmental stage - Contig I...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914487|...pped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  18. AcEST: BP914496 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_E09 561 Adiantum capillus-veneris mRNA. clone: YMU001_000059_E09. BP9144...96 CL1745Contig1 Show BP914496 Clone id YMU001_000059_E09 Library YMU01 Length 561 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_E09. Accession BP914496 Tissue type prothallium Developmental stag...atabase search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914496|Adiantu...rotein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP914496|Adiantum capillus-veneris

  19. AcEST: BP914443 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000059_A02 529 Adiantum capillus-veneris mRNA. clone: YMU001_000059_A02. BP9144...43 CL1901Contig1 Show BP914443 Clone id YMU001_000059_A02 Library YMU01 Length 529 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000059_A02. Accession BP914443 Tissue type prothallium Developmental stag...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP9144

  20. AcEST: BP912219 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000016_E07 496 Adiantum capillus-veneris mRNA. clone: YMU001_000016_E07. BP912219 - Show BP912219...is mRNA. clone: YMU001_000016_E07. Accession BP912219 Tissue type prothallium Developmental stage - Contig I...tion of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912219...e search programs, Nucleic Acids Res. 25:3389-3402. Query= BP912219|Adiantum capillus-veneris mRNA, clone: Y

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. AcEST: BP918432 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000113_D10 502 Adiantum capillus-veneris mRNA. clone: YMU001_000113_D10. BP918432... CL2516Contig1 Show BP918432 Clone id YMU001_000113_D10 Library YMU01 Length 502 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000113_D10. Accession BP918432 Tissue type prothallium Developmental stag...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918432...otein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP918432|

  11. 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

  12. 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

  13. 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

  14. 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

  15. 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

  16. 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

  17. 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_

  18. AcEST: BP915910 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D05 543 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D05. BP915910 - Show BP91591...is mRNA. clone: YMU001_000079_D05. Accession BP915910 Tissue type prothallium Developmental stage - Contig I.... 25:3389-3402. Query= BP915910|Adiantum capillus-veneris mRNA, clone: YMU001_000079_D05. (543 letters) Data...s Res. 25:3389-3402. Query= BP915910|Adiantum capillus-veneris mRNA, clone: YMU00

  19. AcEST: BP915915 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D11 468 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D11. BP915915 - Show BP91591...is mRNA. clone: YMU001_000079_D11. Accession BP915915 Tissue type prothallium Developmental stage - Contig I... programs, Nucleic Acids Res. 25:3389-3402. Query= BP915915|Adiantum capillus-ven...ed BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91591

  20. AcEST: BP915919 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_E03 400 Adiantum capillus-veneris mRNA. clone: YMU001_000079_E03. BP91591...9 CL3486Contig1 Show BP915919 Clone id YMU001_000079_E03 Library YMU01 Length 400 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000079_E03. Accession BP915919 Tissue type prothallium Developmental stag...d BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91591...database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915919|Adiant

  1. AcEST: BP921591 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000151_H01 458 Adiantum capillus-veneris mRNA. clone: YMU001_000151_H01. BP921591 - Show BP921591...is mRNA. clone: YMU001_000151_H01. Accession BP921591 Tissue type prothallium Developmental stage - Contig I...ms, Nucleic Acids Res. 25:3389-3402. Query= BP921591|Adiantum capillus-veneris mRNA, clone: YMU001_000151_H0...LAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP921591

  2. AcEST: BP915913 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D08 427 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D08. BP915913 - Show BP91591...is mRNA. clone: YMU001_000079_D08. Accession BP915913 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= BP91591...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91591

  3. AcEST: BP915917 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_E01 288 Adiantum capillus-veneris mRNA. clone: YMU001_000079_E01. BP915917 - Show BP91591...is mRNA. clone: YMU001_000079_E01. Accession BP915917 Tissue type prothallium Developmental stage - Contig I...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915917|Adiantum capillus-veneris mR...s Res. 25:3389-3402. Query= BP915917|Adiantum capillus-veneris mRNA, clone: YMU00

  4. AcEST: BP915911 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D06 571 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D06. BP91591...1 CL46Contig1 Show BP915911 Clone id YMU001_000079_D06 Library YMU01 Length 571 Definition Adiantum capi...llus-veneris mRNA. clone: YMU001_000079_D06. Accession BP915911 Tissue type prothallium Developmental stage ...: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915911|Adi... Res. 25:3389-3402. Query= BP915911|Adiantum capillus-veneris mRNA, clone: YMU001

  5. AcEST: BP915912 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000079_D07 482 Adiantum capillus-veneris mRNA. clone: YMU001_000079_D07. BP915912 - Show BP91591...is mRNA. clone: YMU001_000079_D07. Accession BP915912 Tissue type prothallium Developmental stage - Contig I...tein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP915912|Adiantum capillus-veneris mR...BLAST: a new generation of protein database search programs, Nucleic Acids Res. 2...5:3389-3402. Query= BP915912|Adiantum capillus-veneris mRNA, clone: YMU001_000079_D07. (482 letters) Databas

  6. AcEST: BP911591 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000006_G06 296 Adiantum capillus-veneris mRNA. clone: YMU001_000006_G06. BP911591 - Show BP911591...is mRNA. clone: YMU001_000006_G06. Accession BP911591 Tissue type prothallium Developmental stage - Contig I...eration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911591|Adiantum capil...of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP911591|Adiantum capillus-vene

  7. AcEST: BP919218 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E11 400 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E11. BP919218 - Show BP91921...is mRNA. clone: YMU001_000122_E11. Accession BP919218 Tissue type prothallium Developmental stage - Contig I... of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919218|Adiantum capillus-ven...leic Acids Res. 25:3389-3402. Query= BP919218|Adiantum capillus-veneris mRNA, clo

  8. AcEST: BP919216 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E09 388 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E09. BP919216 - Show BP91921...is mRNA. clone: YMU001_000122_E09. Accession BP919216 Tissue type prothallium Developmental stage - Contig I...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919216|Adiantum cap...rams, Nucleic Acids Res. 25:3389-3402. Query= BP919216|Adiantum capillus-veneris

  9. AcEST: BP919213 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E06 293 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E06. BP919213 - Show BP91921...is mRNA. clone: YMU001_000122_E06. Accession BP919213 Tissue type prothallium Developmental stage - Contig I...new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919213|Adiantu...ped BLAST and PSI-BLAST: a new generation of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91921

  10. AcEST: BP919211 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E04 158 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E04. BP919211 - Show BP91921...is mRNA. clone: YMU001_000122_E04. Accession BP919211 Tissue type prothallium Developmental stage - Contig I...ucleic Acids Res. 25:3389-3402. Query= BP919211|Adiantum capillus-veneris mRNA, clone: YMU001_000122_E04. (1...Nucleic Acids Res. 25:3389-3402. Query= BP919211|Adiantum capillus-veneris mRNA, clone: YMU001_000122_E04. (

  11. AcEST: BP919214 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E07 486 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E07. BP919214 - Show BP91921...is mRNA. clone: YMU001_000122_E07. Accession BP919214 Tissue type prothallium Developmental stage - Contig I...base search programs, Nucleic Acids Res. 25:3389-3402. Query= BP919214|Adiantum c...Nucleic Acids Res. 25:3389-3402. Query= BP919214|Adiantum capillus-veneris mRNA, clone: YMU001_000122_E07. (

  12. AcEST: BP919215 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E08 525 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E08. BP919215 - Show BP91921...is mRNA. clone: YMU001_000122_E08. Accession BP919215 Tissue type prothallium Developmental stage - Contig I...Nucleic Acids Res. 25:3389-3402. Query= BP919215|Adiantum capillus-veneris mRNA, clone: YMU001_000122_E08. (...eneration of protein database search programs, Nucleic Acids Res. 25:3389-3402. Query= BP91921

  13. AcEST: BP919217 [AcEST

    Lifescience Database Archive (English)

    Full Text Available YMU001_000122_E10 547 Adiantum capillus-veneris mRNA. clone: YMU001_000122_E10. BP91921...7 CL1907Contig1 Show BP919217 Clone id YMU001_000122_E10 Library YMU01 Length 547 Definition Adiantum ca...pillus-veneris mRNA. clone: YMU001_000122_E10. Accession BP919217 Tissue type prothallium Developmental stag... programs, Nucleic Acids Res. 25:3389-3402. Query= BP919217|Adiantum capillus-ven...ds Res. 25:3389-3402. Query= BP919217|Adiantum capillus-veneris mRNA, clone: YMU001_000122_E10. (547 letters

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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