Mutation Research/DNA Repair最新文献

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Human germline mutation in the factor IX gene 因子IX基因的人类种系突变
Mutation Research/DNA Repair Pub Date : 2001-11-01 DOI: 10.1016/S0921-8777(01)00108-2
Steve S. Sommer, William A. Scaringe, Kathleen A. Hill
{"title":"Human germline mutation in the factor IX gene","authors":"Steve S. Sommer,&nbsp;William A. Scaringe,&nbsp;Kathleen A. Hill","doi":"10.1016/S0921-8777(01)00108-2","DOIUrl":"10.1016/S0921-8777(01)00108-2","url":null,"abstract":"<div><p><span><span>The molecular epidemiology of factor IX<span> germline mutations in patients with </span></span>hemophilia B has been studied in detail because it is an advantageous model for analyzing recent germline mutations in humans. It is estimated that mutations have been defined in the majority of nucleotides that are the target for mutation. The likelihood that a factor IX </span>missense mutation<span> will cause disease correlates with the degree of evolutionary conservation of the amino acid. Mutation rates per base-pair have been estimated after careful consideration and correction for biases, predicting about 76 de novo mutations per generation per individual resulting in 0.3 deleterious changes. The male-to-female sex ratio of mutation varies with the type of mutation. There is evidence for a maternal age effect and an excess of non-CpG G:C to A:T transitions. The factor IX mutation pattern is similar among geographically, racially and ethnically diverse human populations. The data support primarily endogenous mechanisms of germline mutation in the factor IX gene. Mutations at splice junctions are compatible with simple rules for predicting disease causing mutations.</span></p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"487 1","pages":"Pages 1-17"},"PeriodicalIF":0.0,"publicationDate":"2001-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00108-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 47
Cisplatin-induced apoptosis in 43-3B and 27-1 cells defective in nucleotide excision repair 顺铂在核苷酸切除修复缺陷的43-3B和27-1细胞中诱导细胞凋亡。
Mutation Research/DNA Repair Pub Date : 2001-09-04 DOI: 10.1016/S0921-8777(01)00095-7
Torsten R Dunkern, Gerhard Fritz, Bernd Kaina
{"title":"Cisplatin-induced apoptosis in 43-3B and 27-1 cells defective in nucleotide excision repair","authors":"Torsten R Dunkern,&nbsp;Gerhard Fritz,&nbsp;Bernd Kaina","doi":"10.1016/S0921-8777(01)00095-7","DOIUrl":"10.1016/S0921-8777(01)00095-7","url":null,"abstract":"<div><p><span>Cisplatin<span><span> is a highly potent cytotoxic and genotoxic agent used in the chemotherapy of various types of tumors. Its cytotoxic effect is supposed to be due to the induction of intra- and interstrand DNA cross-links which are repaired via the nucleotide excision repair<span><span><span> (NER) pathway. Here, we elucidated the mechanism of cisplatin-induced cytotoxicity in mutants derived from CHO-9 cells defective in NER. We compared 43-3B and 27-1 cells deficient for ERCC1 and ERCC3, respectively, with the corresponding wild-type and ERCC1 complemented 43-3B cells. It is shown that cells defective in ERCC1 are more sensitive than cells defective in ERCC3 with regard to cisplatin-induced reproductive cell death. ERCC1 and ERCC3 mutants showed a higher frequency of apoptosis and, to a lesser degree, necrosis compared to repair proficient cells. Induction of apoptosis in both ERCC1 and ERCC3 defective cells was accompanied by decline in Bcl-2 protein level, activation of caspases 8, 9 and 3 and poly(ADP-ribose)polymerase (PARP) </span>cleavage. Since the </span>mutant cells are defective in the repair of cisplatin-induced DNA lesions, the data demonstrate that non-repaired cisplatin-induced </span></span>DNA adducts act as a trigger of the mitochondrial apoptotic pathway by down-regulation of Bcl-2 followed by </span></span>caspase activation.</p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 4","pages":"Pages 249-258"},"PeriodicalIF":0.0,"publicationDate":"2001-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00095-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 27
Ultraviolet radiation alters the phosphorylation of RNA polymerase II large subunit and accelerates its proteasome-dependent degradation 紫外线辐射改变RNA聚合酶II大亚基的磷酸化,加速其蛋白酶体依赖性降解
Mutation Research/DNA Repair Pub Date : 2001-09-04 DOI: 10.1016/S0921-8777(01)00097-0
Zhonghui Luo , Jianhua Zheng , Yi Lu , David B Bregman
{"title":"Ultraviolet radiation alters the phosphorylation of RNA polymerase II large subunit and accelerates its proteasome-dependent degradation","authors":"Zhonghui Luo ,&nbsp;Jianhua Zheng ,&nbsp;Yi Lu ,&nbsp;David B Bregman","doi":"10.1016/S0921-8777(01)00097-0","DOIUrl":"10.1016/S0921-8777(01)00097-0","url":null,"abstract":"<div><p><span><span>It has been shown that ultraviolet (UV) radiation induces the ubiquitination<span> of the large subunit of RNA polymerase II (RNAP II-LS) as well as its proteasomal degradation. Studies in </span></span>mammalian cells have indicated that highly phosphorylated forms of RNAP II-LS are preferentially ubiquitinated, but studies in </span><span><em>Saccharomyces cerevisiae</em></span> have provided evidence that unphosphorylated RNAP II-LS is an equally suitable substrate. In the present study, an antibody (ARNA-3) that recognizes all forms of RNAP II-LS, regardless of the phosphorylation status of its C-terminal domain (CTD), was utilized to evaluate the degradation of total cellular RNAP II-LS in human fibroblasts under basal conditions or after UV-C (10<!--> <!-->J/m<sup>2</sup><span><span>) irradiation. It was found that UV radiation rapidly shifted the phosphorylation profile of RNAP II-LS from a mixture of dephosphorylated and phosphorylated forms to entirely more phosphorylated forms. This shift in phosphorylation status was not blocked by pharmacologic inhibition of either the ERK or p38 pathways, both of which have been implicated in the cellular UV response. In addition to shifting the phosphorylation profile, UV radiation led to net degradation of total RNAP II-LS. UV-induced degradation of RNAP II-LS was also greatly reduced in the presence of the transcriptional and CTD kinase inhibitor DRB. Using a panel of protease inhibitors, it was shown that the bulk of UV-induced degradation is proteasome-dependent. However, the UV-induced loss of hypophosphorylated RNAP II-LS was proteasome-independent. Lastly, UV radiation induced a similar shift to all hyperphosphorylated RNAP II-LS in </span>Cockayne syndrome (CS) cells of complementation groups A or B (CSA or CSB) when compared to appropriate controls. The UV-induced degradation rates of RNAP II-LS were not significantly altered when comparing CSA or CSB to repair competent control cells. The implications for the cellular UV response are discussed.</span></p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 4","pages":"Pages 259-274"},"PeriodicalIF":0.0,"publicationDate":"2001-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00097-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 78
Contents Of Volume 486 第486卷目录
Mutation Research/DNA Repair Pub Date : 2001-09-04 DOI: 10.1016/S0921-8777(01)00103-3
{"title":"Contents Of Volume 486","authors":"","doi":"10.1016/S0921-8777(01)00103-3","DOIUrl":"https://doi.org/10.1016/S0921-8777(01)00103-3","url":null,"abstract":"","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 4","pages":"Pages 285-286"},"PeriodicalIF":0.0,"publicationDate":"2001-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00103-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72032789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Reduced sensitivity to and ras mutation spectrum of N-ethyl-N-nitrosourea-induced thymic lymphomas in adult C.B-17 scid mice 降低对n -乙基-n -亚硝基源诱导的成年C.B-17小鼠胸腺淋巴瘤的敏感性和ras突变谱
Mutation Research/DNA Repair Pub Date : 2001-09-04 DOI: 10.1016/S0921-8777(01)00098-2
Mayumi Nishimura , Shizuko Kakinuma , Shigeharu Wakana , Aya Mukaigawara , Kazuei Mita , Toshihiko Sado , Toshiaki Ogiu , Yoshiya Shimada
{"title":"Reduced sensitivity to and ras mutation spectrum of N-ethyl-N-nitrosourea-induced thymic lymphomas in adult C.B-17 scid mice","authors":"Mayumi Nishimura ,&nbsp;Shizuko Kakinuma ,&nbsp;Shigeharu Wakana ,&nbsp;Aya Mukaigawara ,&nbsp;Kazuei Mita ,&nbsp;Toshihiko Sado ,&nbsp;Toshiaki Ogiu ,&nbsp;Yoshiya Shimada","doi":"10.1016/S0921-8777(01)00098-2","DOIUrl":"10.1016/S0921-8777(01)00098-2","url":null,"abstract":"<div><p><em>Scid</em> mice are defective in the ability to repair DNA double strand breaks and, as a consequence, their cells are radiosensitive. Further, they have been shown to be prone to develop thymic lymphomas (TLs) after small doses of ionizing radiation. Little is known, however, on the role of <em>scid</em> mutation in chemical carcinogenesis. To determine if <em>scid</em> mutation increased predisposition to chemical carcinogenesis, we examined both the susceptibility of <em>scid</em> mice to <em>N</em>-ethyl-<em>N</em>-nitrosourea (ENU)-induced lymphomagenesis and the involvement of <em>ras</em><span> gene activation. Adult female mice at 8 weeks of age were given ENU in their drinking water at 400</span> <!-->ppm for 2–10 weeks. Contrary to expectations, we observed a two to three-fold reduction in TL development in the <em>scid</em> mice. The highest incidence was achieved by ENU treatment for 8 weeks for <em>scid</em> and wild-type C.B-17 mice, of 42 and 85%, respectively (<em>P</em>&lt;0.05). We investigated whether this was attributable to the usage of the <em>ras</em> mutation pathway. There was, however, no significant difference in the frequency and spectrum of K-<em>ras</em> mutation between the <em>scid</em> and wild-type C.B-17 mice. Most of the K-<em>ras</em><span> mutations were either GGT to GAT transition in codon 12 (11/23: 48%) or CAA to CCA transversion in codon 61 (8/23: 35%) that was independent of </span><em>scid</em> background. The incidence of N-<em>ras</em> mutation was very low. These results indicate that <em>scid</em> mice are less susceptible to ENU-induced lymphomagenesis and <em>ras</em><span> gene mutation frequently occurs in both </span><em>scid</em> and wild-type C.B-17 mice.</p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 4","pages":"Pages 275-283"},"PeriodicalIF":0.0,"publicationDate":"2001-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00098-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Repair of DNA interstrand cross-links DNA链间交联的修复
Mutation Research/DNA Repair Pub Date : 2001-09-04 DOI: 10.1016/S0921-8777(01)00092-1
Mies L.G Dronkert , Roland Kanaar
{"title":"Repair of DNA interstrand cross-links","authors":"Mies L.G Dronkert ,&nbsp;Roland Kanaar","doi":"10.1016/S0921-8777(01)00092-1","DOIUrl":"10.1016/S0921-8777(01)00092-1","url":null,"abstract":"<div><p><span>DNA interstrand cross-links (ICLs) are very toxic to dividing cells, because they induce mutations, chromosomal rearrangements and cell death. Inducers of ICLs are important drugs in cancer treatment. We discuss the main properties of several classes of ICL agents and the types of damage they induce. The current insights in ICL repair in bacteria, yeast and </span>mammalian cells<span><span><span> are reviewed. An intriguing aspect of ICLs is that a number of multi-step DNA repair pathways including nucleotide excision repair, </span>homologous recombination and post-replication/translesion repair all impinge on their repair. Furthermore, the breast cancer-associated proteins Brca1 and Brca2, the Fanconi anemia-associated FANC proteins, and </span>cell cycle checkpoint proteins are involved in regulating the cellular response to ICLs. We depict several models that describe possible pathways for the repair or replicational bypass of ICLs.</span></p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 4","pages":"Pages 217-247"},"PeriodicalIF":0.0,"publicationDate":"2001-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00092-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 552
DNA postreplication repair and mutagenesis in Saccharomyces cerevisiae 酿酒酵母DNA复制后修复与诱变
Mutation Research/DNA Repair Pub Date : 2001-08-09 DOI: 10.1016/S0921-8777(01)00091-X
Stacey Broomfield, Todd Hryciw, Wei Xiao
{"title":"DNA postreplication repair and mutagenesis in Saccharomyces cerevisiae","authors":"Stacey Broomfield,&nbsp;Todd Hryciw,&nbsp;Wei Xiao","doi":"10.1016/S0921-8777(01)00091-X","DOIUrl":"10.1016/S0921-8777(01)00091-X","url":null,"abstract":"<div><p><span>DNA postreplication repair (PRR) is defined as an activity to convert DNA damage-induced single-stranded gaps into large molecular weight DNA without actually removing the replication-blocking lesions. In bacteria such as </span><em>Escherichia coli</em><span><span>, this activity requires RecA and the RecA-mediated SOS response and is accomplished by recombination and mutagenic translesion DNA synthesis. Eukaryotic cells appear to share similar DNA damage tolerance pathways; however, some enzymes required for PRR in eukaryotes are rather different from those of </span>prokaryotes. In the yeast </span><span><em>Saccharomyces</em><em> cerevisiae</em></span>, PRR is centrally controlled by <em>RAD6</em> and <em>RAD18</em><span><span>, whose products form a stable complex with single-stranded DNA-binding, ATPase and ubiquitin-conjugating activities. PRR can be further divided into translesion DNA synthesis and error-free modes, the exact molecular events of which are largely unknown. This error-free PRR is analogous to DNA damage-avoidance as defined in </span>mammalian cells, which relies on recombination processes. Two possible mechanisms by which recombination participate in PRR to resolve the stalled replication folk are discussed. Recombination and PRR are also genetically regulated by a DNA helicase and are coupled to the cell-cycle. The PRR processes appear to be highly conserved within eukaryotes, from yeast to human.</span></p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 3","pages":"Pages 167-184"},"PeriodicalIF":0.0,"publicationDate":"2001-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00091-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 254
DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326 人淋巴细胞中8-氧鸟嘌呤DNA糖基酶1 (OGG1)的DNA修复活性不依赖于基因多态性Ser326/Cys326
Mutation Research/DNA Repair Pub Date : 2001-08-09 DOI: 10.1016/S0921-8777(01)00096-9
Kai Janssen , Kirsten Schlink , Walter Götte , Birgit Hippler , Bernd Kaina , Franz Oesch
{"title":"DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326","authors":"Kai Janssen ,&nbsp;Kirsten Schlink ,&nbsp;Walter Götte ,&nbsp;Birgit Hippler ,&nbsp;Bernd Kaina ,&nbsp;Franz Oesch","doi":"10.1016/S0921-8777(01)00096-9","DOIUrl":"10.1016/S0921-8777(01)00096-9","url":null,"abstract":"<div><p><span><span><span>8-Oxoguanine DNA glycosylase 1 (OGG1) is a </span>DNA repair enzyme that excises 7,8-dihydro-8-oxoguanine (8oxoG) from DNA. Since 8oxoG is a highly mispairing lesion, decreased OGG1 expression level could lead to a higher background </span>mutation frequency<span> and could possibly increase the cancer risk of an individual under oxidative stress<span>. In order to analyse the natural variation of OGG1, we measured the DNA repair activity in human lymphocytes of healthy individuals by means of an 8oxoG-containing oligonucleotide assay. The data obtained revealed a two fold interindividual variation of OGG1 activity in lymphocytes. There was no difference in OGG1 activity due to gender and smoking behaviour. Transcriptional analyses of OGG1 showed the expression of two isoforms, 1a and b, in lymphocytes. Structural analysis of the human OGG1 (hOGG1) gene revealed a Ser</span></span></span><sup>326</sup>/Cys<sup>326</sup> polymorphism in the Caucasian population with allele frequencies of 75% for Ser<sup>326</sup> and 25% for Cys<sup>326</sup>. This polymorphism was not associated with altered OGG1 activity. The described routine test system for measuring OGG1 activity in cryopreserved lymphocytes provided highly reproducible results and is a useful tool for risk assessment associated with alterations in the repair of oxidative DNA damage.</p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 3","pages":"Pages 207-216"},"PeriodicalIF":0.0,"publicationDate":"2001-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00096-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 128
Interaction of the yeast Pso5/Rad16 and Sgs1 proteins: influences on DNA repair and aging 酵母Pso5/Rad16和Sgs1蛋白的相互作用:对DNA修复和衰老的影响
Mutation Research/DNA Repair Pub Date : 2001-08-09 DOI: 10.1016/S0921-8777(01)00093-3
Jenifer Saffi , Heidi Feldmann , Ernst-Ludwig Winnacker , João A.P. Henriques
{"title":"Interaction of the yeast Pso5/Rad16 and Sgs1 proteins: influences on DNA repair and aging","authors":"Jenifer Saffi ,&nbsp;Heidi Feldmann ,&nbsp;Ernst-Ludwig Winnacker ,&nbsp;João A.P. Henriques","doi":"10.1016/S0921-8777(01)00093-3","DOIUrl":"10.1016/S0921-8777(01)00093-3","url":null,"abstract":"<div><p>The interaction trap method was used to isolate putative binding partners of Rad16/Pso5, a protein responsible for repair of silent DNA. One of the interactors found was Sgs1, a DNA helicase influencing the life span of <span><em>Saccharomyces cerevisiae</em></span><span>, with homology<span> to the human BLM, WRN and RECQL4<span> proteins. Using the same fusion proteins from the two-hybrid screening, we show evidence that both proteins also interact in vitro. We tested isogenic strains, containing mutant alleles of the two genes in single and double mutant combination, for phenotypic similarity. Life span in </span></span></span><em>sgs1</em>Δ single and <em>sgs1</em>Δ <em>rad16</em>Δ double mutants is about 40% of that of <em>WT</em>, and the <em>rad16</em>/<em>pso5</em><span>Δ single mutant also had its life span reduced to 75%. Sensitivity to different mutagens, whose lesions are poorly repaired in </span><em>rad16</em>/<em>pso5</em>Δ mutants, was tested in <em>sgs1</em>Δ mutants. The <em>sgs1</em><span>Δ conferred sensitivity to MMS, H</span><sub>2</sub>O<sub>2</sub> and was moderately sensitive to UV<sub>254<!--> <!-->nm</sub> (UVC) and 4-NQO. An epistatic interaction between <em>rad16</em> and <em>sgs1</em> mutations after UVC, 4-NQO and H<sub>2</sub>O<sub>2</sub> was observed. Moreover, we found that in a <em>top3</em> background, functional Sgs1p and Rad16p apparently channel MMS, 4-NQO and H<sub>2</sub>O<sub>2</sub><span><span> induced lesions into aberrant DNA repair. Our results demonstrate that Sgs1 is not only involved in genome stability, </span>somatic recombination and aging, but is also implicated, together with Rad16/Pso5, in the repair of specific DNA damage.</span></p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 3","pages":"Pages 195-206"},"PeriodicalIF":0.0,"publicationDate":"2001-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00093-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56180071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 31
Direct transfer of Ku between DNA molecules with nonhomologous ends 具有非同源末端的DNA分子间Ku的直接转移
Mutation Research/DNA Repair Pub Date : 2001-08-09 DOI: 10.1016/S0921-8777(01)00080-5
Chin-Feng Chiu, Tzu-Yang Lin, Wen-Gang Chou
{"title":"Direct transfer of Ku between DNA molecules with nonhomologous ends","authors":"Chin-Feng Chiu,&nbsp;Tzu-Yang Lin,&nbsp;Wen-Gang Chou","doi":"10.1016/S0921-8777(01)00080-5","DOIUrl":"10.1016/S0921-8777(01)00080-5","url":null,"abstract":"<div><p><span>The Ku protein is an essential protein for DNA double-strand-break repair by the pathway of nonhomologous DNA end-joining (NHEJ). A previous study showed that Ku bound to one DNA molecule could transfer directly to another DNA molecule without being released into the solution first. Direct transfer requires the two DNA molecules having homologous cohesive ends with a minimum of four complementary bases. Results of this study reveal that direct transfer activity of Ku is regulated by NaCl and MgCl</span><sub>2</sub>. Increasing either one of the two cations can decrease the required amount of the other. However, the DNA end-binding activity of Ku is not affected by changing the concentration of the cations, indicating that the two activities are regulated independently. Most importantly, the results also show that Ku can transfer directly from one DNA molecule to another one with nonhomologous ends under the condition of 200<!--> <!-->mM NaCl and 5<!--> <!-->mM MgCl<sub>2</sub>. The ability of direct transfer between DNAs with nonhomologous ends suggests that Ku can align or juxtapose two DNA ends during NHEJ.</p></div>","PeriodicalId":100935,"journal":{"name":"Mutation Research/DNA Repair","volume":"486 3","pages":"Pages 185-194"},"PeriodicalIF":0.0,"publicationDate":"2001-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0921-8777(01)00080-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56179903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
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