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Mechanisms and Consequences of Double-Strand DNA Break Formation in Chromatin

机译:机制和双链DNA的后果打破形成染色质

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All organisms suffer double-strand breaks (DSBs) in their DNA as a result of exposure to ionizing radiation. DSBs can also form when replication forks encounter DNA lesions or repair intermediates. The processing and repair of DSBs can lead to mutations, loss of heterozygosity, and chromosome rearrangements that result in cell death or cancer. The most common pathway used to repair DSBs in metazoans (non-homologous DNA end joining) is more commonly mutagenic than the alternative pathway (homologous recombination mediated repair). Thus, factors that influence the choice of pathways used DSB repair can affect an individual's mutation burden and risk of cancer. This review describes radiological, chemical, and biological mechanisms that generate DSBs, and discusses the impact of such variables as DSB etiology, cell type, cell cycle, and chromatin structure on the yield, distribution, and processing of DSBs. The final section focuses on nucleosome-specific mechanisms that influence DSB production, and the possible relationship between higher order chromosome coiling and chromosome shattering (chromothripsis). J. Cell. Physiol. 230: 3-14, 2016. (c) 2015 Wiley Periodicals, Inc.
机译:所有生物遭受双链断裂(双边带)在他们的DNA由于暴露于电离辐射。叉遇到DNA损伤或修复中间体。会导致突变,杂合性丢失,和导致细胞染色体重排死亡或癌症。DNA修复双边带在后生动物(异源加入)是更常用的诱变替代途径(同源重组介导的修复)。双边带维修会影响使用的选择途径一个人的变异的负担和风险癌症。化学和生物机制产生双边带,并讨论了这些变量的影响双边带病因,细胞,细胞周期,染色质结构的产生、分布、和双边带的处理。在nucleosome-specific机制的影响双边带生产,和可能的关系高阶染色体螺旋和之间染色体粉碎(chromothripsis)。杂志。230:3 - 14,2016年。期刊、公司。

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