Mechanisms of double-strand break repair in somatic mammalian cells.
Mechanisms of double-strand break repair in somatic mammalian cells.
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DOI：
10.1042/bj20090942
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发表时间：
2009-09-25
期刊：
影响因子：
--
通讯作者：
Scully R
中科院分区：
文献类型：
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作者：
Hartlerode AJ;Scully R
DNA染色体双链断裂（DSB）是具有潜在危害的DNA损伤，其准确修复对于遗传信息的成功维持和传播至关重要。已经进化出两种主要途径来修复DSB：HR（同源重组）和NHEJ（非同源末端连接）。根据断裂发生的背景，HR和NHEJ可以竞争或合作以固定真核细胞中的DSB。任何一种途径的缺陷都与人类疾病密切相关，包括免疫缺陷和癌症易感性。在这里，我们回顾了目前的知识，如何NHEJ和HR控制在体细胞哺乳动物细胞，并讨论了染色质的背景下，在调节每个途径的作用。我们还审查了两个途径之间的合作和竞争的证据。
DNA chromosomal DSBs (double-strand breaks) are potentially hazardous DNA lesions, and their accurate repair is essential for the successful maintenance and propagation of genetic information. Two major pathways have evolved to repair DSBs: HR (homologous recombination) and NHEJ (non-homologous end-joining). Depending on the context in which the break is encountered, HR and NHEJ may either compete or co-operate to fix DSBs in eukaryotic cells. Defects in either pathway are strongly associated with human disease, including immunodeficiency and cancer predisposition. Here we review the current knowledge of how NHEJ and HR are controlled in somatic mammalian cells, and discuss the role of the chromatin context in regulating each pathway. We also review evidence for both co-operation and competition between the two pathways.