William C. Earnshaw

Jacqueline J.L. Jacobs

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William C. Earnshaw

机译：威廉·C·恩肖

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DNA repair activities at DNA double-strand breaks (DSBs) are under control of regulatory ubiquitylation events governed by the RNF8 and RNF168 ubiquitin-ligases. Defects in this regulatory mechanism, as with mutation of other key DNA damage-response factors, lead to genomic instability and cancer, presumably due to impaired repair of DNA lesions. Recent work revealed that RNF8 and RNF168 also play critical roles at natural chromosome ends, when no longer adequately shielded by telomeres. In contrast to repair of DSBs being needed to maintain genome integrity, repair activities at telomeres create chromosome end-to-end fusions that threaten genome integrity. Upon cell division these telomere fusions give rise to genomic alterations and instability via chromosomal missegregration and initiation of breakage-fusion-bridge cycles. Here, I discuss the role of RNF8 at natural chromosome ends and its (potential) consequences.

机译：DNA双链断裂（DSB）处的DNA修复活性受RNF8和RNF168泛素连接酶控制的调控泛素化事件的控制。与其他关键DNA损伤反应因子的突变一样，这种调节机制的缺陷会导致基因组不稳定和癌症，这可能是由于DNA损伤的修复受损所致。最近的工作表明，当不再被端粒充分屏蔽时，RNF8和RNF168在天然染色体末端也起着关键作用。与维持基因组完整性所需的DSB修复相反，端粒的修复活动产生了威胁基因组完整性的染色体端对端融合。在细胞分裂后，这些端粒融合物通过染色体错配和启动断裂-融合桥循环而引起基因组改变和不稳定性。在这里，我讨论了RNF8在天然染色体末端的作用及其（潜在）后果。

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《Nucleus》 |2012年第2期|共7页
作者
Jacqueline J.L. Jacobs;
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正文语种 eng
中图分类细胞生物学;
关键词
DNA damage; RNF8; genomic instability; telomeres; ubiquitin;

机译：DNA损伤;RNF8;基因组不稳定性;端粒;泛素;

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机译：威廉·C·恩肖
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William C. Earnshaw

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