Complex interactions between the DNA-damage response and mammalian telomeres.
Complex interactions between the DNA-damage response and mammalian telomeres.
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DOI：
10.1038/nsmb.3092
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发表时间：
2015-11
影响因子：
16.8
通讯作者：
Karlseder J
中科院分区：
文献类型：
--
作者：
Arnoult N;Karlseder J
天然的染色体末端类似于双链DNA断裂，但它们不会在健康细胞中激活损伤反应。因此，端粒已经进化到通过抑制多种DNA损伤反应途径来解决“末端保护问题”。在过去的十年里，人们对端粒的看法已经从隐藏染色体末端的简单帽状物发展到在组织基因组中发挥积极作用的复杂机制。在这里，我们将重点关注哺乳动物端粒，并详细总结和解释最近的发现，重点关注修复途径如何被抑制，切除和复制如何被控制，以及这些机制如何在衰老，危机和转化过程中控制细胞命运。
Natural chromosome ends resemble double-stranded DNA breaks, but they do not activate a damage response in healthy cells. Telomeres therefore have evolved to solve the ‘end-protection problem’ by inhibiting multiple DNA damage–response pathways. During the past decade, the view of telomeres has progressed from simple caps that hide chromosome ends to complex machineries that have an active role in organizing the genome. Here we focus on mammalian telomeres and summarize and interpret recent discoveries in detail, focusing on how repair pathways are inhibited, how resection and replication are controlled and how these mechanisms govern cell fate during senescence, crisis and transformation.