NBS1 and multiple regulations of DNA damage response.
NBS1 and multiple regulations of DNA damage response.
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DOI：
10.1093/jrr/rrw031
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发表时间：
2016-08
影响因子：
2
通讯作者：
Komatsu K
中科院分区：
文献类型：
--
作者：
Komatsu K
DNA 损伤反应是经过微调的，有多种途径，包括 DNA 修复、染色质重塑和细胞周期检查点，尽管迄今为止大多数研究都集中在单一途径上。以基因组不稳定为特征的遗传性疾病为 DNA 损伤反应的潜在机制提供了新的见解。 NBS1 是一种导致辐射敏感的常染色体隐性遗传病奈梅亨断裂综合征的蛋白质，是在 DNA 双链断裂 (DSB) 位点首先积累的因子之一。 NBS1 在 C 末端有限范围内的保守区域中与至少 5 个关键蛋白结合，包括 ATM、RPA、MRE11、RAD18 和 RNF20，在响应 DSB 时调节染色质重塑、细胞周期检查点和 DNA 修复。在本文中，我们回顾了这些结合蛋白的功能及其与 NBS1 的综合关联。
DNA damage response is finely tuned, with several pathways including those for DNA repair, chromatin remodeling and cell cycle checkpoint, although most studies to date have focused on single pathways. Genetic diseases characterized by genome instability have provided novel insights into the underlying mechanisms of DNA damage response. NBS1, a protein responsible for the radiation-sensitive autosomal recessive disorder Nijmegen breakage syndrome, is one of the first factors to accumulate at sites of DNA double-strand breaks (DSBs). NBS1 binds to at least five key proteins, including ATM, RPA, MRE11, RAD18 and RNF20, in the conserved regions within a limited span of the C terminus, functioning in the regulation of chromatin remodeling, cell cycle checkpoint and DNA repair in response to DSBs. In this article, we reviewed the functions of these binding proteins and their comprehensive association with NBS1.