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本文引用的文献

1
Bromodomain proteins: repairing DNA damage within chromatin.溴结构域蛋白:修复染色质内的DNA损伤。
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0286.
2
DNA repair goes hip-hop: SMARCA and CHD chromatin remodellers join the break dance.DNA修复跳起嘻哈舞:SMARCA和CHD染色质重塑因子加入霹雳舞行列。
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0285.
3
The tale of a tail: histone H4 acetylation and the repair of DNA breaks.尾巴的故事:组蛋白H4乙酰化与DNA断裂修复
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0284.
4
SUMO, a small, but powerful, regulator of double-strand break repair.SUMO,一种双链断裂修复的小型但强大的调节因子。
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0281.
5
Mechanisms of Ubiquitin-Nucleosome Recognition and Regulation of 53BP1 Chromatin Recruitment by RNF168/169 and RAD18.泛素-核小体识别机制以及RNF168/169和RAD18对53BP1染色质募集的调控
Mol Cell. 2017 May 18;66(4):473-487.e9. doi: 10.1016/j.molcel.2017.04.009. Epub 2017 May 11.
6
The RNF168 paralog RNF169 defines a new class of ubiquitylated histone reader involved in the response to DNA damage.RNF168旁系同源蛋白RNF169定义了一类新的参与DNA损伤应答的泛素化组蛋白阅读器。
Elife. 2017 Apr 13;6:e23872. doi: 10.7554/eLife.23872.
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ZMYM3 regulates BRCA1 localization at damaged chromatin to promote DNA repair.ZMYM3调节BRCA1在受损染色质上的定位以促进DNA修复。
Genes Dev. 2017 Feb 1;31(3):260-274. doi: 10.1101/gad.292516.116. Epub 2017 Feb 27.
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TIRR regulates 53BP1 by masking its histone methyl-lysine binding function.TIRR通过掩盖其组蛋白甲基赖氨酸结合功能来调节53BP1。
Nature. 2017 Mar 9;543(7644):211-216. doi: 10.1038/nature21358. Epub 2017 Feb 27.
9
The p53-binding protein 1-Tudor-interacting repair regulator complex participates in the DNA damage response.p53结合蛋白1-都铎相互作用修复调节复合物参与DNA损伤反应。
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DNA双链断裂后读取染色质特征。

Reading chromatin signatures after DNA double-strand breaks.

作者信息

Wilson Marcus D, Durocher Daniel

机构信息

Macromolecular Machines Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK

The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario, Canada M5G 1X5.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0280.

DOI:10.1098/rstb.2016.0280
PMID:28847817
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5577458/
Abstract

DNA double-strand breaks (DSBs) are DNA lesions that must be accurately repaired in order to preserve genomic integrity and cellular viability. The response to DSBs reshapes the local chromatin environment and is largely orchestrated by the deposition, removal and detection of a complex set of chromatin-associated post-translational modifications. In particular, the nucleosome acts as a central signalling hub and landing platform in this process by organizing the recruitment of repair and signalling factors, while at the same time coordinating repair with other DNA-based cellular processes. While current research has provided a descriptive overview of which histone marks affect DSB repair, we are only beginning to understand how these marks are interpreted to foster an efficient DSB response. Here we review how the modified chromatin surrounding DSBs is read, with a focus on the insights gleaned from structural and biochemical studies.This article is part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and signalling'.

摘要

DNA双链断裂(DSBs)是一种DNA损伤,为了保持基因组完整性和细胞活力,必须对其进行精确修复。对DSBs的反应重塑了局部染色质环境,并且在很大程度上是由一组复杂的与染色质相关的翻译后修饰的沉积、去除和检测来精心安排的。特别是,核小体在这个过程中作为一个核心信号枢纽和着陆平台,通过组织修复和信号因子的募集,同时协调修复与其他基于DNA的细胞过程。虽然目前的研究已经对哪些组蛋白标记影响DSB修复进行了描述性概述,但我们才刚刚开始了解这些标记是如何被解读以促进有效的DSB反应的。在这里,我们回顾了围绕DSBs的修饰染色质是如何被识别的,重点是从结构和生化研究中获得的见解。本文是主题为“DNA修复和信号传导中的染色质修饰剂和重塑剂”的特刊的一部分。