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本文引用的文献

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And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.然而,它在移动:异染色质双链断裂的核与染色质动力学。
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0291.
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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.
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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。
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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
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SCAI promotes DNA double-strand break repair in distinct chromosomal contexts.SCAI在不同的染色体环境中促进DNA双链断裂修复。
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NAD Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair.烟酰胺腺嘌呤二核苷酸(NAD)补充通过线粒体自噬和DNA修复改善共济失调毛细血管扩张症模型的寿命和健康寿命。
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依赖 ATM 的染色质重塑途径及氧化性 DNA 损伤反应

ATM-dependent pathways of chromatin remodelling and oxidative DNA damage responses.

作者信息

Berger N Daniel, Stanley Fintan K T, Moore Shaun, Goodarzi Aaron A

机构信息

Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Departments of Biochemistry & Molecular Biology and Oncology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.

Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Departments of Biochemistry & Molecular Biology and Oncology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1

出版信息

Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0283.

DOI:10.1098/rstb.2016.0283
PMID:28847820
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5577461/
Abstract

Ataxia-telangiectasia mutated (ATM) is a serine/threonine protein kinase with a master regulatory function in the DNA damage response. In this role, ATM commands a complex biochemical network that signals the presence of oxidative DNA damage, including the dangerous DNA double-strand break, and facilitates subsequent repair. Here, we review the current state of knowledge regarding ATM-dependent chromatin remodelling and epigenomic alterations that are required to maintain genomic integrity in the presence of DNA double-strand breaks and/or oxidative stress. We will focus particularly on the roles of ATM in adjusting nucleosome spacing at sites of unresolved DNA double-strand breaks within complex chromatin environments, and the impact of ATM on preserving the health of cells within the mammalian central nervous system.This article is part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and signalling'.

摘要

共济失调毛细血管扩张症突变基因(ATM)是一种丝氨酸/苏氨酸蛋白激酶,在DNA损伤反应中具有主要调节功能。在此过程中,ATM指挥一个复杂的生化网络,该网络能指示氧化性DNA损伤(包括危险的DNA双链断裂)的存在,并促进后续修复。在这里,我们综述了当前关于依赖ATM的染色质重塑和表观基因组改变的知识状态,这些改变是在存在DNA双链断裂和/或氧化应激的情况下维持基因组完整性所必需的。我们将特别关注ATM在复杂染色质环境中未解决的DNA双链断裂位点调节核小体间距的作用,以及ATM对维持哺乳动物中枢神经系统内细胞健康的影响。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。