期刊
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
卷 372, 期 1731, 页码 -出版社
ROYAL SOC
DOI: 10.1098/rstb.2016.0283
关键词
ataxia-telangiectasia mutated; DNA damage; chromatin; brain; neurodegeneration; oxidative stress
类别
资金
- Vanier Canada Graduate Scholarship
- Alberta Innovates Health Solutions
- Izaak Walton Killam Graduate Scholarship
- Achievers in Medical Sciences award
- Canada Research Chairs programme
- Canadian Institutes of Health Research
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'.
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