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’.
ATM-dependent pathways of chromatin remodelling and oxidative DNA damage responses
N. Berger,Fintan Stanley,S. Moore,A. Goodarzi
Published 2017 in Philosophical Transactions of the Royal Society B: Biological Sciences
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
Philosophical Transactions of the Royal Society B: Biological Sciences
- Publication date
2017-10-05
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
- No claims are published for this paper.
CONCEPTS
- No concepts are published for this paper.
REFERENCES
CITED BY
Showing 1-53 of 53 citing papers · Page 1 of 1