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PMID: 24002223 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Push back to respond better: regulatory inhibition of the DNA double-strand break response.

Nature reviews. Molecular cell biology ·Vol. 14 ·No. 10 ·2013-10-00 ·Pages 661-72

Panier S, Durocher D

Abstract

Single DNA lesions such as DNA double-strand breaks (DSBs) can cause cell death or trigger genome rearrangements that have oncogenic potential, and so the pathways that mend and signal DNA damage must be highly sensitive but, at the same time, selective and reversible. When initiated, boundaries must be set to restrict the DSB response to the site of the lesion. The integration of positive and, crucially, negative control points involving post-translational modifications such as phosphorylation, ubiquitylation and acetylation is key for building fast, effective responses to DNA damage and for mitigating the impact of DNA lesions on genome integrity.

MeSH Terms
Acetylation Chromatin/genetics DNA Breaks, Double-Stranded DNA Damage Gene Regulatory Networks Genomic Instability Humans Phosphorylation Signal Transduction Ubiquitination
Chemicals
Chromatin
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Panier Stephanie
1] The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada. [2] Present address: DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, London EN6 3LD, UK.
Durocher Daniel
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Article Info
Journal
Nature reviews. Molecular cell biology
Abbr.
Nat Rev Mol Cell Biol
ISSN
1471-0080
Published
2013-10-00
Epub
2013-00-04
Pages
661-72
Language
English
Region
England
NLM ID
100962782
Subset
IM
Analysis Services
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