Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers

Petra Schwertman; Simon Bekker-Jensen; Niels Mailand

doi:10.1038/nrm.2016.58

Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers

Petra Schwertman, Simon Bekker-Jensen, Niels Mailand

167 Citationer (Scopus)

Abstract

DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition and faithful repair of such damage is crucial for the maintenance of genomic stability, as well as for cell and organismal fitness. Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs) orchestrates and regulates cellular responses to DSBs at multiple levels, often involving extensive crosstalk between these modifications. Recent findings have revealed compelling insights into the complex mechanisms by which ubiquitin and UBLs regulate protein interactions with DSB sites to promote accurate lesion repair and protection of genome integrity in mammalian cells. These advances offer new therapeutic opportunities for diseases linked to genetic instability.

Originalsprog	Engelsk
Tidsskrift	Nature Reviews. Molecular Cell Biology
Vol/bind	17
Udgave nummer	6
Sider (fra-til)	379-94
Antal sider	16
ISSN	1471-0072
DOI	https://doi.org/10.1038/nrm.2016.58
Status	Udgivet - 1 jun. 2016

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10.1038/nrm.2016.58

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Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers

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