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The ubiquitin landscape at DNA double-strand breaks
Correspondence to Roger A. Greenberg: rogergr{at}mail.med.upenn.edu
The intimate relationship between DNA double-strand break (DSB) repair and cancer susceptibility has sparked profound interest in how transactions on DNA and chromatin surrounding DNA damage influence genome integrity. Recent evidence implicates a substantial commitment of the cellular DNA damage response machinery to the synthesis, recognition, and hydrolysis of ubiquitin chains at DNA damage sites. In this review, we propose that, in order to accommodate parallel processes involved in DSB repair and checkpoint signaling, DSB-associated ubiquitin structures must be nonuniform, using different linkages for distinct functional outputs. We highlight recent advances in the study of nondegradative ubiquitin signaling at DSBs, and discuss how recognition of different ubiquitin structures may influence DNA damage responses.
Abbreviations used in this paper: ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3 related; CtIP, CtBP-interacting protein; DSB, double-strand break; DUB, deubiquitinating enzyme; IRIF, ionizing radiation–induced foci; MIU, motif interacting with ubiquitin; PIKK, phosphatidylinositol-3-kinase-related kinase; UIM, ubiquitin interaction motif.
© 2009 Messick and Greenberg
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
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