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PMID: 19948475 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

The ubiquitin landscape at DNA double-strand breaks.

The Journal of cell biology ·Vol. 187 ·No. 3 ·2009-11-02 ·Pages 319-26

Messick TE, Greenberg RA

Abstract

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.

MeSH Terms
Binding Sites DNA Breaks, Double-Stranded DNA Repair/physiology Genomic Instability Models, Molecular Phosphatidylinositol 3-Kinases/physiology Signal Transduction Ubiquitin/chemistry,metabolism Ubiquitination
Chemicals
Ubiquitin Phosphatidylinositol 3-Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Messick Troy E
Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Greenberg Roger A
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Article Info
Journal
The Journal of cell biology
Abbr.
J Cell Biol
ISSN
1540-8140
Published
2009-11-02
Pages
319-26
Language
English
Region
United States
NLM ID
0375356
PMCID
PMC2779242
Subset
IM
Grants
NCI NIH HHS · K08 CA106597 · United States
NCI NIH HHS · 1K08CA106597-01 · United States
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