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Ubiquitylation, neddylation and the DNA damage response.


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Authors

Brown, Jessica S 
Jackson, Stephen P 

Abstract

Failure of accurate DNA damage sensing and repair mechanisms manifests as a variety of human diseases, including neurodegenerative disorders, immunodeficiency, infertility and cancer. The accuracy and efficiency of DNA damage detection and repair, collectively termed the DNA damage response (DDR), requires the recruitment and subsequent post-translational modification (PTM) of a complex network of proteins. Ubiquitin and the ubiquitin-like protein (UBL) SUMO have established roles in regulating the cellular response to DNA double-strand breaks (DSBs). A role for other UBLs, such as NEDD8, is also now emerging. This article provides an overview of the DDR, discusses our current understanding of the process and function of PTM by ubiquitin and NEDD8, and reviews the literature surrounding the role of ubiquitylation and neddylation in DNA repair processes, focusing particularly on DNA DSB repair.

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Keywords

DNA damage response, MLN4924, NEDD8, double-strand break repair, ubiquitin, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Humans, Models, Genetic, NEDD8 Protein, Protein Processing, Post-Translational, Ubiquitin-Protein Ligases, Ubiquitination, Ubiquitins

Journal Title

Open Biol

Conference Name

Journal ISSN

2046-2441
2046-2441

Volume Title

5

Publisher

The Royal Society
Sponsorship
Wellcome Trust (094794/Z/10/Z)
Cancer Research Uk (None)
Wellcome Trust (092096/Z/10/Z)
J.S.B. is funded by the Wellcome Trust Clinical Fellowship (grant no. 094794/Z/10/Z). Research in the Jackson laboratory is funded by Cancer Research UK programme grant C6/A11224, the European Research Council and the European Community Seventh Framework Programme grant agreement no. HEALTH-F2-2010-259893 (DDResponse). Core funding is provided by CRUK (C6946/A14492) and the Wellcome Trust (WT092096). S.P.J. receives his salary from the University of Cambridge UK, supplemented by CRUK.