REVIEW: Regulation of DNA Repair by Ubiquitylation

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G. L. Dianov^*, C. Meisenberg, and J. L. Parsons

Gray Institute for Radiation Oncology and Biology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford OX3 7DQ, UK; fax: (44) 186-561-7334; E-mail: grigory.dianov@rob.ox.ac.uk

^* To whom correspondence should be addressed.

Received August 24, 2010; Revision received October 8, 2010

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Cellular DNA repair is a frontline system that is responsible for maintaining genome integrity and thus preventing premature aging and cancer by repairing DNA lesions and strand breaks caused by endogenous and exogenous mutagens. However, it is also the principal cellular system in cancer cells that counteracts the killing effect of the major cancer treatments, e.g. chemotherapy and ionizing radiation. Although it is clear that an individual’s DNA repair capacity varies, the mechanisms involved in the regulation of repair systems that are responsible for such variations are only just emerging. This knowledge gap is impeding the finding of new cancer therapy targets and the development of novel treatment strategies. In recent years the vital role of post-translational modifications of DNA repair proteins, including ubiquitylation and phosphorylation, has been uncovered. This review will cover recent progress in our understanding of the role of ubiquitylation in the regulation of DNA repair.

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KEY WORDS: DNA repair pathways, regulation of DNA repair systems, post-translational protein modification, ubiquitylation

DOI: 10.1134/S0006297911010093

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