Abstract
Base excision repair (BER) 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 responsible for such variations is 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 BER proteins, including ubiquitylation, has been uncovered. Interestingly, new players in the regulation of BER include proteins encoded by well-known tumour suppressors. This review covers recent progress in our understanding of the post-translational regulation of BER, including the proteins involved, with a specific focus on the role of the ARF (p14) tumour suppressor protein in BER.
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