Base Excision Repair, a Pathway Regulated by Posttranslational Modifications

Abstract

Base excision repair (BER) is an essential DNA repair pathway involved in the maintenance of genome stability and thus in the prevention of human diseases, such as premature aging, neurodegenerative diseases, and cancer. Protein posttranslational modifications (PTMs), including acetylation, methylation, phosphorylation, SUMOylation, and ubiquitylation, have emerged as important contributors in controlling cellular BER protein levels, enzymatic activities, protein-protein interactions, and protein cellular localization. These PTMs therefore play key roles in regulating the BER pathway and are consequently crucial for coordinating an efficient cellular DNA damage response. In this review, we summarize the presently available data on characterized PTMs of key BER proteins, the functional consequences of these modifications at the protein level, and also the impact on BER in vitro and in vivo.

ACKNOWLEDGMENTS

Jason L. Parsons is supported by funding from North West Cancer Research (CR972, CR1016, and CR1074) and by the Medical Research Council via a New Investigator Research Grant (MR/M000354/1).