Base Excision Repair, a Pathway Regulated by Posttranslational Modifications

被引:110
作者
Carter, Rachel J. [1 ]
Parsons, Jason L. [1 ]
机构
[1] Univ Liverpool, Dept Mol & Clin Canc Med, North West Canc Res Ctr, Liverpool L69 3BX, Merseyside, England
基金
英国医学研究理事会;
关键词
THYMINE-DNA GLYCOSYLASE; HUMAN AP-ENDONUCLEASE; E3 UBIQUITIN LIGASE; DEPENDENT PROTEIN-KINASE; CRITICAL LYSINE RESIDUES; CELL NUCLEAR ANTIGEN; POLYMERASE-BETA; POLY(ADP-RIBOSE) POLYMERASE-1; POLYNUCLEOTIDE KINASE/PHOSPHATASE; MEDIATED DEGRADATION;
D O I
10.1128/MCB.00030-16
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1426 / 1437
页数:12
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