Base Excision Repair, a Pathway Regulated by Posttranslational Modifications
Author(s) -
Rachel Carter,
Jason L. Parsons
Publication year - 2016
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.00030-16
Subject(s) - sumo protein , biology , base excision repair , dna repair , acetylation , dna damage , microbiology and biotechnology , ubiquitin , ddb1 , posttranslational modification , phosphorylation , genetics , dna , biochemistry , enzyme , gene , ubiquitin ligase
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 BERin vitro andin vivo .
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