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Base excision repair (BER) is a frontline repair system that is responsible for maintaining genome integrity and thus preventing premature aging, cancer and many other human diseases by repairing thousands of DNA lesions and strand breaks continuously caused by endogenous and exogenous mutagens. This fundamental and essential function of BER not only necessitates tight control of the continuous availability of basic components for fast and accurate repair, but also requires temporal and spatial coordination of BER and cell cycle progression to prevent replication of damaged DNA. The major goal of this review is to critically examine controversial and newly emerging questions about mammalian BER pathways, mechanisms regulating BER capacity, BER responses to DNA damage and their links to checkpoint control of DNA replication.

Original publication

DOI

10.1093/nar/gkt076

Type

Journal article

Journal

Nucleic Acids Res

Publication Date

01/04/2013

Volume

41

Pages

3483 - 3490

Keywords

Animals, DNA Breaks, Double-Stranded, DNA Breaks, Single-Stranded, DNA Damage, DNA Repair, DNA Replication, Genomic Instability, Humans, Protein Processing, Post-Translational, Signal Transduction