Department of Oncology, Gray Institute for Radiation Oncology and Biology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford OX3 7DQ, UK.
Nucleic Acids Res. 2013 Apr 1;41(6):3483-90. doi: 10.1093/nar/gkt076. Epub 2013 Feb 13.
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.
碱基切除修复（BER）是一种前沿的修复系统，负责通过持续修复由内源性和外源性诱变剂引起的数千个 DNA 损伤和链断裂，从而维持基因组的完整性，从而预防过早衰老、癌症和许多其他人类疾病。BER 的这种基本和必要功能不仅需要严格控制基本组件的持续可用性，以实现快速和准确的修复，还需要 BER 与细胞周期进程的时空协调，以防止受损 DNA 的复制。本篇综述的主要目标是批判性地检查有关哺乳动物 BER 途径的有争议和新出现的问题，以及调节 BER 能力的机制、BER 对 DNA 损伤的反应及其与 DNA 复制的检验点控制的联系。
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