期刊
NUCLEIC ACIDS RESEARCH
卷 41, 期 6, 页码 3483-3490出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkt076
关键词
-
资金
- Swiss National Science Foundation
- Oncosuisse
- UBS 'im Auftrag eines Kunden'
- University of Zurich
- Medical Research Council
- Cancer Research UK
- Royal Society
- MRC [MC_PC_12002, MC_U142762994] Funding Source: UKRI
- Medical Research Council [MC_U142762994, MC_PC_12002] Funding Source: researchfish
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据