Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress

被引:168
|
作者
Yan, Shan [1 ]
Sorrell, Melanie [2 ]
Berman, Zachary [1 ]
机构
[1] Univ N Carolina, Dept Biol Sci, Charlotte, NC 28223 USA
[2] Univ N Carolina, J Murrey Atkins Lib, Charlotte, NC 28223 USA
关键词
AP sites; Base excision repair; Homologous repair; Mismatch repair; Nucleotide excision repair; Oxidative stress-induced DNA damage; Reactive oxygen species; NUCLEOTIDE EXCISION-REPAIR; DOUBLE-STRAND BREAK; HISTONE H2AX PHOSPHORYLATION; HUMAN CHECKPOINT SENSOR; UBIQUITIN E3 LIGASE; CELL-CYCLE ARREST; ATAXIA-TELANGIECTASIA; MISMATCH REPAIR; S-PHASE; MRN COMPLEX;
D O I
10.1007/s00018-014-1666-4
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
To maintain genome stability, cells have evolved various DNA repair pathways to deal with oxidative DNA damage. DNA damage response (DDR) pathways, including ATM-Chk2 and ATR-Chk1 checkpoints, are also activated in oxidative stress to coordinate DNA repair, cell cycle progression, transcription, apoptosis, and senescence. Several studies demonstrate that DDR pathways can regulate DNA repair pathways. On the other hand, accumulating evidence suggests that DNA repair pathways may modulate DDR pathway activation as well. In this review, we summarize our current understanding of how various DNA repair and DDR pathways are activated in response to oxidative DNA damage primarily from studies in eukaryotes. In particular, we analyze the functional interplay between DNA repair and DDR pathways in oxidative stress. A better understanding of cellular response to oxidative stress may provide novel avenues of treating human diseases, such as cancer and neurodegenerative disorders.
引用
收藏
页码:3951 / 3967
页数:17
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