G2-M DNA损伤检查点
DNA损伤
DNA修复
支票1
细胞周期检查点
生物
细胞生物学
DNA
基因组不稳定性
检查点激酶2
核苷酸切除修复
细胞周期
遗传学
细胞
作者
Daniël O. Warmerdam,Roland Kanaar
标识
DOI:10.1016/j.mrrev.2009.12.001
摘要
Cell cycle checkpoint activation and DNA repair pathways govern genomic stability after genotoxic stress. Genotoxic insult results in activation of an interwoven network of DNA damage checkpoints and DNA repair pathways. Post-translational modifications on a number of proteins involved in both checkpoint activation and DNA repair play an important role in this cellular response. Genotoxic stress can induce a wide variety of DNA lesions. Among these DNA alterations are double-stranded breaks and single-stranded DNA gaps. Repair of these DNA alterations requires damage recognition and resection. Here we discuss how DNA repair and DNA damage checkpoints cooperate and deal with DNA damage. Processing of DNA lesions by structure-specific nucleases results in DNA–protein intermediates, which form the basis for checkpoint activation and DNA repair. Post-translational modifications like phosphorylation and ubiquitination modulate the DNA damage response in a spatial and temporal manner. Cell cycle-dependent regulation additionally plays a key role in the regulation of both DNA repair and checkpoint activation. We highlight recent advances in in vivo imaging that greatly expand our knowledge on the relationships between DNA damage checkpoints and DNA repair.
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