ATM signaling and 53BP1
ATM signaling and 53BP1
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DOI：
10.1016/j.radonc.2005.06.026
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发表时间：
2005-08-01
影响因子：
5.7
通讯作者：
Halazonetis, TD
中科院分区：
文献类型：
--
作者：
Zgheib, O;Huyen, Y;Halazonetis, TD
ATM（mutated in Ataxia-Telangiectasia）蛋白激酶是高等真核生物中DNA双链断裂（DSB）信号的重要参与者。最近的研究表明，ATM监测DNA双链断裂的存在间接，通过DNA双链断裂诱导的染色质结构的变化。53 BP 1是检测这些染色质结构变化的蛋白质之一，它是一种在所有真核生物中保守的DNA损伤检查点蛋白，也是S.酿酒酵母RAD 9蛋白。我们在这里审查的机制，ATM被激活响应DNA双链断裂，以及关键ATM基板控制细胞周期进程，凋亡和DNA修复。(C)2005 Elsevier爱尔兰有限公司
The ATM (mutated in Ataxia-Telangiectasia) protein kinase is an important player in signaling the presence of DNA double strand breaks (DSBs) in higher eukaryotes. Recent studies suggest that ATM monitors the presence of DNA DSBs indirectly, through DNA DSB-induced changes in chromatin structure. One of the proteins that sense these chromatin structure changes is 53BP1, a DNA damage checkpoint protein conserved in all eukaryotes and the putative ortholog of the S. cerevisiae RAD9 protein. We review here the mechanisms by which ATM is activated in response to DNA DSBs, as well as key ATM substrates that control cell cycle progression, apoptosis and DNA repair. (C) 2005 Elsevier Ireland Ltd.