DNA损伤诱导的ATM激活及ATM依赖的信号通路。

DNA damage-induced activation of ATM and ATM-dependent signaling pathways.

作者信息

Kurz Ebba U, Lees-Miller Susan P

机构信息

Cancer Biology Research Group, Department of Biochemistry and Molecular Biology, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, Canada.

出版信息

DNA Repair (Amst). 2004 Aug-Sep;3(8-9):889-900. doi: 10.1016/j.dnarep.2004.03.029.

DOI:10.1016/j.dnarep.2004.03.029

PMID:15279774

Abstract

Ataxia-telangiectasia mutated (ATM) plays a key role in regulating the cellular response to ionizing radiation. Activation of ATM results in phosphorylation of many downstream targets that modulate numerous damage response pathways, most notably cell cycle checkpoints. In this review, we describe recent developments in our understanding of the mechanism of activation of ATM and its downstream signaling pathways, and explore whether DNA double-strand breaks are the sole activators of ATM and ATM-dependent signaling pathways.

摘要

共济失调毛细血管扩张症突变基因（ATM）在调节细胞对电离辐射的反应中起关键作用。ATM的激活导致许多下游靶点的磷酸化，这些靶点调节众多损伤反应途径，最显著的是细胞周期检查点。在这篇综述中，我们描述了我们对ATM激活机制及其下游信号通路理解的最新进展，并探讨DNA双链断裂是否是ATM及ATM依赖性信号通路的唯一激活剂。