摘要
Ataxia-telangiectasia mutated(ATM)plays a key role in regulating the cellular response to ionizing radiation.The tumor-suppressor gene ATM,mutations in which cause the human genetic disease ataxia telangiecta-sia,encodes a key protein kinase that controls the cellular response to double-stranded breaks.Activation of ATM results in phosphorylation of many downstream targets that modulate numerous damage response pathways,most notably cell cycle checkpoints.Here,we highlight some of the new developments in thefield in our understanding of the mechanism of activation of ATM and its signaling pathways,explore whether DNA double-strand breaks are the sole activators of ATM and ATM-dependent signaling pathways,and address some of the prominent,unanswered questions related to ATM and its function.The scope of this article is to provide a brief overview of the recent literature on this subject and to raise questions that could be addressed in future studies.
基金
support of the National Natural Science Foundation of China(Grant No.20872095)was gratefully acknowledged.
