Lee J-H, Paull T T
Department of Molecular Genetics and Microbiology, Institute of Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Oncogene. 2007 Dec 10;26(56):7741-8. doi: 10.1038/sj.onc.1210872.
The ataxia-telangiectasia-mutated (ATM) protein kinase is rapidly and specifically activated in response to DNA double-strand breaks in eukaryotic cells. In this review, we summarize recent insights into the mechanism of ATM activation, focusing on the role of the Mre11/Rad50/Nbs1 (MRN) complex in this process. We also compare observations of the ATM activation process in different biological systems and highlight potential candidates for cellular factors that may participate in regulating ATM activity in human cells.
共济失调毛细血管扩张症突变（ATM）蛋白激酶在真核细胞中响应DNA双链断裂时会迅速且特异性地被激活。在本综述中，我们总结了关于ATM激活机制的最新见解，重点关注Mre11/Rad50/Nbs1（MRN）复合物在此过程中的作用。我们还比较了不同生物系统中ATM激活过程的观察结果，并强调了可能参与调节人类细胞中ATM活性的细胞因子的潜在候选者。
