The David and Inez Myers Laboratory for Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
Nat Rev Mol Cell Biol. 2013 Apr;14(4):197-210. doi: 10.1038/nrm3546. Epub 2013 Mar 13.
The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signalling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. Although most ATM research has focused on this function, evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress. Moreover, it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.
蛋白激酶共济失调毛细血管扩张突变(ATM)最为人所知的是其在面对 DNA 双链断裂(DSBs)时作为 DNA 损伤反应的顶端激活剂的作用。在 DSBs 的诱导之后,ATM 调动了对特定刺激做出反应并直接或间接地修饰广泛靶标的最广泛的信号网络之一。尽管大多数 ATM 研究都集中在这个功能上,但有证据表明 ATM 介导的磷酸化在对其他类型的遗传毒性应激的反应中起作用。此外,已经明显的是,ATM 在涉及维持细胞内稳态的其他细胞信号通路中是活跃的。