Rotman G, Shiloh Y
Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel.
Hum Mol Genet. 1998;7(10):1555-63. doi: 10.1093/hmg/7.10.1555.
The identification of ATM , the gene responsible for the pleiotropic recessive disease ataxia telangiectasia, has initiated extensive research to determine the functions of its multifaceted protein product. The ATM protein belongs to a family of protein kinases that share similarities at their C-terminal region with the catalytic domain of phosphatidylinositol 3-kinases. Studies with ataxia telangiectasia (A-T) cells and Atm-deficient mice have shown that ATM is a key regulator of multiple signaling cascades which respond to DNA strand breaks induced by damaging agents or by normal processes, such as meiotic or V(D)J recombination. These responses involve the activation of cell cycle checkpoints, DNA repair and apoptosis. Other roles outside the cell nucleus might be carried out by the cytoplasmic fraction of ATM. In addition, ATM appears to function as a 'caretaker', suppressing tumorigenesis in specific T cell lineages.
共济失调毛细血管扩张症是一种多效性隐性疾病,负责该疾病的基因ATM的鉴定引发了广泛研究,以确定其多功能蛋白质产物的功能。ATM蛋白属于蛋白激酶家族,其在C末端区域与磷脂酰肌醇3激酶的催化结构域具有相似性。对共济失调毛细血管扩张症(A-T)细胞和Atm缺陷小鼠的研究表明,ATM是多种信号级联反应的关键调节因子,这些信号级联反应可响应由损伤剂或正常过程(如减数分裂或V(D)J重组)诱导的DNA链断裂。这些反应涉及细胞周期检查点的激活、DNA修复和细胞凋亡。ATM的细胞质部分可能在细胞核外发挥其他作用。此外,ATM似乎起着“守护者”的作用,抑制特定T细胞谱系中的肿瘤发生。