Hosoi H, Sawada T
Dept. of Pediatrics, Kyoto Prefectural University of Medicine.
Nihon Rinsho. 2000 Jul;58(7):1505-10.
Ataxia-telangiectasia(AT), an autosomal recessive disorder characterized by cerebellar degeneration, immunodeficiency, cancer predisposition and radiation sensitivity, is caused by mutations in a gene named ATM(AT, mutated), which encodes a 370 kDa serine-threonine kinase, whose catalytic domain is structurally related to the catalytic subunit of phosphatidylinositol 3-kinase(PI3K). ATM has been recently revealed to be involved in DNA damage recognition and cell cycle control in response to ionizing radiation damage. Further investigations of the multiple roles of ATM will explain other disease features, such as cerebellar degeneration in ATM in the near future. This review summarizes some of the recent research developments in ATM functions and their relationship to the clinical phenotypes of AT.
共济失调毛细血管扩张症(AT)是一种常染色体隐性疾病,其特征为小脑变性、免疫缺陷、癌症易感性和辐射敏感性,由名为ATM(AT突变)的基因突变引起,该基因编码一种370 kDa的丝氨酸 - 苏氨酸激酶,其催化结构域在结构上与磷脂酰肌醇3激酶(PI3K)的催化亚基相关。最近发现ATM参与了对电离辐射损伤的DNA损伤识别和细胞周期控制。对ATM多种作用的进一步研究将在不久的将来解释其他疾病特征,如ATM中的小脑变性。本综述总结了ATM功能的一些最新研究进展及其与AT临床表型的关系。