Structural insights into the activation of ATM kinase

• 来源期刊: 细胞研究（英文版）
• 年，卷（期）: 2019,（8）
• 页码范围: 683-685
• 页数: 3页
• 语种: 英文

摘要

Dear Editor, ATM (ataxia telangiectasia-mutated) is a master regulator in response to DNA damage and activates downstream pathways involved in cell cycle checkpoints,DNA damage repair,transcription regulation,immune response,central nervous system development and metabolism.1,2 Loss of ATM activity in human results in the pleiotropic neurodegeneration disorder ataxia-telangiectasia (A-T) that is characterized by immunodeficiency,cancer predisposition,premature aging and insulin-resistant diabetes.3-5 Despite extensive studies over the past two decades,6,7 it remains controversial how ATM is activated.Particularly,whether ATM exists in a monomeric form,whether the monomer is more active than dimer,and how dimer-to-monomer transition affects the ATM kinase activity,remain controversial.