ATM's Role in the Repair of DNA Double-Strand Breaks

Ataxia telangiectasia mutated (ATM) is a central kinase that activates an extensive network of responses to cellular stress via a signaling role. ATM is activated by DNA double strand breaks (DSBs) and by oxidative stress, subsequently phosphorylating a plethora of target proteins. In the last several decades, newly developed molecular biological techniques have uncovered multiple roles of ATM in response to DNA damage-e.g., DSB repair, cell cycle checkpoint arrest, apoptosis, and transcription arrest. Combinational dysfunction of these stress responses impairs the accuracy of repair, consequently leading to dramatic sensitivity to ionizing radiation (IR) in ataxia telangiectasia (A-T) cells. In this review, we summarize the roles of ATM that focus on DSB repair.

Automated summary

ATM is a central kinase that activates a wide range of responses to cellular stress through signaling. It plays multiple roles in response to DNA damage, particularly focusing on DSB repair. Dysfunction in stress responses impairs repair accuracy, leading to dramatic sensitivity to ionizing radiation in ataxia telangiectasia (A-T) cells.