ATM’s role in the repair of DNA double-strand breaks

Atsushi Shibata, Penny A. Jeggo

Research output: Contribution to journalReview articlepeer-review

37 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number1370
JournalGenes
Volume12
Issue number9
DOIs
Publication statusPublished - 2021 Sept
Externally publishedYes

Keywords

  • ATM
  • DNA double-strand break
  • Homologous recombination
  • Ionizing radiation
  • Non-homologous end joining

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

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