論文

2021年8月31日

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

Genes
  • Atsushi Shibata
  • ,
  • Penny A. Jeggo

12
9
開始ページ
1370
終了ページ
1370
記述言語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/genes12091370
出版者・発行元
MDPI AG

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.

リンク情報
DOI
https://doi.org/10.3390/genes12091370
URL
https://www.mdpi.com/2073-4425/12/9/1370/pdf
ID情報
  • DOI : 10.3390/genes12091370
  • eISSN : 2073-4425

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