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

Atsushi Shibata1, Penny A Jeggo2

  • 1Signal Transduction Program, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Gunma 371-8511, Japan.

Genes
|September 28, 2021
PubMed

Insights

Ataxia telangiectasia mutated (ATM) is a key kinase in cellular stress response. This review focuses on ATM

Area of Science:

  • Molecular biology
  • Cellular biology
  • Genetics

Background:

  • Ataxia telangiectasia mutated (ATM) is a central kinase.
  • ATM is activated by DNA double-strand breaks (DSBs) and oxidative stress.
  • ATM regulates DNA damage response pathways.

Purpose of the Study:

  • To review the roles of ATM in DNA double-strand break (DSB) repair.
  • To highlight ATM's function in maintaining genomic stability.

Main Methods:

  • Literature review of molecular biological techniques.
  • Analysis of ATM's signaling pathways in response to DNA damage.

Main Results:

  • ATM plays critical roles in DSB repair, cell cycle checkpoint control, apoptosis, and transcription.
  • ATM dysfunction leads to impaired DNA repair accuracy and ionizing radiation sensitivity in ataxia telangiectasia (A-T) cells.

Conclusions:

  • ATM is essential for orchestrating cellular responses to DNA damage.
  • Understanding ATM's role in DSB repair is crucial for A-T research and potential therapeutic strategies.
Keywords:
ATMDNA double-strand breakhomologous recombinationionizing radiationnon-homologous end joining

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