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The ATM protein kinase: regulating the cellular response to genotoxic stress, and more

Yosef Shiloh1, Yael Ziv

  • 1The David and Inez Myers Laboratory for Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. yossih@post.tau.ac.il

Nature Reviews. Molecular Cell Biology
|March 15, 2013
PubMed

Insights

The protein kinase ataxia-telangiectasia mutated (ATM) is crucial for DNA double-strand break repair. Emerging evidence shows ATM also responds to other genotoxic stresses and maintains cellular homeostasis.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • The protein kinase ataxia-telangiectasia mutated (ATM) is primarily recognized for its role in DNA double-strand break (DSB) response.
  • ATM initiates an extensive signaling network upon DSB induction, affecting numerous cellular targets.

Purpose of the Study:

  • To explore the broader functions of ATM beyond its canonical role in DSB repair.
  • To investigate ATM's involvement in responses to various genotoxic stresses.
  • To understand ATM's participation in cellular homeostasis pathways.

Main Methods:

  • The study reviews existing literature and experimental evidence on ATM signaling.
  • Analysis of ATM-mediated phosphorylation in response to different cellular stresses.
  • Investigation of ATM's role in pathways regulating cellular balance.

Main Results:

  • ATM's function extends beyond DSB repair, playing a role in responses to other genotoxic stresses.
  • ATM-mediated phosphorylation is implicated in diverse cellular signaling networks.
  • ATM is actively involved in pathways crucial for maintaining cellular homeostasis.

Conclusions:

  • ATM possesses multifaceted roles in cellular stress response and homeostasis.
  • Further research into ATM's non-canonical functions is warranted.
  • ATM represents a key regulator of cellular integrity under various conditions.

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