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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
|July 13, 2013
PubMed

Insights

The protein kinase ataxia-telangiectasia mutated (ATM) is crucial for DNA repair and cellular homeostasis. It activates extensive signaling networks in response to DNA damage and participates in other cellular pathways.

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) repair.
  • ATM initiates a significant signaling cascade upon DSB induction, impacting numerous cellular targets.

Purpose of the Study:

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

Main Methods:

  • Literature review and analysis of existing research on ATM signaling.
  • Examination of studies investigating ATM-mediated phosphorylation in different cellular contexts.

Main Results:

  • ATM plays a critical role in the DNA damage response, particularly for DSBs.
  • Evidence indicates ATM-mediated phosphorylation is involved in responding to other genotoxic stresses.
  • ATM is implicated in cellular signaling pathways essential for maintaining homeostasis.

Conclusions:

  • ATM's functions extend beyond DSB repair, encompassing responses to diverse genotoxic insults.
  • ATM actively participates in cellular signaling networks vital for maintaining overall cell health and stability.

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