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The role of ATM and ATR in DNA damage-induced cell cycle control

Aaron A Goodarzi1, Wesley D Block, Susan P Lees-Miller

  • 1Departments of Biochemistry & Molecular Biology and Biological Sciences, University of Calgary, 2500 University Drive, N.W., Calgary, AB T2N 1N4, Canada.

Progress in Cell Cycle Research
|November 5, 2003
PubMed

Insights

Ataxia-Telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) are key kinases in DNA damage response. Targeting these pathways offers potential for developing novel therapeutics against various diseases.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Ataxia-Telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) are serine/threonine protein kinases.
  • They are crucial in the cellular response to DNA damage.
  • ATM and ATR belong to the phosphatidyl inositol 3-kinase-like kinase (PIKK) family.

Purpose of the Study:

  • To review the roles of ATM and ATR in DNA damage response pathways.
  • To explore the therapeutic potential of targeting ATM and ATR.

Main Methods:

  • Literature review of ATM and ATR functions.
  • Analysis of DNA damage response mechanisms.
  • Discussion of therapeutic strategies targeting ATM and ATR.

Main Results:

  • ATM activation by ionizing radiation induces cell cycle arrest at G1/S, S, and G2/M phases.
  • ATR is essential for cell cycle arrest in response to bulky DNA lesions caused by agents like UV radiation.
  • ATM and ATR play distinct yet cooperative roles in maintaining genomic stability.

Conclusions:

  • ATM and ATR are vital regulators of the DNA damage response.
  • Targeting ATM and ATR pathways presents a promising avenue for novel therapeutic development.
  • Further research into ATM and ATR signaling could lead to innovative cancer treatments.

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