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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Cleavage of ATM during radiation-induced apoptosis: caspase-3-like apoptotic protease as a candidate

X Tong1, B Liu, Y Dong

  • 1Beijing Institute of Radiation Medicine, PR China.

International Journal of Radiation Biology
|November 1, 2000
PubMed
Abstract

Insights

Ionizing radiation induces apoptosis by cleaving ATM (ataxia-telangiectasia mutated), a key DNA repair protein. This cleavage, mediated by caspase-3, is essential for efficient apoptosis induction.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Radiation Oncology

Background:

  • The ATM (ataxia-telangiectasia mutated) protein is crucial for DNA damage response, cell cycle control, and genomic stability.
  • Apoptosis, or programmed cell death, is a vital process regulated by complex molecular pathways.

Purpose of the Study:

  • To investigate the relationship between ionizing radiation-induced apoptosis and the integrity of the ATM protein.
  • To understand ATM's role in DNA damage sensing, repair, and cell-cycle checkpoint control during radiation-induced cell death.

Main Methods:

  • U937 cells were exposed to gamma radiation.
  • Assessed apoptosis markers including Sub-G1 DNA content, DNA fragmentation, and active caspase-3.
  • Measured ATM cleavage in vitro and in vivo using Western blotting and other assays.

Main Results:

  • ATM undergoes specific cleavage during ionizing radiation-induced apoptosis.
  • ATM cleavage kinetics correlated with increased Sub-G1 DNA content and caspase-3 activation.
  • In vitro studies indicated that caspase-3 or related proteases cleave ATM at specific aspartic acid-glycine (DIVD/G) sites.

Conclusions:

  • ATM is among several DNA repair proteins (e.g., PARP, DNA-PK, HsRad51) that are cleaved during apoptosis.
  • Inactivation of DNA repair mechanisms, including ATM cleavage, appears necessary for efficient apoptosis execution.

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