Protective roles for ATM in cellular response to oxidative stress

Noriaki Takao, Yingzhu Li, Ken Ichi Yamamoto

Research output: Contribution to journalArticle

80 Citations (Scopus)

Abstract

ATM (ataxia telangiectasia mutated), the gene mutated in ataxia telangiectasia, is related to a family of large phosphatidylinositol 3-kinase domain-containing proteins involved in cell cycle control and DNA repair. We found that ATM-/- DT40 cells were more susceptible than wild-type cells to apoptosis induced not only by ionizing radiation and bleomycin but also by non-DNA-damaging apoptotic stimuli such as C2-ceramide. Furthermore, the apoptosis induced by C2-ceramide and H2O2 was blocked by anti-oxidants, indicating that the ATM-/- DT40 cells had a heightened susceptibility to apoptosis induced by reactive oxygen intermediates (ROI), presumably due to defective ROI-detoxification activities. In support of this hypothesis, we found that more ROI were generated in ATM-/- DT40 cells than in wild-type cells, following treatment with the above apoptotic stimuli. These results indicate that ATM plays important roles in the maintenance of the cell homeostasis in response to oxidative damage.

Original languageEnglish
Pages (from-to)133-136
Number of pages4
JournalFEBS Letters
Volume472
Issue number1
DOIs
Publication statusPublished - Apr 21 2000
Externally publishedYes

Keywords

  • Apoptosis
  • Ataxia telangiectasia mutated
  • Gene targeting
  • Reactive oxygen intermediate

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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