ATM, a paradigm for a stress-responsive signal transducer in higher vertebrate cells.

Ken ichi Yamamoto, Masahiko Kobayashi, Hiroko Shimizu

Research output: Contribution to journalReview article

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Abstract

ATM, the gene mutated in ataxia telangiectasia, is related to a family of large phosphatidylinositol 3-kinase domain-containing protein kinases involved in cell cycle control and DNA repair. To define the physiological roles of ATM in higher vertebrate cells, we created an ATM-deficient DT40 cell line, which, despite of the lack of p53 expression, displays multiple p53-independent defects in cell cycle checkpoint control and in maintenance of chromosomal DNA. ATM -/- DT40 cells also show a mild impairment in homologous recombination repair, which is independent of its checkpoint control defects. These ATM deficient DT40 clones thus provide a useful model system for analyzing p53-independent ATM functions in cellular response to double-strand break. Furthermore, we observe various abnormalities in cellular response to noxious stress such as oxidative stress in ATM -/- DT40 cells, indicating that ATM plays important roles not only in cellular response to DNA damage but also in the maintenance of the cell homeostasis in response to oxidative damage.

Original languageEnglish
Pages (from-to)327-339
Number of pages13
JournalSub-cellular biochemistry
Volume40
Publication statusPublished - 2006

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ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology
  • Cancer Research

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