ATM, a paradigm for a stress-responsive signal transducer in higher vertebrate cells.
作者： Ken-ichi Yamamoto , Masahiko Kobayashi , Hiroko Shimizu
DOI: 10.1007/978-1-4020-4896-8_19
关键词: Ataxia-telangiectasia 、 Kinase 、 Gene 、 Cell 、 Oxidative stress 、 Anatomy 、 Cell biology 、 Homologous recombination 、 DNA repair 、 Biology 、 DNA damage
摘要: ATM, the gene mutated in ataxia telangiectasia, is related to a family of large phosphatidylinositol 3-kinase domain-containing protein kinases involved cell cycle control and DNA repair. To define physiological roles ATM higher vertebrate cells, we created an ATM-deficient DT40 line, which, despite lack p53 expression, displays multiple p53-independent defects checkpoint maintenance chromosomal DNA. -/- cells also show mild impairment homologous recombination repair, which independent its defects. These deficient clones thus provide useful model system for analyzing functions cellular response double-strand break. Furthermore, observe various abnormalities noxious stress such as oxidative indicating that plays important not only damage but homeostasis damage.
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