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Activation of the ATM kinase by ionizing radiation and phosphorylation of p53.

Science (New York, N.Y.) | Sep 11, 1998

The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents. The gene product mutated in ataxia telangiectasia, ATM, acts upstream of p53 in a signal transduction pathway initiated by ionizing radiation. Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner. Ionizing radiation, but not ultraviolet radiation, rapidly enhanced this p53-directed kinase activity of endogenous ATM. These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo.

Pubmed ID: 9733515 RIS Download

Mesh terms: Ataxia Telangiectasia Mutated Proteins | Cell Cycle Proteins | Cell Line | DNA Damage | DNA-Activated Protein Kinase | DNA-Binding Proteins | Enzyme Activation | Humans | Lymphocytes | Mutation | Nuclear Proteins | Phosphatidylinositol 3-Kinases | Phosphorylation | Phosphoserine | Protein Kinases | Protein-Serine-Threonine Kinases | Proteins | Radiation, Ionizing | Recombinant Fusion Proteins | Recombinant Proteins | Signal Transduction | Transfection | Tumor Suppressor Protein p53 | Tumor Suppressor Proteins | Ultraviolet Rays

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Associated grants

  • Agency: NCI NIH HHS, Id: CA71387
  • Agency: NIEHS NIH HHS, Id: ES05777

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