A specific DNA-binding protein activated by ionizing radiation in normal cells and constitutively present in ataxia telangiectasia cells.
Exposure of mammalian cells to ionizing radiation gives rise to a complex series of changes. This response is characterized by the induction of a variety of genes and the activation of pre-existing proteins. We describe here activation of a specific DNA-binding protein by ionizing radiation. The response was dose-dependent and specific for ionizing radiation. The binding factor appears to be normally present in the cytoplasm and responds to radiation by translocation to the nucleus, or is activated within the nucleus by an unknown mechanism. The radiation-induced activation of this protein appears to be mediated through a protein kinase C-associated pathway. A DNA-binding factor recognizing the same binding motif was found to be abnormally distributed in cells from patients with the human genetic disease, ataxia telangiectasia. The protein was constitutively present in the nucleus and the cytoplasm of ataxia telangiectasia cells and did not respond to radiation.
Teale
B
B
Queensland Cancer Fund Research Unit, Queensland Institute of Medical Research, Bancroft Centre, Brisbane, Australia.
Lavin
M F
MF
D001260:Ataxia Telangiectasia / Q000378:metabolism*; D001483:Base Sequence; D002478:Cells, Cultured; D004247:DNA / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism / Q000528:radiation effects*; D006801:Humans; D008969:Molecular Sequence Data; D009838:Oligodeoxyribonucleotides; D011493:Protein Kinase C / Q000378:metabolism; D011839:Radiation, Ionizing; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D004268:DNA-Binding Proteins; D009838:Oligodeoxyribonucleotides; D004247:DNA; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate