title: Cellular response to DNA damage. Link between p53 and DNA-PK.
abstract: Cells which lack DNA-activated protein kinase (DNA-PK) are very susceptible to ionizing radiation and display an inability to repair double strand DNA breaks. DNA-PK is a member of a protein kinase family that includes ATR and ATM which have strong homology in their carboxy-terminal kinase domain with PL-3 kinase. ATM has been proposed to act upstream of p53 in cellular response to ionizing radiation. DNA-PK may similarly interact with p53 in cellular growth control and in mediation of the response to ionizing radiation.
authors: Institut de biologie structurale J.-P.-Ebel, Grenoble, France.
authors: I
authors: I
authors: Salles-Passador
authors: A
authors: A
authors: Fotedar
authors: R
authors: R
authors: Fotedar
mesh_terms: D000818:Animals; D001260:Ataxia Telangiectasia / Q000235:genetics; D002477:Cells / Q000378:metabolism / Q000528:radiation effects*; D004249:DNA Damage; D051747:DNA-Activated Protein Kinase; D004268:DNA-Binding Proteins / Q000378:metabolism; D016158:Genes, p53; D006801:Humans; D009687:Nuclear Proteins; D009842:Oligopeptides / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D017434:Protein Structure, Tertiary
chemical_list: D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D009842:Oligopeptides; D051747:DNA-Activated Protein Kinase; C497263:PRKDC protein, human; D017346:Protein Serine-Threonine Kinases