BID as a double agent in cell life and death.
DNA damage leads to the activation of ATM and ATR, which in turn either cause cell cycle arrest and DNA repair or apoptosis. We have demonstrated that DNA damage leads to ATM-mediated BID phosphorylation, and that this phosphorylation regulates a novel, pro-survival function of BID important for S phase arrest. Thus, BID, a member from the core apoptotic regulatory machinery (BCL-2 family) receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death.
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel. atan.gross@weizmann.ac.il
Atan
A
Gross
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D064007:Ataxia Telangiectasia Mutated Proteins; D051023:BH3 Interacting Domain Death Agonist Protein / Q000235:genetics*; D018797:Cell Cycle Proteins / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics*; D018816:Genes, cdc / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics*
D051023:BH3 Interacting Domain Death Agonist Protein; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases