Abstract
Double strand breaks (DSBs) occur in chromosomal DNA as a result of exposure of cells to ionizing radiation (IR). DSBs induce cellular responses that lead to cell cycle checkpoint, DNA repair, and apoptosis. The ataxia telangiectasia mutated (ATM) kinase plays a centarl role in these responses, and the pathways in these responses form complicated networks through non linear relationships. Upon indction of DSBs, activeated ATM phosphorylates many proteins that are involved in DSB responses. In a process of our previous research to clarify functions of 53BP1 in DSB responses, we identified a few proteins which cross-react to anti-phospho ATM antibody after treatement of cells with IR. To identify a new ATM target, cell lysates from IR-exposed cells were subjected to immunoprecipitation with anti-phospho ATM antibody. The precipitated proteins were resolved by SDS-PAGE, and analyzed by LC-MS/MS. We would like to present a protein that is phosphorylated after exposure of cells to IR in a ATM-depnedent manner.
