The interaction of CtIP with DNA damage response proteins

摘要: In the course of this study it was established that CtlP associates in vivo with, and directly binds to, DNA damage mediator proteins containing BRCT domains: 53BP1, MDC1, TopBP1 NBS1. The binding sites on all these have been mapped establishing which regions interact with NBS1 vice versa. This implies is involved response many levels interacting mediate different aspects sensing signalling. CtIP's nuclear localization before after determined its colocalization other damaged responsive examined. It found CtIP sensor such as MRN complex (Mre11, Rad50 NBS1) RPA70, signal transducer PIKK kinases ATM, ATR SMG1 53BP1 MDC1. All those are detecting repairing double stranded or single lesions. Moreover has a major influence phosphorylation events induced during repair processes thus could be an inducer kinase activity. deletion causes impairment important take part pathways NBS1, Chk1 RPA70. However, impaired only occurs to lesions collapse replication forks. pathway malfunctioning depleted cells. previously reported phosphorylated Ser664 Ser745 by ATM breaks. I two possible new sites: Ser506 Ser555. They potentially CtlP's redistribution but remains elucidated.