作者: S Sakamoto , K Iijima , D Mochizuki , K Nakamura , K Teshigawara
关键词: DNA repair 、 Cancer research 、 Mutant 、 Sister chromatids 、 Biology 、 Nuclease 、 DNA-binding protein 、 DNA 、 Cell biology 、 Carcinogenesis 、 Homologous recombination
摘要: The proteins responsible for radiation sensitive disorders, NBS1, kinase ataxia-telangiectasia-(A-T)-mutated (ATM) and MRE11, interact through the C-terminus of NBS1 in response to generation DNA double-strand breaks (DSBs) are all implicated checkpoint regulation DSB repair, such as homologous recombination (HR). We measured ability several mutant clones A-T cells regulate HR repair using DR-GFP or SCneo systems. ATM deficiency did not reduce frequency an induced DSB, it was confirmed by findings that frequencies only slightly affected deletion ATM-binding site at extreme NBS1. In contrast, HR-regulating is dramatically reduced MRE11-binding domain markedly inhibited mutations FHA/BRCT domains N-terminus. This impaired capability consistent with a failure observe MRE11 foci formation. Furthermore, normal sister chromatid completely absence domains. These results suggested N- C-terminal major regulatory pathways, very likely recruitment retention nuclease sites ATM-independent fashion.