Homologous recombination repair is regulated by domains at the N- and C-terminus of NBS1 and is dissociated with ATM functions

作者: S Sakamoto , K Iijima , D Mochizuki , K Nakamura , K Teshigawara

DOI: 10.1038/SJ.ONC.1210428

关键词: DNA repairCancer researchMutantSister chromatidsBiologyNucleaseDNA-binding proteinDNACell biologyCarcinogenesisHomologous 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.

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