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摘要Objective:Recently,a Ku-independent DNA double-strand break (DSB) repair pathway termed altemative-NHEJ (Alt-NHEJ) was identified.However,the mechanism remain unknown.This article is to investigate what is the mechanism of the cellular components that play a role in Alt-NHEJ.Method:In this study,we down-regulated Ku70 by Ku70shRNA in human cells.and we present the association of PARP1 with the double strand breaks DNA using biochemical fractionation and immunostainning.Moreover,inhibition the activity of PARP1 impairs the DSB repair and the cell survival in response to Ncs treatment.Result:In this study,we found PARP1 was recruited to chromatin in response to neocarzinostatin (Ncs) induced DSB in the absence of Ku70 by using a fractionation protocol and immunostainning.Meanwhile,inhibition of PARP1 impair the Ncs induced DSB repair and led to significantly sencitivity of the cells to Ncs(P<0.01).Conclusion:These data support the involvement of PARP1 in the Alt-NHEJ pathway.