Cadmium delays non-homologous end joining (NHEJ) repair via inhibition of DNA-PKcs phosphorylation and downregulation of XRCC4 and Ligase IV

Weiwei Li,Xueyan Gu,Xiaoning Zhang, Jinxin Kong,Nan Ding,Yongmei Qi, Yingmei Zhang,Jufang Wang,Dejun Huang

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis（2015）

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摘要

•Cadmium (Cd) exposure delayed the repair of DNA damage induced by X-ray.•Cd exposure altered the phosphorylation of DNA-PKcs on Thr-2609 and Ser-2056 sites.•Cd impaired the formation of XRCC4 and Ligase IV foci, and down-regulated their protein expression.•Zinc mitigated the effects of Cd on DDR by regulating pDNA-PKcs (Thr-2609), XRCC4 and Ligase IV.

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关键词

Heavy metal cadmium (Cd),DNA damage repair (DDR),Non-homologous end joining (NHEJ),DNA-dependent protein kinase,X-ray cross-complementing protein 4,DNA Ligase IV

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