ZHU Xiang,CAO Bao-shan,ZHANG Zhao-hui,MA Li-wen,SU Xu,LIANG Li.Roel of Lys63-linked TAK1 poly-ubiquitination at lysine 158 in radiation-induced NF-κB activity[J].Chinese Journal of Radiological Medicine and Protection,2013,33(3):235-238
Roel of Lys63-linked TAK1 poly-ubiquitination at lysine 158 in radiation-induced NF-κB activity
Received:February 19, 2013  
DOI:10.3760/cma.j.issn.0254-5098.2013.03.004
KeyWords:Radiation effect  Transforming growth factor-β-activating kinase 1  Polyubiquitination  Nuclear factor-kappa B  Signaling pathway
FundProject:卫生行业科研专项(201002009)
Author NameAffiliationE-mail
ZHU Xiang 100191, 北京大学第三医院病理科  
CAO Bao-shan Department of Tumor Chemotherapy and Radiation Sickness, Peking University Third Hospital, Beijing 100191, China  
ZHANG Zhao-hui Department of Tumor Chemotherapy and Radiation Sickness, Peking University Third Hospital, Beijing 100191, China  
MA Li-wen Department of Tumor Chemotherapy and Radiation Sickness, Peking University Third Hospital, Beijing 100191, China  
SU Xu 中国疾病预防控制中心辐射防护与核安全医学所  
LIANG Li 100191, 北京大学第三医院病理科 liang.dr@163.com 
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Abstract::
      Objective To study the role of the transforming growth factor-β-activating kinase 1 (TAK1) poly-ubiquitination in radiation-induced NF-κB activation.Methods FLAG-TAK1 and HA-Ub-K63 plasmids were transiently transfected into HEK-293T cells. The radiation effect on TAK1 ubiquitination was detected by immunoprecipitation and Western blot, which was further confirmed in FLAG-TAK1 HeLa stable cell line. Results At 1 h after irradiation, Lys 63-link TAK1 ubiquitination was induced in the HEK-293T cells with plasmids transfection. This result was further confirmed by using a FLAG-TAK1 stably expressed HeLa cell line. Radiation-induced IKKs and p38 phosphorylation were greatly impaired in MEFs reconstituted with TAK1 K158R mutant compared to ones with wild-type TAK1. Conclusions Lys63-linked TAK1 poly-ubiquitination at Lys-58 plays a key role in the process of radiation-induced NF-κB activation.
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