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作 者:Xueer Wang Honghai Zhang Zhugui Shao Wanxin Zhuang Chao Sui Feng Liu Xiaorong Chen Jinxiu Hou Lingli Kong Hansen Liu Yi Zheng Bingyu Liu Tian Chen Lei Zhang Xinming Jia Chengjiang Gao
机构地区:[1]Shandong Provincial Key Laboratory of Infection and Immunity&Department of Immunology,School of Biomedical Sciences,Shandong University,Jinan,Shandong,China [2]Department of Pathogenic Biology,School of Biomedical Sciences,Shandong University,Jinan,Shandong,China [3]Clinical Medicine Scientific and Technical Innovation Center,Shanghai Tenth People’s Hospital,Tongji University School of Medicine,Shanghai,China
出 处:《Signal Transduction and Targeted Therapy》2021年第9期2794-2808,共15页信号转导与靶向治疗(英文)
基 金:This work was supported by grants from the National Natural Science Foundation of China(81930039,31730026,81525012);the Key Research and Development Projects of Shandong Province(2019GSF108133).
摘 要:Spleen tyrosine kinase(SYK)is a non-receptor tyrosine kinase,which plays an essential role in both innate and adaptive immunity.However,the key molecular mechanisms that regulate SYK activity are poorly understood.Here we identified the E3 ligase TRIM31 as a crucial regulator of SYK activation.We found that TRIM31 interacted with SYK and catalyzed K27-linked polyubiquitination at Lys375 and Lys517 of SYK.This K27-linked polyubiquitination of SYK promoted its plasma membrane translocation and binding with the C-type lectin receptors(CLRs).
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