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TRAF6和IFN-λR1相互作用后的泛素化变化对IFN-λ1信号通路的影响 被引量：1

Molecular Mechnism of the Respective Inhibition Effect of IFN-λ1 to NF-κB and TRAF6 to ISRE
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摘要 目的研究IFN-λ1抑制NF-κB激活和TRAF6抑制ISRE激活的分子机制。方法利用细胞培养、细胞转染、免疫共沉淀、SDS-PAGE及Western blot等方法检测IFN-λ1对TRAF6泛素化,以及泛素连接酶TRAF6对IFN-λ1的受体IFN-λR1泛素化的作用。结果 IFN-λ1会抑制TRAF6的自身泛素化,TRAF6能泛素化受体IFN-λR1,并且IFN-λ1会增加IFN-λR1与泛素K63位点的结合。结论 IFN-λ1抑制了NF-κB的激活的原因是IFN-λ1能够抑制TRAF6的自身泛素化。TRAF6能泛素化IFN-λR1,从而抑制ISRE的激活。 Objective To investigate the molecular mechnism of IFN - λ1 depressing the activation of NF - KB and TRAF6 inhibi- ting the activation of ISRE. Methods Cell culture, cell transfection, immunoprecipitation and Western blot were used to check the influence of IFN - λ1 in TRAF6 ubiquitination and the function of TRAF6 in IFN - λR1 ubiquitination. Results IFN - λ1 depressed the self- ubiquitination of TRAF6 and TRAF6 can ubiquitate IFN - λR1. IFN - 3,1 promoted the linkage of IFN - ）λR1 with K63 Ub protein. Conclusion IFN - hi depressed the activation of NF -κB because of the decreased self - ubiquitination of TRAF6 evoked by the IFN - λ1. The over - expression of TRAF6 ubiquitated the IFN - 3,R1, and then inhibited the following activation of ISRE.
作者 张俊文 杨霞 米蕊芳 刘福生 陈虹 黄秉仁
机构地区 首都医科大学附属北京天坛医院/北京市神经外科研究所脑肿瘤研究中心 中国医学科学院基础医学研究所/清华大学医学部北京协和医学院基础学院医学分子生物学国家重点实验室
出处 《医学研究杂志》 2016年第9期43-48,共6页 Journal of Medical Research
基金 国家自然科学基金资助项目(81372354,81302186) 北京市自然科学基金资助项目(7132034) 生物医用材料北京实验室基金资助项目(京教函【2013】133号) 北京市卫生系统高层次卫生技术人才培养计划(2013-2-018) 北京市神经外科研究所创新基金资助项目(所青年-2014-003)
关键词 IFN—λ1 IFN-λR1 TRAF6 NF—κB ISRE IFN-λ1 IFN-λR1 TRAF6 NF-κB ISRE
分类号 R73-36 [医药卫生—肿瘤]
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参考文献11

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二级参考文献12

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医学研究杂志
2016年 第9期

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