BS69 cooperates with TRAF3 in the regulation of Epstein-Barr virus-derived LMP1/CTAR1-induced NF-κB activation

BS69 cooperates with TRAF3 in the regulation of Epstein-Barr virus-derived LMP1/CTAR1-induced NF-κB activation
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DOI:
10.1016/j.febslet.2010.01.060
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发表时间:
2010-03-05
期刊:
影响因子:
3.5
通讯作者:
Matsuda, Tadashi
Matsuda, Tadashi
中科院分区:
生物学3区
文献类型:
--
作者:
Ikeda, Osamu;Miyasaka, Yuto;Matsuda, Tadashi

文献摘要

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EB病毒潜伏膜蛋白1(LMP 1)通过两个C末端区域CTAR 1和CTAR 2激活NF-κ B信号通路。先前的研究表明,BS 69,一种多结构域细胞蛋白,通过干扰TRADD和LMP 1/CTAR 2之间的复合物形成来调节LMP 1/CTAR 2介导的NF-κ B活化。在这里,我们发现BS 69直接与LMP 1/CTAR 1结构域相互作用,并调节LMP 1/CTAR 1介导的NF-κ B活化和随后的IL-6产生。关于所涉及的机制,我们发现BS 69直接与TRAF 3相互作用,TRAF 3是NF-κ B激活的负调节因子。此外,小干扰RNA介导的敲低实验揭示TRAF 3参与BS 69介导的对LMP 1/CTAR 1诱导的NF-κ B活化的抑制。(uniprotkb:P03230)与BS 69发生物理相互作用(MI:0915)(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)MINT-7556646:TRAF6(uniprotkb:Q9 Y 4K 3)物理相互作用(MI:0915),带BS 69(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)MINT-7556658,MINT-7556670:TRAF3(uniprotkb:Q13114)物理相互作用(MI:0915)带BS 69(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)MINT-7556607:TRAF1(uniprotkb:Q13077)物理相互作用(MI:0915)带BS 69(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)MINT-7556634:TRAF5(uniprotkb:O 00463)物理相互作用(MI:0915),带BS 69(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)MINT-7556622:TRAF2(uniprotkb:Q12933)物理相互作用(MI:0915)与BS 69(uniprotkb:Q15326)通过抗标签共免疫沉淀(MI:0007)(C)2010欧洲生物化学学会联合会。由Elsevier B出版。V.保留所有权利。
Epstein-Barr virus latent membrane protein 1 (LMP1) activates NF-kappa B signaling pathways through two C-terminal regions, CTAR1 and CTAR2. Previous studies have demonstrated that BS69, a multidomain cellular protein, regulates LMP1/CTAR2-mediated NF-kappa B activation by interfering with the complex formation between TRADD and LMP1/CTAR2. Here, we found that BS69 directly interacted with the LMP1/CTAR1 domain and regulated LMP1/CTAR1-mediated NF-kappa B activation and subsequent IL-6 production. Regarding the mechanisms involved, we found that BS69 directly interacted with TRAF3, a negative regulator of NF-kappa B activation. Furthermore, small-interfering RNA-mediated knockdown experiments revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-kappa B activation.Structured summary:MINT-7556591: lmp1 (uniprotkb: P03230) physically interacts (MI:0915) with BS69 (uniprotkb:Q15326) by anti tag coimmunoprecipitation (MI: 0007)MINT-7556646: TRAF6 (uniprotkb:Q9Y4K3) physically interacts (MI: 0915) with BS69 (uniprotkb: Q15326) by anti tag coimmunoprecipitation (MI: 0007)MINT-7556658, MINT-7556670: TRAF3 (uniprotkb:Q13114) physically interacts (MI: 0915) with BS69 (uniprotkb: Q15326) by anti tag coimmunoprecipitation (MI: 0007)MINT-7556607: TRAF1 (uniprotkb:Q13077) physically interacts (MI: 0915) with BS69 (uniprotkb: Q15326) by anti tag coimmunoprecipitation (MI: 0007)MINT-7556634: TRAF5 (uniprotkb:O00463) physically interacts (MI: 0915) with BS69 (uniprotkb: Q15326) by anti tag coimmunoprecipitation (MI: 0007)MINT-7556622: TRAF2 (uniprotkb:Q12933) physically interacts (MI: 0915) with BS69 (uniprotkb: Q15326) by anti tag coimmunoprecipitation (MI: 0007) (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.