BS69负向调节由爱泼斯坦-巴尔病毒衍生的LMP1诱导的经典核因子κB激活。
BS69 negatively regulates the canonical NF-kappaB activation induced by Epstein-Barr virus-derived LMP1.
作者信息
Ikeda Osamu, Sekine Yuichi, Mizushima Akihiro, Oritani Kenji, Yasui Teruhito, Fujimuro Masahiro, Muromoto Ryuta, Nanbo Asuka, Matsuda Tadashi
机构信息
Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-Ku Kita 12 Nishi 6, Sapporo, Japan.
出版信息
FEBS Lett. 2009 May 19;583(10):1567-74. doi: 10.1016/j.febslet.2009.04.022. Epub 2009 Apr 18.
Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) activates NF-kappaB signaling pathways through the two C-terminal regions, CTAR1 and CTAR2. BS69 has previously been shown to be involved in LMP1-induced c-Jun N-terminal kinase activation through CTAR2 by interacting with tumor necrosis factor (TNFR) receptor-associated factor 6. In the present study, our manipulation of BS69 expression clearly indicates that BS69 negatively regulates LMP1-mediated NF-kappaB activation and up-regulates IL-6 mRNA expression and IkappaB degradation. Our immunoprecipitation experiments suggest that BS69 decreases complex formation between LMP1 and TNFR-associated death domain protein (TRADD).
爱泼斯坦-巴尔病毒（EBV）潜伏膜蛋白1（LMP1）通过两个C末端区域CTAR1和CTAR2激活核因子κB信号通路。先前已表明，BS69通过与肿瘤坏死因子（TNFR）受体相关因子6相互作用，参与LMP1通过CTAR2诱导的c-Jun氨基末端激酶激活。在本研究中，我们对BS69表达的调控清楚地表明，BS69负向调节LMP1介导的核因子κB激活，并上调白细胞介素-6 mRNA表达和IκB降解。我们的免疫沉淀实验表明，BS69减少了LMP1与TNFR相关死亡结构域蛋白（TRADD）之间的复合物形成。
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