BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activation
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概要
- 論文の詳細を見る
Epstein-Barr virus latent membrane protein 1 (LMP1) activates NF-κB 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-κB 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-κB activation and subsequent IL-6 production. Regarding the mechanisms involved, we found that BS69 directly interacted with TRAF3, a negative regulator of NF-κB activation. Furthermore, small-interfering RNA-mediated knockdown experiments revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-κB activation.
- 2010-03-05
著者
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Oritani K
Osaka Univ. Osaka Jpn
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Oritani Kenji
大阪大学 血液・腫瘍内科学
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Muromoto Ryuta
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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Sugio Y
Kyushu Univ. Fukuoka Jpn
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Sudo Yoshikazu
The Second Department Of Medicine Kyoto Prefectural University Of Medicine
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Sekine Yuichi
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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Matsuda Tadashi
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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Sugio Y
Miyazaki Prefectural Miyazaki Hospital Miyazaki Jpn
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Ikeda Osamu
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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Mizushima Akihiro
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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Nanbo Asuka
Department Of Immunology Graduate School Of Pharmaceutical Sciences Hokkaido University
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