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BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activation
Title: | BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activation |
Other Titles: | Physical and functional interactions between BS69 and LMP1/CTAR1 |
Authors: | Ikeda, Osamu Browse this author | Miyasaka, Yuto Browse this author | Yoshida, Ryuji Browse this author | Mizushima, Akihiro Browse this author | Oritani, Kenji Browse this author | Sekine, Yuichi Browse this author →KAKEN DB | Kuroda, Makoto Browse this author | Yasui, Teruhito Browse this author | Fujimuro, Masahiro Browse this author | Muromoto, Ryuta Browse this author →KAKEN DB | Nanbo, Asuka Browse this author →KAKEN DB | Matsuda, Tadashi Browse this author |
Keywords: | BS69 | EBV | LMP1 | TRAF3 | NF-κB | transcription |
Issue Date: | 5-Mar-2010 |
Publisher: | Elsevier |
Journal Title: | FEBS Letters |
Volume: | 584 |
Issue: | 5 |
Start Page: | 865 |
End Page: | 872 |
Publisher DOI: | 10.1016/j.febslet.2010.01.060 |
PMID: | 20138174 |
Abstract: | 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. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/42639 |
Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 松田 正
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