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

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/42639

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)

Submitter: 松田 正

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