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BS69 negatively regulates the canonical NF-κB activation induced by Epstein-Barr virus-derived LMP1
| Title: | BS69 negatively regulates the canonical NF-κB activation induced by Epstein-Barr virus-derived LMP1 |
| Authors: | Ikeda, Osamu Browse this author | | Sekine, Yuichi Browse this author | | Mizushima, Akihiro Browse this author | | Oritani, Kenji Browse this author | | Yasui, Teruhito Browse this author | | Fujimuro, Masahiro Browse this author | | Muromoto, Ryuta Browse this author | | Nanbo, Asuka Browse this author | | Matsuda, Tadashi Browse this author →KAKEN DB |
| Keywords: | EBV | | LMP1 | | BS69 | | NF-κB | | TRADD |
| Issue Date: | 19-May-2009 |
| Publisher: | Elsevier |
| Journal Title: | FEBS Letters |
| Volume: | 583 |
| Issue: | 10 |
| Start Page: | 1567 |
| End Page: | 1574 |
| Publisher DOI: | 10.1016/j.febslet.2009.04.022 |
| PMID: | 19379743 |
| Abstract: | Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) activates NF-κB 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-κB activation and up-regulates IL-6 mRNA expression and IκB degradation. Our immunoprecipitation experiments suggest that BS69 decreases complex formation between LMP1 and TNFR-associated death domain protein (TRADD). |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/38441 |
| 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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