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STAP-2 Negatively Regulates both Canonical and Noncanonical NF-κB Activation Induced by Epstein-Barr Virus-Derived Latent Membrane Protein 1

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Title: STAP-2 Negatively Regulates both Canonical and Noncanonical NF-κB Activation Induced by Epstein-Barr Virus-Derived Latent Membrane Protein 1
Authors: Ikeda, Osamu Browse this author
Sekine, Yuichi Browse this author
Yasui, Teruhito Browse this author
Oritani, Kenji Browse this author
Sugiyma, Kenji Browse this author
Muromoto, Ryuta Browse this author
Ohbayashi, Norihiko Browse this author
Yoshimura, Akihiko Browse this author
Matsuda, Tadashi Browse this author
Issue Date: Aug-2008
Publisher: American Society for Microbiology
Journal Title: Molecular and Cellular Biology
Volume: 28
Issue: 16
Start Page: 5027
End Page: 5042
Publisher DOI: 10.1128/MCB.00194-08
Abstract: The signal-transducing adaptor protein 2 (STAP-2) is a recently identified adaptor protein that contains a pleckstrin homology (PH) and Src homology 2 (SH2)-like domains, as well as a proline-rich domain in its C-terminal region. In previous studies, we demonstrated that STAP-2 binds to MyD88 and IKK-α or IKK-β and modulates NF-κB signaling in macrophages. In the present study, we found that ectopic expression of STAP-2 inhibited Epstein-Barr virus (EBV) LMP1-mediated NF-κB signaling and interleukin-6 expression. Indeed, STAP-2 associated with LMP1 through its PH and SH2-like domains, and these proteins interacted with each other in EBV-positive human B cells. We found, furthermore, that STAP-2 regulated LMP1-mediated NF-κB signaling through direct or indirect interactions with the tumor necrosis factor receptor (TNFR)- associated factor 3 (TRAF3) and TNFR-associated death domain (TRADD) proteins. STAP-2 mRNA was induced by the expression of LMP1 in human B cells. Furthermore, transient expression of STAP-2 in EBV-positive human B cells decreased cell growth. Finally, STAP-2 knockout mouse embryonic fibroblasts showed enhanced LMP1-induced cell growth. These results suggest that STAP-2 acts as an endogenous negative regulator of EBV LMP1-mediated signaling through TRAF3 and TRADD.
Rights: Copyright © 2008, American Society for Microbiology
Type: article
URI: http://hdl.handle.net/2115/34635
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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