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FEBS Lett. 2009 May 19;583(10):1567-74. doi: 10.1016/j.febslet.2009.04.022. Epub 2009 Apr 18.

BS69 negatively regulates the canonical NF-kappaB activation induced by Epstein-Barr virus-derived LMP1.

Author information

1
Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-Ku Kita 12 Nishi 6, Sapporo, Japan.

Abstract

Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) activates NF-kappaB 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-kappaB activation and up-regulates IL-6 mRNA expression and IkappaB degradation. Our immunoprecipitation experiments suggest that BS69 decreases complex formation between LMP1 and TNFR-associated death domain protein (TRADD).

PMID:
19379743
DOI:
10.1016/j.febslet.2009.04.022
[Indexed for MEDLINE]
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