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KMID : 0620920070390010056
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Experimental & Molecular Medicine
2007 Volume.39 No. 1 p.56 ~ p.64
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STP-A11, an oncoprotein of Herpesvirus saimiri augments both NF-kB and AP-1 transcription activity through TRAF6
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Jeong Su-Nam
Cho Il-Rae
An Won-Gun
Jhun Byung-Hak
Chung Young-Hwa
Lee Bok-Soo
Park Kee-Rang
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Abstract
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Herpesvirus saimiri (HVS), a member of the g- herpesvirus family, encodes an oncoprotein called Saimiri Transforming Protein (STP) which is required for lymphoma induction in non-human primates. However, a detailed mechanism of STP-A11-induced oncogenesis has not been revealed yet. We first report that STP-A11 oncoprotein interacts with TNF-? receptor-associated factor (TRAF) 6 in vivo and in vitro. Mutagenesis analysis of the TRAF6-binding motif 10PQENDE15 in STP-A11 reveals that Glu (E)12 residue is critical for binding to TRAF6 and NF-kB activation. Interestingly, co-expression of E12A mutant, lack of TRAF6 binding, with cellular Src (Src) results in decreased transcriptional activity of Stat3 and AP-1, a novel target of STP-A11 compared to that of wild type. Furthermore, the presence of STP-A11 enhances the association of TRAF6 with Src and induces the translocation of both TRAF6 and Src to a nonionic detergent-insoluble fraction. Taken together, these studies suggest that STP-A11 oncoprotein up-regulates both NF-kB and AP-1 transcription activity through TRAF6, which would ultimately contribute cellular transformation.
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KEYWORD
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herpesvirus 2 saimirine, NF- B, oncogene protein pp60 (v-src), Src, TNF receptor-associated factor 6, transcription factor AP-1
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