This Article Full Text (PDF) Other Versions of this Article: JVI.02448-06v1 81/9/4837    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ho, C.-H. Articles by Chen, C.-J. Search for Related Content PubMed PubMed Citation Articles by Ho, C.-H. Articles by Chen, C.-J.

 Previous Article  |  Next Article 

J. Virol. doi:10.1128/JVI.02448-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Epstein-Barr Virus Transcription Activator Rta Upregulates Decoy Receptor 3 Expression by Binding to its Promoter

Institute of Microbiology and Immunology, Department of Otolaryngology, National Yang-Ming University, Taipei, Taiwan, Department of Otolaryngology, and Immunology Research Center, Taipei Veterans General Hospital, Taipei, Taiwan

^* To whom correspondence should be addressed. Email: cjchen{at}ym.edu.tw.

	Abstract

Decoy receptor 3 (DcR3) is a soluble decoy receptor belonging to the tumor necrosis factor receptor (TNFR) superfamily that is overexpressed in various malignant tumor types. DcR3 has been implicated in tumor cell survival by inhibiting apoptosis and by interfering with immune surveillance. Previous study showed that DcR3 expression is associated with Epstein-Barr virus (EBV)-positive lymphomas, but rarely with non-EBV-positive B cell lymphomas, suggesting that the presence of EBV may affect DcR3 expression. Here we demonstrated enhanced DcR3 expression upon EBV reactivation in P3HR1 cells and in EBV-infected 293 cells. This enhancement, however, could not be detected in 293 cells infected with BRLF1-deleted EBV. We found that EBV transactivator, Rta, could upregulate DcR3 expression by direct binding to an Rta responsive element (RRE) located in DcR3 promoter region and this RRE is important for Rta-mediated DcR3 expression. Overexpressing CREB-binding protein (CBP) further enhanced Rta-dependent DcR3 expression, suggesting Rta-dependent DcR3 transcription activity is mediated by CBP. Previously Rta was shown to enhance phophatidylinositol-3 kinase (PI3-K) activity. However, Rta-transduced PI3-K activity plays a minor role in DcR3 expression. This is the first report to demonstrate Rta upregulates a cellular gene by direct binding to an RRE.

This article has been cited by other articles:

• Levine, S. J. (2008). Molecular Mechanisms of Soluble Cytokine Receptor Generation. J. Biol. Chem. 283: 14177-14181 [Abstract] [Full Text]  
• Hsu, M., Wu, S.-Y., Chang, S.-S., Su, I.-J., Tsai, C.-H., Lai, S.-J., Shiau, A.-L., Takada, K., Chang, Y. (2008). Epstein-Barr Virus Lytic Transactivator Zta Enhances Chemotactic Activity through Induction of Interleukin-8 in Nasopharyngeal Carcinoma Cells. J. Virol. 82: 3679-3688 [Abstract] [Full Text]