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Journal of Virology, May 2009, p. 5269-5277, Vol. 83, No. 10
0022-538X/09/$08.00+0     doi:10.1128/JVI.00097-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The LMP1 Promoter Can Be Transactivated Directly by NF-{kappa}B{triangledown}

Constantinos Demetriades1 and George Mosialos1,2*

School of Biology, Aristotle University of Thessaloniki, University Campus, 54124 Thessaloniki, Greece,1 Institute of Immunology, Biomedical Sciences Research Center Al. Fleming, 34 Al. Fleming Str., 16672 Vari, Greece2

Received 15 January 2009/ Accepted 17 February 2009

A bioinformatic analysis identified two putative NF-{kappa}B binding sites in the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) promoter. The ability of p65RelA to interact with the LMP1 promoter was shown by in vitro and in vivo assays. Using an EBV-transformed lymphoblastoid cell line as a reporter system for the activity of the +40/–328 LMP1 promoter region, the functional importance of NF-{kappa}B and other transcription factor binding sites was demonstrated. p65RelA could also induce LMP1 expression from the EBV genome in Daudi and P3HR1 Burkitt's lymphoma cell lines. Finally, it was shown that p65RelA could cooperate with EBNA2 or the aryl hydrocarbon receptor in the transactivation of the LMP1 promoter. Our study established the importance of NF-{kappa}B and several cis-acting elements in the regulation of the LMP1 promoter in a latency III environment and highlighted a complex interplay between NF-{kappa}B and other transcription factors in this process.

* Corresponding author. Mailing address: School of Biology, Aristotle University of Thessaloniki, University Campus, 54124 Thessaloniki, Greece. Phone and fax: 302310998907. E-mail: gmosialo{at}bio.auth.gr

{triangledown} Published ahead of print on 11 March 2009.

Journal of Virology, May 2009, p. 5269-5277, Vol. 83, No. 10
0022-538X/09/$08.00+0     doi:10.1128/JVI.00097-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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