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Originally published In Press as doi:10.1074/jbc.M003758200 on October 16, 2000

J. Biol. Chem., Vol. 276, Issue 2, 984-992, January 12, 2001
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Characterization of Intercellular Adhesion Molecule-1 Regulation by Epstein-Barr Virus-encoded Latent Membrane Protein-1 Identifies Pathways That Cooperate with Nuclear Factor kappa B to Activate Transcription*

Anja M. Mehl, J. Eike FloettmannDagger , Matthew Jones, Paul Brennan, and Martin Rowe§

From the Department of Medicine, Tenovus Building, University of Wales College of Medicine, Cardiff CF14 4XX, United Kingdom

The latent membrane protein-1 (LMP1) of Epstein-Barr virus induces gene transcription, phenotypic changes, and oncogenic transformation. One cellular gene induced by LMP1 is that for intercellular adhesion molecule-1 (ICAM-1), which participates in a wide range of inflammatory and immune responses. ICAM-1 may enhance the immune recognition of cells transformed by Epstein-Barr virus, and thus combat development of malignancy. Despite growing understanding of the various signaling functions of LMP1, the molecular mechanisms by which LMP1 induces ICAM-1 are not understood. Here, we demonstrate that transcriptional activation by LMP1 is absolutely dependent upon a variant NF-kappa B motif within the tumor necrosis factor alpha  (TNFalpha ) response element of the ICAM-1 promoter. Although the TNFalpha response element is sufficient for TNFalpha induction of the ICAM-1 promoter, LMP1 also required the cooperation of additional upstream sequences for optimal induction. Inhibitor studies of known LMP1-induced signaling pathways ruled out the involvement of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase, and the Janus-activating tyrosine kinase 3 (JAK3), and confirmed NF-kappa B as a critical factor for induction of ICAM-1. However, although constitutive activation of NF-kappa B efficiently induced promoter activity, it was not sufficient to induce either ICAM-1 mRNA or ICAM-1 protein. Using signaling defective LMP1 mutants and deacetylation inhibitors, we showed that the C-terminal activator region 1 of LMP1 delivers a new cooperating signal to induce ICAM-1 mRNA.

* This work was supported by EC BioMed-2 Program Grant BMH4-97-2567, by Leukaemia Research Fund (London) Grants 9533 and 9842, and by a grant from the Wellcome Trust.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Present address: Dept. of Biochemistry, Astra-Zeneca, Loughborough LE11 5RH, United Kingdom.

§ To whom correspondence should be addressed. Tel.: 44-2920-742579; Fax: 44-2920-743868; E-mail: rowem@cf.ac.uk.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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