vIRF3 encoded by Kaposi's sarcoma-associated herpesvirus inhibits T-cell factor-dependent transcription via a CREB-binding protein interaction motif

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Kaposi's sarcoma-associated herpesvirus (KSHV) is an etiological agent of Kaposi's sarcoma and primary effusion lymphoma. Like other herpesviruses, KSHV has two distinct life cycles: latent and lytic. Among KSHV latent genes, viral interferon regulatory factor 3 (vIRF3), which shares homology with cellular IRFs, is a multifunctional protein. To identify unknown functions of vIRF3, we performed luciferase-reporter assays in the presence of vIRF3. These analyses revealed that overexpression of vIRF3 inhibited T-cell factor (TCF)-dependent transcriptional activity. This TCF-dependent transcription was associated with the Wnt signaling pathway, which normally regulates embryonic development, but contributes to oncogenesis under dysregulated conditions. Using a mutagenesis analysis, we identified a CREB-binding protein-interaction motif (LXXLL) in vIRF3 as an important region for its inhibitory activity. Collectively, our findings provide insight into the dysregulation of host signaling pathways in KSHV-infected cells. (C) 2016 Elsevier Inc. All rights reserved
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Issue Date
2016-10
Language
English
Article Type
Article
Keywords

INTERFERON-REGULATORY FACTOR-3; GENE-EXPRESSION; BETA-CATENIN; LATENT; LANA2; IDENTIFICATION; ACTIVATION; TARGET; SIGNAL; ALPHA

Citation

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.479, no.4, pp.697 - 702

ISSN
0006-291X
DOI
10.1016/j.bbrc.2016.09.150
URI
http://hdl.handle.net/10203/214837
Appears in Collection
BS-Journal Papers(저널논문)
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