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NF kappa B-mediated activation of the cellular FUT3, 5 and 6 gene cluster by herpes simplex virus type 1

Journal article
Authors Rickard Nordén
Ebba Samuelsson
Kristina Nyström
Published in Glycobiology
Volume 27
Issue 11
Pages 999-1005
ISSN 0959-6658
Publication year 2017
Published at Institute of Biomedicine, Department of Infectious Medicine
Pages 999-1005
Language en
Links dx.doi.org/10.1093/glycob/cwx079
Keywords FUT3, FUT5, FUT6, Herpes simplex virus type 1, NF kappa B, fucosyl-transferase genes, dependent protein-kinase, transcriptional, regulation, sialyl-le(x) expression, adhesion molecules, carcinoma, cells, infected cells, lewis enzyme, host, cancer, Biochemistry & Molecular Biology, ates of america, v106, p19491
Subject categories Biochemistry and Molecular Biology

Abstract

Herpes simplex virus type 1 has the ability to induce expression of a human gene cluster located on chromosome 19 upon infection. This gene cluster contains three fucosyltransferases (encoded by FUT3, FUT5 and FUT6) with the ability to add a fucose to an N-acetylglucosamine residue. Little is known regarding the transcriptional activation of these three genes in human cells. Intriguingly, herpes simplex virus type 1 activates all three genes simultaneously during infection, a situation not observed in uninfected tissue, pointing towards a virus specific mechanism for transcriptional activation. The aim of this study was to define the underlying mechanism for the herpes simplex virus type 1 activation of FUT3, FUT5 and FUT6 transcription. The transcriptional activation of the FUT-gene cluster on chromosome 19 in fibroblasts was specific, not involving adjacent genes. Moreover, inhibition of NF kappa B signaling through panepoxydone treatment significantly decreased the induction of FUT3, FUT5 and FUT6 transcriptional activation, as did siRNA targeting of p65, in herpes simplex virus type 1 infected fibroblasts. NF kappa B and p65 signaling appears to play an important role in the regulation of FUT3, FUT5 and FUT6 transcriptional activation by herpes simplex virus type 1 although additional, unidentified, viral factors might account for part of the mechanism as direct interferon mediated stimulation of NF kappa B was not sufficient to induce the fucosyltransferase encoding gene cluster in uninfected cells.

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