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dc.creatorOussaief, Lassad
dc.creatorRamírez Mayorga, Vanessa
dc.creatorHippocrate, Aurélie
dc.creatorArbach, Hratch
dc.creatorCochet, Chantal
dc.creatorProust, Alexis
dc.creatorRaphaël, Martine
dc.creatorKhelifa, Ridha
dc.creatorJoab, Irène
dc.description.abstractTransforming growth factor beta 1 (TGF-β1) signal transduction has been implicated in many second-messenger pathways, including the NF-κB pathway. We provide evidence of a novel TGF-β1-mediated pathway that leads to extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, which in turn induces expression of an Epstein-Barr virus (EBV) protein, ZEBRA, that is responsible for the induction of the viral lytic cycle. This pathway includes two unexpected steps, both of which are required to control ERK 1/2 phosphorylation: first, a quick and transient activation of NF-κB, and second, downregulation of inducible nitric oxide synthase (iNOS) activity that requires the participation of NF-κB activity. Although necessary, NF-κB alone is not sufficient to produce downregulation of iNOS, suggesting that another uncharacterized event(s) is involved in this pathway. Dissection of the steps involved in the switch from the EBV latent cycle to the lytic cycle will be important to understand how virus-host relationships modulate the innate immune system.es_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.sourceJournal of Virol, vol. 85(13), pp. 6502–6512es_ES
dc.subjectNitric Oxide Synthasees_ES
dc.subjectGrowth Factores_ES
dc.subjectBeta 1es_ES
dc.subject579. 2 Virus y organismos subviraleses_ES
dc.titleNF-κB-Mediated Modulation of Inducible Nitric Oxide Synthase Activity Controls Induction of the Epstein-Barr Virus Productive Cycle by Transforming Growth Factor Beta 1es_ES
dc.description.procedenceUCR::Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto de Investigaciones en Salud (INISA)es_ES

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internacional