Conditional up-regulation of IL-2 production by p38 MAPK inactivation is mediated by increased Erk1/2 activity

dc.contributor.authorKogkopoulou, O.en
dc.contributor.authorTzakos, E.en
dc.contributor.authorMavrothalassitis, G.en
dc.contributor.authorBaldari, C. T.en
dc.contributor.authorPaliogianni, F.en
dc.contributor.authorYoung, H. A.en
dc.contributor.authorThyphronitis, G.en
dc.date.accessioned2015-11-24T16:33:44Z
dc.date.available2015-11-24T16:33:44Z
dc.identifier.issn0741-5400-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7701
dc.rightsDefault Licence-
dc.subjectt lymphocytesen
dc.subjectprotein kinasesen
dc.subjecttranscription factorsen
dc.subjectsignal transductionen
dc.subjectactivated protein-kinaseen
dc.subjectt-cell-activationen
dc.subjectsignal-transduction pathwaysen
dc.subjectnuclear factoren
dc.subjectinhibitionen
dc.subjectexpressionen
dc.subjecttranscriptionen
dc.subjectstimulationen
dc.subjectdifferentiationen
dc.subjectcomponentsen
dc.titleConditional up-regulation of IL-2 production by p38 MAPK inactivation is mediated by increased Erk1/2 activityen
heal.abstractThe p38 mitogen-activated protein kinase regulates many cellular processes in almost all eukaryotic cell types. In T cells, p38 was shown to regulate thymic development and cytokine production. Here, the role of p38 on interleukin-2 (IL-2) production by human peripheral blood CD4(+) T cells was examined. When T cells were stimulated under weak stimulation conditions, pharmaceutical and molecular p38 inhibitors induced a dramatic increase of IL-2 production. In contrast, IL-2 levels were not affected significantly when strong stimulation was provided to T cells. The increase in IL-2 production, following p38 inhibition, was associated with a strong up-regulation of extracellular signal-regulated kinase (Erk)1/2 activity. Furthermore the Erk inhibitor U0126 was able to counteract the effect of p38 inhibition on IL-2 production, supporting the conclusion that p38 mediates its effect through Erk. These results suggest that the p38 kinase, through its ability to control Erk activation levels, acts as a gatekeeper, which prevents inappropriate IL-2 production. Also, the finding that p38 acts in a strength-of-stimulation-dependent way provides an explanation for previously reported, contradictory results regarding the role of this kinase in IL-2 expression.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primaryDoi 10.1189/Jlb.0705418-
heal.identifier.secondary<Go to ISI>://000243015200020-
heal.identifier.secondaryhttp://www.jleukbio.org/content/79/5/1052.full.pdf-
heal.journalNameJ Leukoc Biolen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate2006-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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