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  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18432
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dc.contributor.authorMarkopoulou, S.en
dc.contributor.authorKontargiris, E.en
dc.contributor.authorBatsi, C.en
dc.contributor.authorTzavaras, T.en
dc.contributor.authorTrougakos, I.en
dc.contributor.authorBoothman, D. A.en
dc.contributor.authorGonos, E. S.en
dc.contributor.authorKolettas, E.en
dc.date.accessioned2015-11-24T18:52:45Z-
dc.date.available2015-11-24T18:52:45Z-
dc.identifier.issn1742-4658-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18432-
dc.rightsDefault Licence-
dc.subjectApoptosis/*drug effectsen
dc.subjectCell Cycle Proteins/metabolismen
dc.subjectCell Lineen
dc.subjectCell Nucleus/*drug effects/*metabolismen
dc.subjectCell Proliferation/drug effectsen
dc.subjectClusterin/genetics/*metabolismen
dc.subjectHumansen
dc.subjectProto-Oncogene Proteins c-bcl-2/genetics/metabolismen
dc.subjectProto-Oncogene Proteins c-fos/genetics/*metabolismen
dc.subjectUp-Regulation/drug effectsen
dc.subjectVanadium/*pharmacologyen
dc.titleVanadium-induced apoptosis of HaCaT cells is mediated by c-fos and involves nuclear accumulation of clusterinen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1111/j.1742-4658.2009.07093.x-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/19531052-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1111/j.1742-4658.2009.07093.x/asset/j.1742-4658.2009.07093.x.pdf?v=1&t=h0dhuokt&s=1c3e3dae0c3fee4b553b3617ec7b7b1eef2fd8e2-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2009-
heal.abstractVanadium exerts a variety of biological effects, including antiproliferative responses through activation of the respective signaling pathways and the generation of reactive oxygen species. As epidermal cells are exposed to environmental insults, human keratinocytes (HaCaT) were used to investigate the mechanism of the antiproliferative effects of vanadyl(IV) sulfate (VOSO(4)). Treatment of HaCaT cells with VOSO(4) inhibited proliferation and induced apoptosis in a dose-dependent manner. Inhibition of proliferation was associated with downregulation of cyclins D1 and E, E2F1, and the cyclin-dependent kinase inhibitors p21(Cip1/Waf1) and p27(Kip1). Induction of apoptosis correlated with upregulation of the c-fos oncoprotein, changes in the expression of clusterin (CLU), an altered ratio of antiapoptotic to proapoptotic Bcl-2 protein family members, and poly(ADP-ribose) polymerase-1 cleavage. Forced overexpression of c-fos induced apoptosis in HaCaT cells that correlated with secretory CLU downregulation and upregulation of nuclear CLU (nCLU), a pro-death protein. Overexpression of Bcl-2 protected HaCaT cells from vanadium-induced apoptosis, whereas secretory CLU overexpression offered no cytoprotection. In contrast, nCLU sensitized HaCaT cells to apoptosis. Our data suggest that vanadium-mediated apoptosis was promoted by c-fos, leading to alterations in CLU isoform processing and induction of the pro-death nCLU protein.en
heal.journalNameFEBS Jen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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