Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20308
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dc.contributor.authorDamalas, A.en
dc.contributor.authorVelimezi, G.en
dc.contributor.authorKalaitzakis, A.en
dc.contributor.authorLiontos, M.en
dc.contributor.authorPapavassiliou, A. G.en
dc.contributor.authorGorgoulis, V.en
dc.contributor.authorAngelidis, C.en
dc.date.accessioned2015-11-24T19:06:10Z-
dc.date.available2015-11-24T19:06:10Z-
dc.identifier.issn1097-0215-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20308-
dc.rightsDefault Licence-
dc.subject*Apoptosisen
dc.subjectBlotting, Westernen
dc.subjectCell Proliferationen
dc.subjectFlow Cytometryen
dc.subjectGene Expression Regulation, Neoplasticen
dc.subjectHSP72 Heat-Shock Proteins/genetics/*metabolismen
dc.subject*Heat-Shock Responseen
dc.subjectHumansen
dc.subjectImmunoprecipitationen
dc.subjectLuciferases/metabolismen
dc.subjectNeoplasms/genetics/metabolism/pathologyen
dc.subject*Oxidative Stressen
dc.subjectRNA, Messenger/geneticsen
dc.subjectRNA, Small Interfering/geneticsen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectTumor Cells, Cultureden
dc.subjectTumor Suppressor Protein p14ARF/antagonists & inhibitors/genetics/*metabolismen
dc.subjectUp-Regulationen
dc.subjectbeta Catenin/genetics/*metabolismen
dc.titleLoss of p14(ARF) confers resistance to heat shock- and oxidative stress-mediated cell death by upregulating beta-cateninen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1002/ijc.25510-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/20549705-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1002/ijc.25510/asset/25510_ftp.pdf?v=1&t=h0dnm3ch&s=b5f169b405f087425a8f2063963cd2f6259f404d-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2011-
heal.abstractThe p14(ARF) is a key tumor suppressor induced mainly by oncogenic stimuli. Although p14(ARF) does not seem to respond to DNA damage, there are very few data regarding its role in other forms of stress, such as heat shock (HS) and oxidative stress (OS). Here, we report that suppression of p14(ARF) increased resistance to cell death when cells were treated with H(2) O(2) or subjected to HS. In this setting, protection from cell death was mediated by elevated levels and activity of beta-catenin, as downregulation of beta-catenin alleviated the protective role of p14(ARF) silencing. Moreover, Hsp70 was shown to regulate beta-catenin protein levels by interacting with p14(ARF) , suggesting that Hsp70, p14(ARF) and beta-catenin form a regulatory network. This novel pathway triggers cell death signals when cells are exposed to HS and OS.en
heal.journalNameInt J Canceren
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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