Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/23032
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dc.contributor.authorPetropoulou, C.en
dc.contributor.authorTrougakos, I. P.en
dc.contributor.authorKolettas, E.en
dc.contributor.authorToussaint, O.en
dc.contributor.authorGonos, E. S.en
dc.date.accessioned2015-11-24T19:30:10Z-
dc.date.available2015-11-24T19:30:10Z-
dc.identifier.issn0014-5793-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23032-
dc.rightsDefault Licence-
dc.subjectAntigens, Differentiation/biosynthesis/genetics/*isolation & purificationen
dc.subjectCell Aging/*physiologyen
dc.subjectClusterinen
dc.subjectDiploidyen
dc.subjectFibroblasts/cytology/*physiologyen
dc.subjectGlycoproteins/biosynthesis/genetics/*isolation & purificationen
dc.subjectHumansen
dc.subjectMolecular Chaperones/biosynthesis/genetics/*isolation & purificationen
dc.subjectOxidative Stress/physiologyen
dc.subjectRecombinant Proteins/biosynthesisen
dc.subjectUp-Regulationen
dc.titleClusterin/apolipoprotein J is a novel biomarker of cellular senescence that does not affect the proliferative capacity of human diploid fibroblastsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11741605-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0014579301031507/1-s2.0-S0014579301031507-main.pdf?_tid=b8d9bc05985860b1f09f7f2a6d2f15ec&acdnat=1333000694_553717e9eac488f82619d39f0617c32e-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2001-
heal.abstractNormal human fibroblasts have a limited replicative potential in culture and eventually reach a state of irreversible growth arrest, termed senescence. In a previous study aiming to identify genes that are differentially regulated during cellular senescence we have cloned clusterin/apolipoprotein J (Apo J), a 80 kDa secreted glycoprotein. In the current report we pursue our studies and show that senescence of human diploid fibroblasts is accompanied by up-regulation of both Apo J mRNA and protein levels, but with no altered biogenesis, binding partner profile or intracellular distribution of the two Apo J forms detected. To analyze the causal relationship between senescence and Apo J protein accumulation, we stably overexpressed the Apo J gene in primary as well as in SV40 T antigen-immortalized human fibroblasts and we showed no alteration of the proliferative capacity of the transduced cells. Despite previous reports on tumor-derived cell lines, overexpression of Apo J in human fibroblasts did not provide protection against apoptosis or growth arrest induced by hydrogen peroxide. Overall, our results suggest that Apo J overexpression does not induce senescence but it is rather a secondary consequence of the senescence phenotype. To our knowledge this is the first report that provides a functional analysis of human Apo J during replicative senescence.en
heal.journalNameFEBS Letten
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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