Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/24561
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dc.contributor.authorThomas, C. G.en
dc.contributor.authorVezyraki, P. E.en
dc.contributor.authorKalfakakou, V. P.en
dc.contributor.authorEvangelou, A. M.en
dc.date.accessioned2015-11-24T19:41:58Z-
dc.date.available2015-11-24T19:41:58Z-
dc.identifier.issn0021-9541-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24561-
dc.rightsDefault Licence-
dc.subjectAntioxidants/pharmacologyen
dc.subjectAscorbic Acid/*pharmacologyen
dc.subjectCell Cycle/*drug effectsen
dc.subjectCell Cycle Proteins/*metabolismen
dc.subjectCell Line, Tumoren
dc.subjectDNA/antagonists & inhibitors/biosynthesisen
dc.subjectEnzyme Activation/drug effectsen
dc.subjectG2 Phase/*drug effectsen
dc.subjectHeLa Cellsen
dc.subjectHumansen
dc.subjectKineticsen
dc.subjectMitosis/*drug effectsen
dc.subjectModels, Biologicalen
dc.subjectS Phase/*drug effectsen
dc.subjectcdc25 Phosphatases/*metabolismen
dc.titleVitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation and the subcellular localization of Cdc25C phosphataseen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1002/jcp.20405-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15887239-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1002/jcp.20405/asset/20405_ftp.pdf?v=1&t=h0c6japx&s=34c2a57cbace42707143596ce9f283f2a7cfacfd-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2005-
heal.abstractRegulation of cell cycle progression involves redox (oxidation-reduction)-dependent modification of proteins including the mitosis-inducing phosphatase Cdc25C. The role of vitamin C (ascorbic acid, ASC), a known modulator of the cellular redox status, in regulating mitotic entry was investigated in this study. We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis. High concentrations of Vitamin C caused transient S and G2 arrest in both cell lines by delaying the activation of the M-phase promoting factor (MPF), Cdc2/cyclin-B complex. Although vitamin C did not inhibit the accumulation of cyclin-B1, it may have increased the level of Cdc2 inhibitory phosphorylation. This was achieved by transiently maintaining Cdc25C, the activator of Cdc2, both in low levels and in a phosphorylated on Ser216 inactive form that binds to 14-3-3 proteins contributing thus to the nuclear exclusion of Cdc25C. As expected, vitamin C prevented the nuclear accumulation of Cdc25C in both cell lines. In conclusion, it seems that vitamin C induces transient cell cycle arrest, at least in part, by delaying the accumulation and the activation of Cdc25C.en
heal.journalNameJ Cell Physiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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