Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/19773
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dc.contributor.authorLazaridis, I.en
dc.contributor.authorCharalampopoulos, I.en
dc.contributor.authorAlexaki, V. I.en
dc.contributor.authorAvlonitis, N.en
dc.contributor.authorPediaditakis, I.en
dc.contributor.authorEfstathopoulos, P.en
dc.contributor.authorCalogeropoulou, T.en
dc.contributor.authorCastanas, E.en
dc.contributor.authorGravanis, A.en
dc.date.accessioned2015-11-24T19:02:12Z-
dc.date.available2015-11-24T19:02:12Z-
dc.identifier.issn1545-7885-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/19773-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subject*Apoptosisen
dc.subjectDehydroepiandrosterone/*metabolismen
dc.subjectHEK293 Cellsen
dc.subjectHumansen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectNerve Tissue Proteins/genetics/*metabolismen
dc.subjectNeurogenesisen
dc.subjectNeurons/*pathologyen
dc.subjectPC12 Cellsen
dc.subjectPhosphorylationen
dc.subjectPhylogenyen
dc.subjectProto-Oncogene Proteins c-bcl-2/metabolismen
dc.subjectRNA Interferenceen
dc.subjectRatsen
dc.subjectReceptor, trkA/genetics/*metabolismen
dc.subjectReceptors, Nerve Growth Factor/genetics/*metabolismen
dc.subjectSignal Transductionen
dc.subjectTransfectionen
dc.titleNeurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosisen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1371/journal.pbio.1001051-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/21541365-
heal.identifier.secondaryhttp://www.plosbiology.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pbio.1001051&representation=PDF-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2011-
heal.abstractThe neurosteroid dehydroepiandrosterone (DHEA), produced by neurons and glia, affects multiple processes in the brain, including neuronal survival and neurogenesis during development and in aging. We provide evidence that DHEA interacts with pro-survival TrkA and pro-death p75(NTR) membrane receptors of neurotrophin nerve growth factor (NGF), acting as a neurotrophic factor: (1) the anti-apoptotic effects of DHEA were reversed by siRNA against TrkA or by a specific TrkA inhibitor; (2) [(3)H]-DHEA binding assays showed that it bound to membranes isolated from HEK293 cells transfected with the cDNAs of TrkA and p75(NTR) receptors (K(D): 7.4 +/- 1.75 nM and 5.6 +/- 0.55 nM, respectively); (3) immobilized DHEA pulled down recombinant and naturally expressed TrkA and p75(NTR) receptors; (4) DHEA induced TrkA phosphorylation and NGF receptor-mediated signaling; Shc, Akt, and ERK1/2 kinases down-stream to TrkA receptors and TRAF6, RIP2, and RhoGDI interactors of p75(NTR) receptors; and (5) DHEA rescued from apoptosis TrkA receptor positive sensory neurons of dorsal root ganglia in NGF null embryos and compensated NGF in rescuing from apoptosis NGF receptor positive sympathetic neurons of embryonic superior cervical ganglia. Phylogenetic findings on the evolution of neurotrophins, their receptors, and CYP17, the enzyme responsible for DHEA biosynthesis, combined with our data support the hypothesis that DHEA served as a phylogenetically ancient neurotrophic factor.en
heal.journalNamePLoS Biolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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