Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/57717
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dc.contributor.authorMello da Luz, Marcio Henrique [UNIFESP]
dc.contributor.authorGlezer, Isaias [UNIFESP]
dc.contributor.authorXavier, Andre Machado [UNIFESP]
dc.contributor.authorPaiva da Silva, Marcelo Alberti [UNIFESP]
dc.contributor.authorMonteiro, Jessica [UNIFESP]
dc.contributor.authorPino, Volejnik [UNIFESP]
dc.contributor.authorZamith, Thiago Panaro [UNIFESP]
dc.contributor.authorVieira, Taynara Fernanda [UNIFESP]
dc.contributor.authorAntonio, Bruno Brito [UNIFESP]
dc.contributor.authorMoreira Antunes, Hanna Karen [UNIFESP]
dc.contributor.authorMartins, Vilma Regina
dc.contributor.authorLee, Kil Sun [UNIFESP]
dc.date.accessioned2020-08-14T13:44:32Z-
dc.date.available2020-08-14T13:44:32Z-
dc.date.issued2016
dc.identifierhttp://dx.doi.org/10.1007/s11064-016-1885-1
dc.identifier.citationNeurochemical Research. New York, v. 41, n. 7, p. 1691-1699, 2016.
dc.identifier.issn0364-3190
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57717-
dc.description.abstractCellular prion protein (PrPC) is a glycoprotein of the plasma membrane that plays pleiotropic functions by interacting with multiple signaling complexes at the cell surface. Recently, a number of studies have reported the involvement of PrPC in dopamine metabolism and signaling, including its interactions with tyrosine hydroxylase (TH) and dopamine receptors. However, the outcomes reported by independent studies are still debatable. Therefore in this study, we investigated the effects of PrPC on the TH expression during the differentiation of N2a cells with dibutyryl-cAMP, a well-known cAMP analog that activates TH transcription. Upon differentiation, TH was induced with concomitant reduction of PrPC at protein level, but not at mRNA level. shRNA-mediated PrPC reduction increased the basal level of TH at both mRNA and protein levels without dibutyryl-cAMP treatment. This phenotype was reversed by re-expression of PrPC. PrPC knockdown also potentiated the effect of dibutyryl-cAMP on TH expression. Our findings suggest that PrPC has suppressive effects on TH expression. As a consequence, altered PrPC functions may affect the regulation of dopamine metabolism and related neurological disorders.en
dc.description.sponsorshipFAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo)
dc.description.sponsorshipCAPES (Coordenacao de Aperfeicoamento de pessoal de Nivel Superior)
dc.description.sponsorshipCNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico)
dc.description.sponsorshipEMU (programa de equipamentos multiusuarios)
dc.format.extent1691-1699
dc.language.isoeng
dc.publisherSpringer/Plenum Publishers
dc.relation.ispartofNeurochemical Research
dc.rightsAcesso restrito
dc.subjectCellular prion proteinen
dc.subjectDopamine metabolismen
dc.subjectTyrosine hydroxylaseen
dc.subjectGene expressionen
dc.titleExpression of Tyrosine Hydroxylase is Negatively Regulated Via Prion Proteinen
dc.typeArtigo
dc.description.affiliationUniv Fed Sao Paulo, Dept Bioquim, Edificio Pesquisa 2,Rua Pedro de Toledo 669, BR-04039032 Sao Paulo, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Psicobiol, BR-04039032 Sao Paulo, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Biociencia, BR-04039032 Sao Paulo, SP, Brazil
dc.description.affiliationAC Camargo Canc Ctr, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Bioquim, Edificio Pesquisa 2,Rua Pedro de Toledo 669, BR-04039032 Sao Paulo, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Psicobiol, BR-04039032 Sao Paulo, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Biociencia, BR-04039032 Sao Paulo, SP, Brazil
dc.description.sponsorshipIDFAPESP: 2013/22413-5
dc.description.sponsorshipIDFAPESP: 2013/07937-8
dc.description.sponsorshipIDCNPq: 467566/2014-3
dc.identifier.doi10.1007/s11064-016-1885-1
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000377474000018
dc.coverageNew York
dc.citation.volume41
dc.citation.issue7
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