Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/74840
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampCalegari, Vivian Cristinept_BR
dc.contributor.authorunicampPicardi, Paty Karollpt_BR
dc.contributor.authorunicampInoue, Rosana Yuript_BR
dc.contributor.authorunicampFranchini, Kleber Gomespt_BR
dc.contributor.authorunicampVelloso, Lício Augustopt_BR
dc.contributor.authorunicampSaad, Mário José Abdallapt_BR
dc.typeArtigopt_BR
dc.titleSuppressor of cytokine signaling-3 provides a novel interface in the cross-talk between angiotensin II and insulin signaling systemspt_BR
dc.title.alternativeen
dc.contributor.authorVelloso, L.A.pt_BR
dc.contributor.authorCalegari, V.C.pt_BR
dc.contributor.authorSaad, M.J.A.pt_BR
dc.contributor.authorAlves, M.pt_BR
dc.contributor.authorInoue, R.Y.pt_BR
dc.contributor.authorPicardi, P.K.pt_BR
dc.contributor.authorFranchini, K.G.pt_BR
unicamp.author.emaillavelloso@fcm.unicamp.brpt_BR
unicamp.authorUniv Estadual Campinas, Dept Internal Med, BR-13081970 Campinas, SP, Brazilpt_BR
dc.subjectAngiotensina IIpt_BR
dc.subjectProteínas de ligação a DNApt_BR
dc.subjectExpressão gênicapt_BR
dc.subjectMiócitos cardíacospt_BR
dc.subject.otherlanguageAngiotensin IIpt_BR
dc.subject.otherlanguageDNA-binding proteinspt_BR
dc.subject.otherlanguageGene expressionpt_BR
dc.subject.otherlanguageMyocytes, Cardiacpt_BR
dc.subject.wosRat Cardiac Myocytespt_BR
dc.subject.wosPhosphatidylinositol 3-kinasept_BR
dc.subject.wosTyrosine Phosphorylationpt_BR
dc.subject.wosReceptor Substrate-1pt_BR
dc.subject.wosConverting Enzymept_BR
dc.subject.wosPotential Rolept_BR
dc.subject.wosMuscle-cellspt_BR
dc.subject.wosIntact Ratpt_BR
dc.subject.wosResistancept_BR
dc.subject.wosGlucosept_BR
dc.description.abstractAngiotensin II inhibits insulin-induced activation of phosphatidylinositol 3-kinase through a mechanism, at least in part, dependent on serine phosphorylation of the insulin receptor and insulin receptor substrates (IRS)-1/2. Recent evidence shows that suppressor of cytokine signaling-3 (SOCS-3) is induced by insulin and angiotensin II and participates in the negative control of further stimulation of each of these signaling systems independently. In the present study, we evaluated the interaction of angiotensin II-induced SOCS-3 with the insulin signaling pathway in the heart of living rats. A single iv dose of angiotensin II promotes a significant increase of SOCS-3 in heart, an effect that lasts up to 180 min. Once induced, SOCS-3 interacts with the insulin receptor, JAK-2, IRS-1, and IRS-2. The inhibition of SOCS-3 expression by a phosphorthioate-modified antisense oligonucleotide partially restores angiotensin II-induced inhibition of insulin-induced insulin receptor, IRS-1 and IRS-2 tyrosine phosphorylation, and IRS-1 and IRS-2 association with p85-phosphatidylinositol 3-kinase and [Ser(473)] phosphorylation of Akt. Moreover, the inhibition of SOCS-3 expression partially reverses angiotensin II-induced inhibition of insulin-stimulated glucose transporter-4 translocation to the cell membrane. These results are reproduced in isolated cardiomyocytes. Thus, SOCS-3 participates, as a late event, in the negative crosstalk between angiotensin II and insulin, producing an inhibitory effect on insulin-induced glucose transporter-4 translocationpt
dc.description.noteo TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.pt
dc.relation.ispartofEndocrinologypt_BR
dc.relation.ispartofabbreviationEndocrinol.pt_BR
dc.publisher.cityCary, NCpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherOxford University Presspt_BR
dc.date.issued2005pt_BR
dc.identifier.citationEndocrinology. Endocrine Soc, v. 146, n. 2, n. 579, n. 588, 2005.pt_BR
dc.language.isoengpt_BR
dc.description.volume146pt_BR
dc.description.issuenumber2pt_BR
dc.description.firstpage579pt_BR
dc.description.lastpage588pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.sourceWOSpt_br
dc.identifier.issn0013-7227pt_BR
dc.identifier.eissn1945-7170pt_BR
dc.identifier.wosidWOS:000226295300008pt_BR
dc.identifier.doi10.1210/en.2004-0466pt_BR
dc.identifier.urlhttps://academic.oup.com/endo/article/146/2/579/2878096pt_BR
dc.description.sponsorshipFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2014-11-14T03:17:31Z
dc.date.available2015-11-26T16:04:02Z-
dc.date.accessioned2014-11-14T03:17:31Z
dc.date.accessioned2015-11-26T16:04:02Z-
dc.description.provenanceMade available in DSpace on 2014-11-14T03:17:31Z (GMT). No. of bitstreams: 1 WOS000226295300008.pdf: 770535 bytes, checksum: a6c0c816ac4e5573763f2100f9014c4f (MD5) Previous issue date: 2005 Bitstreams deleted on 2020-05-18T20:40:45Z: WOS000226295300008.pdf,. Added 1 bitstream(s) on 2020-05-19T14:30:26Z : No. of bitstreams: 2 000226295300008.pdf: 849524 bytes, checksum: 87263cfd104fa08a865dab20dcf910d5 (MD5) WOS000226295300008.pdf.txt: 53540 bytes, checksum: 7bc7798710891a22316f860d7b237e8b (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T16:04:02Z (GMT). No. of bitstreams: 2 WOS000226295300008.pdf: 770535 bytes, checksum: a6c0c816ac4e5573763f2100f9014c4f (MD5) WOS000226295300008.pdf.txt: 53540 bytes, checksum: 7bc7798710891a22316f860d7b237e8b (MD5) Previous issue date: 2005en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/74840pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/74840
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/74840-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.description.abstractalternative-
dc.identifier.source000226295300008-
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-0190-6635pt_BR
dc.creator.orcid0000-0003-4544-6105pt_BR
dc.creator.orcid0000-0002-4806-7218pt_BR
dc.type.formArtigo original-
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