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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorOGATA, Fernando Toshio-
dc.contributor.authorBATISTA, Wagner Luiz-
dc.contributor.authorSARTORI, Adriano-
dc.contributor.authorGESTEIRA, Tarsis Ferreira-
dc.contributor.authorMASUTANI, Hiroshi-
dc.contributor.authorARAI, Roberto Jun-
dc.contributor.authorYODOI, Junji-
dc.contributor.authorSTERN, Arnold-
dc.contributor.authorMONTEIRO, Hugo Pequeno-
dc.date.accessioned2014-04-25T22:02:35Z-
dc.date.available2014-04-25T22:02:35Z-
dc.date.issued2013-
dc.identifier.citationPLOS ONE, v.8, n.12, article ID e84588, 16p, 2013-
dc.identifier.issn1932-6203-
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/5212-
dc.description.abstractThioredoxin (TRX-1) is a multifunctional protein that controls the redox status of other proteins. TRX-1 can be found in the extracellular milieu, cytoplasm and nucleus, and it has distinct functions in each environment. Previously, we studied the intracellular localization of TRX-1 and its relationship with the activation of the p21Ras - ERK1/2 MAP Kinases signaling pathway. In situations where this pathway was activated by stress conditions evoked by a nitrosothiol, S-nitroso-N-acetylpenicillamine (SNAP), TRX-1 accumulated in the nuclear compartment due to nitrosylation of p21Ras and activation of downstream ERK1/2 MAP kinases. Presently, we demonstrate that ERK1/2 MAP Kinases activation and spatial distribution within cells trigger TRX-1 nuclear translocation through downregulation of the physiological inhibitor of TRX-1, Thioredoxin Interacting Protein (TXN1P). Once activated by the oxidants, SNAP and H2O2, the ERK1/2 MAP kinases migrate to the nucleus. This is correlated with down-regulation of TXN1P. In the presence of the MEK inhibitors (PD98059 or U0126), or in cells transfected with the Protein Enriched in Astrocytes (PEA-15), a cytoplasmic anchor of ERK1/2 MAP kinases, TRX-1 nuclear migration and TXNIP down-regulation are no longer observed in cells exposed to oxidants. On the other hand, over-expression of TXNIP abolishes nuclear migration of TRX-1 under nitrosative/oxidative stress conditions, whereas gene silencing of TXNIP facilitates nuclear migration even in the absence of stress conditions. Studies based on the TXNIP promoter support this regulation. In conclusion, changes in TRX-1 compartmentalization under nitrosative/oxidative stress conditions are dependent on the expression levels of TXNIP, which are regulated by cellular compartmentalization and activation of the ERK1/2 MAP kinases.-
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo - FAPESP [07/59617-6, 09/52730-7, 12/10470-1, 06/53791-1, 09/50708-4]-
dc.language.isoeng-
dc.publisherPUBLIC LIBRARY SCIENCE-
dc.relation.ispartofPlos One-
dc.rightsopenAccess-
dc.subject.otheraortic endothelial-cells-
dc.subject.othernitric-oxide synthase-
dc.subject.otherredox regulation-
dc.subject.othermap kinase-
dc.subject.othertranscriptional activity-
dc.subject.otheroxidative stress-
dc.subject.otherpc12 cells-
dc.subject.otherbinding-
dc.subject.otherglucose-
dc.subject.otherras-
dc.titleNitrosative/Oxidative Stress Conditions Regulate Thioredoxin-Interacting Protein (TXNIP) Expression and Thioredoxin-1 (TRX-1) Nuclear Localization-
dc.typearticle-
dc.rights.holderCopyright PUBLIC LIBRARY SCIENCE-
dc.identifier.doi10.1371/journal.pone.0084588-
dc.identifier.pmid24376827-
dc.subject.wosMultidisciplinary Sciences-
dc.type.categoryoriginal article-
dc.type.versionpublishedVersion-
hcfmusp.author.externalOGATA, Fernando Toshio:Univ Fed Sao Paulo, Dept Bioquim Biol Mol, Sao Paulo, Brazil; Univ Fed Sao Paulo, CTCMol, Ctr Cellular & Mol Therapy, Sao Paulo, Brazil-
hcfmusp.author.externalBATISTA, Wagner Luiz:Univ Fed Sao Paulo, Dept Ciencias Biol, Sao Paulo, Brazil-
hcfmusp.author.externalSARTORI, Adriano:Univ Fed Sao Paulo, Dept Bioquim Biol Mol, Sao Paulo, Brazil; Univ Fed Sao Paulo, CTCMol, Ctr Cellular & Mol Therapy, Sao Paulo, Brazil-
hcfmusp.author.externalGESTEIRA, Tarsis Ferreira:Univ Fed Sao Paulo, Dept Bioquim Biol Mol, Sao Paulo, Brazil; Univ Fed Sao Paulo, CTCMol, Ctr Cellular & Mol Therapy, Sao Paulo, Brazil-
hcfmusp.author.externalMASUTANI, Hiroshi:Kyoto Univ, Dept Biol Responses, Kyoto, Japan-
hcfmusp.author.externalYODOI, Junji:Kyoto Univ, Dept Biol Responses, Kyoto, Japan-
hcfmusp.author.externalSTERN, Arnold:NYU, Sch Med, Dept Pharmacol, New York, NY USA-
hcfmusp.author.externalMONTEIRO, Hugo Pequeno:Univ Fed Sao Paulo, Dept Bioquim Biol Mol, Sao Paulo, Brazil; Univ Fed Sao Paulo, CTCMol, Ctr Cellular & Mol Therapy, Sao Paulo, Brazil-
hcfmusp.description.articlenumbere84588-
hcfmusp.description.issue12-
hcfmusp.description.volume8-
hcfmusp.origemWOS-
hcfmusp.origem.id2-s2.0-84893186874-
hcfmusp.origem.idWOS:000328745100178-
hcfmusp.publisher.citySAN FRANCISCO-
hcfmusp.publisher.countryUSA-
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dc.description.indexMEDLINE-
hcfmusp.remissive.sponsorshipFAPESP-
hcfmusp.citation.scopus27-
hcfmusp.scopus.lastupdate2022-06-24-
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