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Campo DC Valor Lengua/Idioma
dc.creatorSerrano Nascimento, Caroline-
dc.creatorNicola, Juan Pablo-
dc.creatorda Silva Teixeira, Silvania-
dc.creatorPoyares, Leonice Lourenço-
dc.creatorLellis Santos, Camilo-
dc.creatorBordin, Silvana-
dc.creatorMasini, Ana María-
dc.creatorNunes, Maria Tereza-
dc.date2018-05-30T17:34:30Z-
dc.date2018-05-30T17:34:30Z-
dc.date2016-05-
dc.date2018-05-22T21:49:22Z-
dc.date.accessioned2019-04-29T15:56:32Z-
dc.date.available2019-04-29T15:56:32Z-
dc.identifierSerrano Nascimento, Caroline; Nicola, Juan Pablo; da Silva Teixeira, Silvania; Poyares, Leonice Lourenço; Lellis Santos, Camilo; et al.; Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway; Elsevier Ireland; Molecular and Cellular Endocrinology; 426; 5-2016; 73-90-
dc.identifier0303-7207-
dc.identifierhttp://hdl.handle.net/11336/46658-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/305838-
dc.descriptionTranscriptional mechanisms associated with iodide-induced downregulation of NIS expression remain uncertain. Here, we further analyzed the transcriptional regulation of NIS gene expression by excess iodide using PCCl3 cells. NIS promoter activity was reduced in cells treated for 12-24 h with 10<sup>-5</sup> to 10<sup>-3</sup> M NaI. Site-directed mutagenesis of Pax8 and NF-κB cis-acting elements abrogated the iodide-induced NIS transcription repression. Indeed, excess iodide (10<sup>-3</sup>M) excluded Pax8 from the nucleus, decreased p65 total expression and reduced their transcriptional activity. Importantly, p65-Pax8 physical interaction and binding to NIS upstream enhancer were reduced upon iodide treatment. PI3K/Akt pathway activation by iodide-induced ROS production is involved in the transcriptional repression of NIS expression. In conclusion, the results indicated that excess iodide transcriptionally represses NIS gene expression through the impairment of Pax8 and p65 transcriptional activity. Furthermore, the data presented herein described novel roles for PI3K/Akt signaling pathway and oxidative status in the thyroid autoregulatory phenomenon.-
dc.descriptionFil: Serrano Nascimento, Caroline. Universidade de Sao Paulo; Brasil-
dc.descriptionFil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina-
dc.descriptionFil: da Silva Teixeira, Silvania. Universidade de Sao Paulo; Brasil-
dc.descriptionFil: Poyares, Leonice Lourenço. Universidade de Sao Paulo; Brasil-
dc.descriptionFil: Lellis Santos, Camilo. Universidade de Sao Paulo; Brasil-
dc.descriptionFil: Bordin, Silvana. Universidade de Sao Paulo; Brasil-
dc.descriptionFil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina-
dc.descriptionFil: Nunes, Maria Tereza. Universidade de Sao Paulo; Brasil-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherElsevier Ireland-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1016/j.mce.2016.02.006-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0303720716300338-
dc.rightsinfo:eu-repo/semantics/restrictedAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectEXCESS IODIDE-
dc.subjectNA+/I- SYMPORTER-
dc.subjectREACTIVE OXYGEN SPECIES-
dc.subjectPI3K/AKT PATHWAY-
dc.subjectOtras Ciencias Biológicas-
dc.subjectCiencias Biológicas-
dc.subjectCIENCIAS NATURALES Y EXACTAS-
dc.titleExcess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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