Iodide excess regulates its own efflux: a possible involvement of pendrin. - Wikidata - awgldk - TriplyDB

Iodide excess regulates its own efflux: a possible involvement of pendrin.

Iodide excess regulates its own efflux: a possible involvement of pendrin.

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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen.

P2860

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P2860

Iodide excess regulates its own efflux: a possible involvement of pendrin.

http://www.wikidata.org/entity/Q37148716

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 20 January 2016

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

@en

Iodide excess regulates its own efflux: a possible involvement of pendrin.

@nl

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P356

AJPCELL.00210.2015

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American Journal of Physiology - Cell Physiology

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Iodide excess regulates its own efflux: a possible involvement of pendrin.

@en

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Caroline Serrano-Nascimento

http://www.w3.org/2001/XMLSchema#string

Jamile Calil-Silveira

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Maria Tereza Nunes

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Peter Andreas Kopp

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P2860

The Pendred syndrome gene encodes a chloride-iodide transport protein

Anoctamin 1 is apically expressed on thyroid follicular cells and contributes to ATP- and calcium-activated iodide efflux

Thyroid iodide efflux: a team effort?

Physiological and molecular basis of thyroid hormone action

Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells

Bacterial lipopolysaccharide stimulates the thyrotropin-dependent thyroglobulin gene expression at the transcriptional level by involving the transcription factors thyroid transcription factor-1 and paired box domain transcription factor 8

Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species

Regulation of thyroid oxidative state by thioredoxin reductase has a crucial role in thyroid responses to iodide excess.

Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein.

CHANGES IN THYROIDAL FUNCTION DURING ADAPTATION TO LARGE DOSES OF IODIDE.

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C576-82

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scholarly article

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10.1152/AJPCELL.00210.2015

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P433

7

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310

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2016-01-20T00:00:00Z

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26791486

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4971809

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