{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T17:52:29Z","timestamp":1791827549772,"version":"4.3.4"},"reference-count":91,"publisher":"The Endocrine Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,3,1]]},"abstract":"<jats:p>Thyroid hormones are essential for normal development and metabolism. Thyroid hormone biosynthesis requires iodide uptake into the thyrocytes and efflux into the follicular lumen, where it is organified on selected tyrosyls of thyroglobulin. Uptake of iodide into the thyrocytes is mediated by an intrinsic membrane glycoprotein, the sodium-iodide symporter (NIS), which actively cotransports two sodium cations per each iodide anion. NIS-mediated transport of iodide is driven by the electrochemical sodium gradient generated by the Na+\/K+-ATPase. NIS is expressed in the thyroid, the salivary glands, gastric mucosa, and the lactating mammary gland. TSH and iodide regulate iodide accumulation by modulating NIS activity via transcriptional and posttranscriptional mechanisms. Biallelic mutations in the NIS gene lead to a congenital iodide transport defect, an autosomal recessive condition characterized by hypothyroidism, goiter, low thyroid iodide uptake, and a low saliva\/plasma iodide ratio. Pendrin is an anion transporter that is predominantly expressed in the inner ear, the thyroid, and the kidney. Biallelic mutations in the SLC26A4 gene lead to Pendred syndrome, an autosomal recessive disorder characterized by sensorineural deafness, goiter, and impaired iodide organification. In thyroid follicular cells, pendrin is expressed at the apical membrane. Functional in vitro data and the impaired iodide organification observed in patients with Pendred syndrome support a role of pendrin as an apical iodide transporter.<\/jats:p><jats:p>This review shows how the sodium-iodide symporter mediates the active transport of iodide at the basolateral membrane of thyrocytes and discusses biallelic mutations in NIS and the effects of pendrin.<\/jats:p>","DOI":"10.1210\/en.2008-1437","type":"journal-article","created":{"date-parts":[[2009,2,7]],"date-time":"2009-02-07T04:40:17Z","timestamp":1233981617000},"page":"1084-1090","source":"Crossref","is-referenced-by-count":189,"title":["The Sodium-Iodide Symporter NIS and Pendrin in Iodide Homeostasis of the Thyroid"],"prefix":"10.1210","volume":"150","author":[{"given":"Aigerim","family":"Bizhanova","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Metabolism, and Molecular Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kopp","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Metabolism, and Molecular Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2009,2,5]]},"reference":[{"key":"2020071613032576800_R1","doi-asserted-by":"crossref","first-page":"48","DOI":"10.1210\/er.2001-0029","article-title":"The sodium\/iodide symporter (NIS): characterization, regulation, and medical significance.","volume":"24","author":"Dohan","year":"2003","journal-title":"Endocr Rev"},{"key":"2020071613032576800_R2","first-page":"52","author":"Kopp","year":"2005"},{"key":"2020071613032576800_R3","first-page":"77","author":"Arvan","year":"2005"},{"key":"2020071613032576800_R4","doi-asserted-by":"crossref","first-page":"839","DOI":"10.1210\/endo.141.2.7303","article-title":"Pendrin, the protein encoded by the Pendred syndrome gene (PDS), is an apical porter of iodide in the thyroid and is regulated by thyroglobulin in FRTL-5 cells.","volume":"141","author":"Royaux","year":"2000","journal-title":"Endocrinology"},{"key":"2020071613032576800_R5","doi-asserted-by":"crossref","first-page":"440","DOI":"10.1038\/7783","article-title":"The Pendred syndrome gene encodes a chloride-iodide transport protein.","volume":"21","author":"Scott","year":"1999","journal-title":"Nat Genet"},{"key":"2020071613032576800_R6","doi-asserted-by":"crossref","first-page":"458","DOI":"10.1038\/379458a0","article-title":"Cloning and characterization of the thyroid iodide transporter.","volume":"379","author":"Dai","year":"1996","journal-title":"Nature"},{"key":"2020071613032576800_R7","first-page":"904","author":"Mazaferri","year":"2000"},{"key":"2020071613032576800_R8","doi-asserted-by":"crossref","first-page":"339","DOI":"10.1006\/bbrc.1996.1358","article-title":"Cloning of the human sodium iodide symporter.","volume":"226","author":"Smanik","year":"1996","journal-title":"Biochem Biophys Res Commun"},{"key":"2020071613032576800_R9","doi-asserted-by":"crossref","first-page":"3555","DOI":"10.1210\/endo.138.8.5262","article-title":"Expression, exon-intron organization, and chromosome mapping of the human sodium iodide symporter.","volume":"138","author":"Smanik","year":"1997","journal-title":"Endocrinology"},{"key":"2020071613032576800_R10","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1016\/0304-4157(94)90003-5","article-title":"A functional superfamily of sodium\/solute symporters.","volume":"1197","author":"Reizer","year":"1994","journal-title":"Biochim Biophys Acta"},{"key":"2020071613032576800_R11","doi-asserted-by":"crossref","first-page":"22657","DOI":"10.1074\/jbc.273.35.22657","article-title":"N-linked glycosylation of the thyroid Na+\/I\u2212 symporter (NIS). 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