| Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells. | |
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MedLine Citation:
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PMID: 22116361 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Pendred syndrome is an autosomal recessive disorder defined by sensorineural deafness, goiter and a partial organification defect of iodide. It is caused by biallelic mutations in the multifunctional anion transporter pendrin/SLC26A4. In human thyroid tissue, pendrin is localized at the apical membrane of thyroid follicular cells. The clinical phenotype of patients with Pendred syndrome and the fact that pendrin can mediate iodide efflux in transfected cells suggest that this anion exchanger may be involved in mediating iodide efflux into the follicular lumen, a key step in thyroid hormone biosynthesis. This concept has, however, been questioned. This review discusses supporting evidence as well as arguments questioning a role of pendrin in mediating iodide efflux in thyrocytes. |
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Authors:
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Aigerim Bizhanova; Peter Kopp |
Publication Detail:
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Type: Journal Article Date: 2011-11-18 |
Journal Detail:
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Title: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology Volume: 28 ISSN: 1421-9778 ISO Abbreviation: Cell. Physiol. Biochem. Publication Date: 2011 |
Date Detail:
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Created Date: 2011-11-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9113221 Medline TA: Cell Physiol Biochem Country: Switzerland |
Other Details:
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Languages: eng Pagination: 485-90 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 S. Karger AG, Basel. |
Affiliation:
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Division of Endocrinology, Metabolism and Molecular Medicine, Feinberg School of Medicine, Northwestern University, Chicago, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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