Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells.

Details

Serval ID
serval:BIB_CA5A73C1EF67
Type
Article: article from journal or magazin.
Collection
Publications
Title
Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells.
Journal
Cellular physiology and biochemistry
Author(s)
Bizhanova A., Kopp P.
ISSN
1421-9778 (Electronic)
ISSN-L
1015-8987
Publication state
Published
Issued date
2011
Peer-reviewed
Oui
Volume
28
Number
3
Pages
485-490
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Abstract
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.
Keywords
Goiter, Nodular/pathology, Hearing Loss, Sensorineural/pathology, Humans, Iodides/metabolism, Ion Transport, Membrane Transport Proteins/genetics, Membrane Transport Proteins/metabolism, Mutation, Sulfate Transporters, Thyroid Gland/cytology, Thyroid Gland/metabolism, Thyroid Hormones/biosynthesis
Pubmed
Web of science
Open Access
Yes
Create date
28/12/2020 16:31
Last modification date
29/12/2020 7:26
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