title: Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells.
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.
authors: Division of Endocrinology, Metabolism and Molecular Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
authors: Aigerim
authors: A
authors: Bizhanova
authors: Peter
authors: P
authors: Kopp
mesh_terms: D006044:Goiter, Nodular / Q000473:pathology; D006319:Hearing Loss, Sensorineural / Q000473:pathology; D006801:Humans; D007454:Iodides / Q000378:metabolism*; D017136:Ion Transport; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D000076988:Sulfate Transporters; D013961:Thyroid Gland / Q000166:cytology / Q000378:metabolism*; D013963:Thyroid Hormones / Q000096:biosynthesis
chemical_list: D007454:Iodides; D026901:Membrane Transport Proteins; C085609:SLC26A4 protein, human; D000076988:Sulfate Transporters; D013963:Thyroid Hormones