Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux. - Wikidata - wikimedia - TriplyDB

Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux.

Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux.

http://www.wikidata.org/entity/Q40600626

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Thyroid iodide efflux: a team effort?Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells Further characterisation of the recently described SLC26A4 c.918+2T>C mutation and reporting of a novel variant predicted to be damaging.Efficient molecular genetic diagnosis of enlarged vestibular aqueducts in East Asians.SLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueduct.TSH regulates pendrin membrane abundance and enhances iodide efflux in thyroid cells.Lactaturia and loss of sodium-dependent lactate uptake in the colon of SLC5A8-deficient mice.Modulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and Apigenin Developmental expression of solute carrier family 26A member 4 (SLC26A4/pendrin) during amelogenesis in developing rodent teeth Expression of pendrin in benign and malignant human thyroid tissues.Functional assessment of allelic variants in the SLC26A4 gene involved in Pendred syndrome and nonsyndromic EVA Analysis of cellular localization and function of carboxy-terminal mutants of pendrin Functional characterization of pendrin mutations found in the Israeli and Palestinian populations.Pendrin function and regulation in Xenopus oocytes Identification of allelic variants of pendrin (SLC26A4) with loss and gain of function.Minireview: The sodium-iodide symporter NIS and pendrin in iodide homeostasis of the thyroid Iodide excess regulates its own efflux: a possible involvement of pendrin.Reduction of cellular expression levels is a common feature of functionally affected pendrin (SLC26A4) protein variants.Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression.American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Iodine mediated mechanisms and thyroid carcinoma.Genetic causes of nonsyndromic hearing loss in Iran in comparison with other populations.Mis-trafficking of bicarbonate transporters: implications to human diseases.Molecular and functional characterization of human pendrin and its allelic variants.Pendrin: the thyrocyte apical membrane iodide transporter?Thiocyanate: a review and evaluation of the kinetics and the modes of action for thyroid hormone perturbations.Chemistry and Biology in the Biosynthesis and Action of Thyroid Hormones.Functional coupling of TRPC2 cation channels and the calcium-activated anion channels in rat thyroid cells: implications for iodide homeostasis.Combining transfer of TTF-1 and Pax-8 gene: a potential strategy to promote radioiodine therapy of thyroid carcinoma.Pendrin overexpression affects cell volume recovery, intracellular pH and chloride concentration after hypotonicity-induced cell swelling.Fast fluorometric method for measuring pendrin (SLC26A4) Cl-/I- transport activity.Mutation screening of the SLC26A4 gene in a cohort of 192 Chinese patients with congenital hypothyroidism.The Cl-/HCO3- exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance.Identification of two heterozygous deafness mutations in SLC26A4 (PDS) in a Chinese family with two siblings.Iodide Binding in Sodium-Coupled Cotransporters.Distinct and novel SLC26A4/Pendrin mutations in Chinese and U.S. patients with nonsyndromic hearing loss.The Effect on Sodium/Iodide Symporter and Pendrin in Thyroid Colloid Retention Developed by Excess Iodide Intake.Atrophic thyroid follicles and inner ear defects reminiscent of cochlear hypothyroidism in Slc26a4-related deafness.Chemie und Biologie der Schilddrüsenhormon-Biosynthese und -Wirkung Expert specification of the ACMG/AMP variant interpretation guidelines for genetic hearing loss

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P2860

Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux.

http://www.wikidata.org/entity/Q40600626

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2004 nî lūn-bûn

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Functional characterization of ...... mediated apical iodide efflux.

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Functional characterization of ...... mediated apical iodide efflux.

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Aniket R Sidhaye

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Catherine Waeber Stephan

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Eun Jig Lee

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Jonas Rutishauser

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Mary P Gillam

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Peter Kopp

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P2860

The Pendred syndrome gene encodes a chloride-iodide transport protein

Purification of a novel flavoprotein involved in the thyroid NADPH oxidase. Cloning of the porcine and human cdnas

Cloning of two human thyroid cDNAs encoding new members of the NADPH oxidase family

Achondrogenesis type IB is caused by mutations in the diastrophic dysplasia sulphate transporter gene

Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)

Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea

The diastrophic dysplasia gene encodes a novel sulfate transporter: positional cloning by fine-structure linkage disequilibrium mapping

Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion

Non-syndromic hearing loss associated with enlarged vestibular aqueduct is caused by PDS mutations

Prestin is the motor protein of cochlear outer hair cells

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13004-13010

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10.1074/JBC.M313648200

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13

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279

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14715652

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