ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011
Analysis of cellular localization and function of carboxy-terminal mutants of pendrin.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Comparative analysis of functional assay evidence use by ClinGen Variant Curation Expert Panels.Genome medicine · 2019Pooled it
- The ZBTB16/CUL3/ROC1 ubiquitin ligase drives the degradation of pathogenic pendrin (SLC26A4) protein variants.Journal of biomedical science · 2026Article
- Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7.Communications biology · 2019Article
- Expert specification of the ACMG/AMP variant interpretation guidelines for genetic hearing loss.Human mutation · 2018Article
- A Novel Frameshift Mutation ofClinical and experimental otorhinolaryngology · 2017Article
- Atrophic thyroid follicles and inner ear defects reminiscent of cochlear hypothyroidism in Slc26a4-related deafness.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- Protein phosphatase 1 coordinates CFTR-dependent airway epithelial HCO3- secretion by reciprocal regulation of apical and basolateral membrane Cl(-)-HCO3- exchangers.British journal of pharmacology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIodide uptake at the basolateral membrane and iodide efflux at the apical membrane of thyrocytes, essential steps in the biosynthesis of thyroid hormone, are stimulated by thyroid stimulating hormone (TSH). Pendrin (SLC26A4) is inserted into the apical membrane of thyrocytes and thought to be involved in mediating iodide efflux.
methodsWe determined the effects of carboxy-terminal mutations of pendrin on the cellular localization and the ability to transport iodide.
resultsAfter exposure to forskolin, the membrane abundance of wild type pendrin and iodide efflux increase. Truncation mutants lead to complete intracellular retention. Elimination of the distal part of the sulfate transporter and antisigma factor antagonist (STAS) domain with retention of the putative protein kinase A (PKA) phosphorylation site (RKDT 714-717) results in residual membrane insertion and a partial loss of function. Deletion of the PKA site results in decreased basal function and membrane insertion and abolishes the response to forskolin.
conclusionPendrin membrane abundance and its ability to mediate iodide efflux increase after activation of the PKA pathway. Elimination of the PKA site abolishes the response to forskolin but partial basal function and membrane insertion are maintained.
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