Pendrin, the protein encoded by the Pendred syndrome gene (PDS), is an apical porter of iodide in the thyroid and is regulated by thyroglobulin in FRTL-5 cells.
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Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretionWNK4 regulates apical and basolateral Cl- flux in extrarenal epitheliaTranscriptional control of SLC26A4 is involved in Pendred syndrome and nonsyndromic enlargement of vestibular aqueduct (DFNB4)In Vivo Noninvasive Imaging for Gene TherapyLoss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model.Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway DiseasesGenetic disorders coupled to ROS deficiencyThyroid iodide efflux: a team effort?Collecting duct intercalated cell function and regulationControversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cellsDifferences in the pathogenicity of the p.H723R mutation of the common deafness-associated SLC26A4 gene in humans and miceQTL Mapping of Endocochlear Potential Differences between C57BL/6J and BALB/cJ mice.Further characterisation of the recently described SLC26A4 c.918+2T>C mutation and reporting of a novel variant predicted to be damaging.KCNK5 channels mostly expressed in cochlear outer sulcus cells are indispensable for hearingIntegration of human and mouse genetics reveals pendrin function in hearing and deafnessTranscriptional regulation of the pendrin gene.Localization and functional studies of pendrin in the mouse inner ear provide insight about the etiology of deafness in pendred syndrome.Comprehensive molecular etiology analysis of nonsyndromic hearing impairment from typical areas in China.Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.Macrophage invasion contributes to degeneration of stria vascularis in Pendred syndrome mouse modelThyroglobulin increases thyroid cell proliferation via the suppression of specific microRNAs.Iodine excess as an environmental risk factor for autoimmune thyroid disease.Common molecular etiologies are rare in nonsyndromic Tibetan Chinese patients with hearing impairment.Efficient molecular genetic diagnosis of enlarged vestibular aqueducts in East Asians.Epithelial anion transporter pendrin contributes to inflammatory lung pathology in mouse models of Bordetella pertussis infectionTargeting of the hair cell proteins cadherin 23, harmonin, myosin XVa, espin, and prestin in an epithelial cell model.Altered ion transport by thyroid epithelia from CFTR(-/-) pigs suggests mechanisms for hypothyroidism in cystic fibrosis.The sodium iodide symporter and thyroid disease.Hearing loss associated with enlargement of the vestibular aqueduct: mechanistic insights from clinical phenotypes, genotypes, and mouse models.Origins and frequencies of SLC26A4 (PDS) mutations in east and south Asians: global implications for the epidemiology of deafnessGenetics of congenital hypothyroidismMouse models for pendrin-associated loss of cochlear and vestibular functionSLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueduct.TSH regulates pendrin membrane abundance and enhances iodide efflux in thyroid cells.Probing the Effect of Two Heterozygous Mutations in Codon 723 of SLC26A4 on Deafness Phenotype Based on Molecular Dynamics SimulationsModulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and ApigeninPropylthiouracil increases sodium/iodide symporter gene expression and iodide uptake in rat thyroid cells in the absence of TSH.Regulation of dual oxidase expression and H2O2 production by thyroglobulin.Pendred syndrome in two Galician families: insights into clinical phenotypes through cellular, genetic, and molecular studies.Developmental expression of solute carrier family 26A member 4 (SLC26A4/pendrin) during amelogenesis in developing rodent teeth
P2860
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P2860
Pendrin, the protein encoded by the Pendred syndrome gene (PDS), is an apical porter of iodide in the thyroid and is regulated by thyroglobulin in FRTL-5 cells.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
@zh-sg
2000年學術文章
@yue
2000年學術文章
@zh
2000年學術文章
@zh-hant
name
Pendrin, the protein encoded b ...... thyroglobulin in FRTL-5 cells.
@en
type
label
Pendrin, the protein encoded b ...... thyroglobulin in FRTL-5 cells.
@en
prefLabel
Pendrin, the protein encoded b ...... thyroglobulin in FRTL-5 cells.
@en
P2093
P356
P1433
P1476
Pendrin, the protein encoded b ...... thyroglobulin in FRTL-5 cells.
@en
P2093
P304
P356
10.1210/EN.141.2.839
P407
P577
2000-02-01T00:00:00Z