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    SLC26A6 solute carrier family 26 member 6 [ Homo sapiens (human) ]

    Gene ID: 65010, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Up-Regulation of SLC26A6 in Hepatocellular Carcinoma and Its Diagnostic and Prognostic Significance.

    Up-Regulation of SLC26A6 in Hepatocellular Carcinoma and Its Diagnostic and Prognostic Significance.
    Zhu Y, Huang Y, Chen L, Guo L, Wang L, Li M, Liang Y.

    03/19/2022
    Characterization of pendrin in urinary extracellular vesicles in a rat model of aldosterone excess and in human primary aldosteronism.

    Characterization of pendrin in urinary extracellular vesicles in a rat model of aldosterone excess and in human primary aldosteronism.
    Ochiai-Homma F, Kuribayashi-Okuma E, Tsurutani Y, Ishizawa K, Fujii W, Odajima K, Kawagoe M, Tomomitsu Y, Murakawa M, Asakawa S, Hirohama D, Nagura M, Arai S, Yamazaki O, Tamura Y, Fujigaki Y, Nishikawa T, Shibata S., Free PMC Article

    01/29/2022
    SLC26A6 and NADC1: Future direction of nephrolithiasis and calculusrelated hypertension research (Review).

    SLC26A6 and NADC‑1: Future direction of nephrolithiasis and calculus‑related hypertension research (Review).
    Yang X, Yao S, An J, Jin H, Wang H, Tuo B.

    01/8/2022
    TNFalpha and IL-17 alkalinize airway surface liquid through CFTR and pendrin.

    TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin.
    Rehman T, Thornell IM, Pezzulo AA, Thurman AL, Romano Ibarra GS, Karp PH, Tan P, Duffey ME, Welsh MJ., Free PMC Article

    10/24/2020
    Novel SLC26A6 gene polymorphism rs184187143 is associated with diabetic ketoacidosis of gestational diabetes.

    Novel SLC26A6 gene polymorphism rs184187143 is associated with diabetic ketoacidosis of gestational diabetes.
    Zhang FM, Tian SX, Geng Y, Wei CL, Li N, Zhang XG, Xie JP.

    10/10/2020
    In colonic epithelial cells, microRNA-125a-5p can modulate PAT-1 expression posttranscriptionally via mRNA degradation.

    miR-125a-5p: a novel regulator of SLC26A6 expression in intestinal epithelial cells.
    Anbazhagan AN, Priyamvada S, Borthakur A, Saksena S, Gill RK, Alrefai WA, Dudeja PK., Free PMC Article

    03/28/2020
    pendrin mediates most HCO3(-) secretion across airway surface epithelium during inflammation and enhances electrogenic chloride secretion via CFTR.

    Pendrin Mediates Bicarbonate Secretion and Enhances Cystic Fibrosis Transmembrane Conductance Regulator Function in Airway Surface Epithelia.
    Kim D, Huang J, Billet A, Abu-Arish A, Goepp J, Matthes E, Tewfik MA, Frenkiel S, Hanrahan JW.

    02/22/2020
    ADO inhibits oxalate transport by reducing PAT1 surface expression as shown by biotinylation studies. We conclude that ADO inhibits oxalate transport by lowering PAT1 surface expression in C2 cells through signaling pathways including the A2B AR, PKC, and phospholipase C

    Adenosinergic signaling inhibits oxalate transport by human intestinal Caco2-BBE cells through the A(2B) adenosine receptor.
    Jung D, Alshaikh A, Ratakonda S, Bashir M, Amin R, Jeon S, Stevens J, Sharma S, Ahmed W, Musch M, Hassan H., Free PMC Article

    07/6/2019
    IL13 increases pendrin abundance to the cell surface via Rho/actin signaling, an effect reversed by theophylline.

    Interleukin-13 increases pendrin abundance to the cell surface in bronchial NCI-H292 cells via Rho/actin signaling.
    Russo A, Ranieri M, Di Mise A, Dossena S, Pellegrino T, Furia E, Nofziger C, Debellis L, Paulmichl M, Valenti G, Tamma G.

    12/22/2018
    Results indicate that the variant G539R in the SLC26A6 gene is associated with kidney stone risk, providing a clear clue to further achieve insight into oxalate transport in kidney stone formation.

    In Silico Screening and Molecular Dynamic Study of Nonsynonymous Single Nucleotide Polymorphisms Associated with Kidney Stones in the SLC26A6 Gene.
    Lu X, Sun D, Xu B, Pan J, Wei Y, Mao X, Yu D, Liu H, Gao B.

    08/11/2018
    Results indicate the involvement of SLC26A6 along with SLC26A3 in transporting HCO3(-) essential for embryo cleavage, possibly working in concert with CFTR through a Cl(-) recycling pathway.

    Involvement of Cl(-)/HCO3(-) exchanger SLC26A3 and SLC26A6 in preimplantation embryo cleavage.
    Lu YC, Yang J, Fok KL, Ye YH, Jin L, Chen ZY, Zhang XM, Huang HF, Chan HC., Free PMC Article

    05/5/2018
    Endogenous oestrogen upregulates the expressions and functional activities of CFTR and SLC26A6 in duodenal mucosa.

    Oestrogen upregulates the expression levels and functional activities of duodenal mucosal CFTR and SLC26A6.
    Jin H, Wen G, Deng S, Wan S, Xu J, Liu X, Xie R, Dong H, Tuo B.

    12/30/2017
    IL-4 induces demethylation of specific CpG sites within the pendrin promoter. These epigenetic alterations are cell type specific, and may in part dictate pendrin mRNA transcription

    Interleukin-4 Induces CpG Site-Specific Demethylation of the Pendrin Promoter in Primary Human Bronchial Epithelial Cells.
    Scantamburlo G, Vanoni S, Dossena S, Soyal SM, Bernardinelli E, Civello DA, Patsch W, Paulmichl M, Nofziger C.

    06/24/2017
    Helicobacter pylori infection impairs the expressions and functional activities of duodenal mucosal bicarbonate transport proteins, CFTR and SLC26A6, which contributes to the development of duodenal ulcer.

    Effects of Helicobacter pylori Infection on the Expressions and Functional Activities of Human Duodenal Mucosal Bicarbonate Transport Proteins.
    Wen G, Jin H, Deng S, Xu J, Liu X, Xie R, Tuo B.

    02/18/2017
    Molecular dynamics simulations of the STAS domains of rat prestin and human pendrin reveal conformational motions in conserved flexible regions.

    Molecular dynamics simulations of the STAS domains of rat prestin and human pendrin reveal conformational motions in conserved flexible regions.
    Sharma AK, Zelikovic I, Alper SL.

    08/6/2016
    Data show that SLC26A6 variants do not alter the risk for the development of chronic pancreatitis.

    Genetic analysis of the bicarbonate secreting anion exchanger SLC26A6 in chronic pancreatitis.
    Balázs A, Ruffert C, Hegyi E, Hritz I, Czakó L, Takács T, Szepes Z, Németh BC, Gervain J, Izbéki F, Halász A, Kelemen D, Szmola R, Novák J, Crai S, Illés A, Vincze Á, Molnár Z, Varga M, Bod B, Farkas G Jr, Sümegi J, Szepes A, Dubravcsik Z, Lásztity N, Párniczky A, Hamvas J, Andorka C, Veres G, Szentkereszty Z, Rakonczay Z Jr, Maléth J, Sahin-Tóth M, Rosendahl J, Hegyi P, Hungarian Pancreatic Study Group.

    07/30/2016
    In the intestinal epithelium, PAT-1 (SLC26A6) could mediate apical oxalate influx or apical oxalate efflux depending on the magnitude and direction prevailing counterion driver gradients as well as the relative affinities of the transported anions.

    Parsing apical oxalate exchange in Caco-2BBe1 monolayers: siRNA knockdown of SLC26A6 reveals the role and properties of PAT-1.
    Freel RW, Morozumi M, Hatch M., Free PMC Article

    07/12/2010
    lysophosphatidic acid stimulates apical Cl(-)/OH(-) exchange activity and surface levels of SCL26A3 and SCL26A6 in intestinal epithelial cells

    Mechanisms of lysophosphatidic acid (LPA) mediated stimulation of intestinal apical Cl-/OH- exchange.
    Singla A, Dwivedi A, Saksena S, Gill RK, Alrefai WA, Ramaswamy K, Dudeja PK., Free PMC Article

    02/22/2010
    Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator)

    Identification of neuroglycan C and interacting partners as potential susceptibility genes for schizophrenia in a Southern Chinese population.
    So HC, Fong PY, Chen RY, Hui TC, Ng MY, Cherny SS, Mak WW, Cheung EF, Chan RC, Chen EY, Li T, Sham PC.

    12/2/2009
    Though the SLC26A6 206M polymorphism did not correlate with kidney stone development in primary hyperparathyroidism, PHPT stone-formers harbouring the M allele had a lower hypercalciuria

    Analysis of the 206M polymorphic variant of the SLC26A6 gene encoding a Cl- oxalate transporter in patients with primary hyperparathyroidism.
    Corbetta S, Eller-Vainicher C, Frigerio M, Valaperta R, Costa E, Vicentini L, Baccarelli A, Beck-Peccoz P, Spada A, Corbetta S, Eller-Vainicher C, Frigerio M, Valaperta R, Costa E, Vicentini L, Baccarelli A, Beck-Peccoz P, Spada A.

    01/21/2010
    involvement of IRF-1 in the regulation of SLC26A6 gene expression by IFNgamma in the human intestine

    Characterization of the 5'-flanking region and regulation of expression of human anion exchanger SLC26A6.
    Saksena S, Dwivedi A, Singla A, Gill RK, Tyagi S, Borthakur A, Alrefai WA, Ramaswamy K, Dudeja PK., Free PMC Article

    01/21/2010
    SLC26A6 was effectively ruled out as the disease gene in this non-PH1/PH2 cohort. Phenotypic and functional analysis excluded a significant effect of identified variants on oxalate excretion.

    Phenotypic and functional analysis of human SLC26A6 variants in patients with familial hyperoxaluria and calcium oxalate nephrolithiasis.
    Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS, Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS., Free PMC Articles: PMC2710965, PMC2710965

    01/21/2010
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (2) articles

    Analysis of the 206M polymorphic variant of the SLC26A6 gene encoding a Cl- oxalate transporter in patients with primary hyperparathyroidism.
    Corbetta S, Eller-Vainicher C, Frigerio M, Valaperta R, Costa E, Vicentini L, Baccarelli A, Beck-Peccoz P, Spada A, Corbetta S, Eller-Vainicher C, Frigerio M, Valaperta R, Costa E, Vicentini L, Baccarelli A, Beck-Peccoz P, Spada A.

    Phenotypic and functional analysis of human SLC26A6 variants in patients with familial hyperoxaluria and calcium oxalate nephrolithiasis.
    Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS, Monico CG, Weinstein A, Jiang Z, Rohlinger AL, Cogal AG, Bjornson BB, Olson JB, Bergstralh EJ, Milliner DS, Aronson PS.

    11/5/2008
    Low extracellular Cl(-) affinity and electroneutrality of oxalate efflux characterizing human SLC26A6 explain the high human susceptibility to nephrolithiasis relative to mice. SLC26A6 sequence variant(s) are candidate risk modifiers for nephrolithiasis.

    Species differences in Cl- affinity and in electrogenicity of SLC26A6-mediated oxalate/Cl- exchange correlate with the distinct human and mouse susceptibilities to nephrolithiasis.
    Clark JS, Vandorpe DH, Chernova MN, Heneghan JF, Stewart AK, Alper SL., Free PMC Article

    01/21/2010
    No mutation was found in the coding regions and intron-exon boundaries of the genes for CA II, CA IV, CA XIV, kNCB1, NHE3, NHE8, NHRF1, NHRF2 and SLC26A6 amplified from genomic DNA of family members with pRTA.

    Familial pure proximal renal tubular acidosis--a clinical and genetic study.
    Katzir Z, Dinour D, Reznik-Wolf H, Nissenkorn A, Holtzman E.

    01/21/2010
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