Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Am J Physiol Cell Physiol
2010 Jun 01;2986:C1363-75. doi: 10.1152/ajpcell.00004.2010.
Show Gene links
Show Anatomy links
Regulated transport of sulfate and oxalate by SLC26A2/DTDST.
Heneghan JF
,
Akhavein A
,
Salas MJ
,
Shmukler BE
,
Karniski LP
,
Vandorpe DH
,
Alper SL
.
???displayArticle.abstract???
Nephrolithiasis in the Slc26a6(-/-) mouse is accompanied by 50-75% reduction in intestinal oxalate secretion with unchanged intestinal oxalate absorption. The molecular identities of enterocyte pathways for oxalate absorption and for Slc26a6-independent oxalate secretion remain undefined. The reported intestinal expression of SO(4)(2-) transporter SLC26A2 prompted us to characterize transport of oxalate and other anions by human SLC26A2 and mouse Slc26a2 expressed in Xenopus oocytes. We found that hSLC26A2-mediated [(14)C]oxalate uptake (K(1/2) of 0.65 +/- 0.08 mM) was cis-inhibited by external SO(4)(2-) (K(1/2) of 3.1 mM). hSLC26A2-mediated bidirectional oxalate/SO(4)(2-) exchange exhibited extracellular SO(4)(2-) K(1/2) of 1.58 +/- 0.44 mM for exchange with intracellular [(14)C]oxalate, and extracellular oxalate K(1/2) of 0.14 +/- 0.11 mM for exchange with intracellular (35)SO(4)(2-). Influx rates and K(1/2) values for mSlc26a2 were similar. hSLC26A2-mediated oxalate/Cl(-) exchange and bidirectional SO(4)(2-)/Cl(-) exchange were not detectably electrogenic. Both SLC26A2 orthologs exhibited nonsaturable extracellular Cl(-) dependence for efflux of intracellular [(14)C]oxalate, (35)SO(4)(2-), or (36)Cl(-). Rate constants for (36)Cl(-) efflux into extracellular Cl(-), SO(4)(2-), and oxalate were uniformly 10-fold lower than for oppositely directed exchange. Acidic extracellular pH (pH(o)) inhibited all modes of hSLC26A2-mediated anion exchange. In contrast, acidic intracellular pH (pH(i)) selectively activated exchange of extracellular Cl(-) for intracellular (35)SO(4)(2-) but not for intracellular (36)Cl(-) or [(14)C]oxalate. Protein kinase C inhibited hSLC26A2 by reducing its surface abundance. Diastrophic dysplasia mutants R279W and A386V of hSLC26A2 exhibited similar reductions in uptake of both (35)SO(4)(2-) and [(14)C]oxalate. A386V surface abundance was reduced, but R279W surface abundance was at wild-type levels.
Aronson,
Mechanisms of chloride transport in the proximal tubule.
1997, Pubmed
Aronson,
Mechanisms of chloride transport in the proximal tubule.
1997,
Pubmed
Barmeyer,
Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells.
2007,
Pubmed
Beaugé,
The squid axon Na/Ca2+ exchanger shows ping pong kinetics only when the Ca2+(i)-regulatory site is saturated.
2009,
Pubmed
Burckhardt,
Pathways of NH3/NH4+ permeation across Xenopus laevis oocyte cell membrane.
1992,
Pubmed
,
Xenbase
Chernova,
Acute regulation of the SLC26A3 congenital chloride diarrhoea anion exchanger (DRA) expressed in Xenopus oocytes.
2003,
Pubmed
,
Xenbase
Chernova,
Functional comparison of mouse slc26a6 anion exchanger with human SLC26A6 polypeptide variants: differences in anion selectivity, regulation, and electrogenicity.
2005,
Pubmed
,
Xenbase
Clark,
Species differences in Cl- affinity and in electrogenicity of SLC26A6-mediated oxalate/Cl- exchange correlate with the distinct human and mouse susceptibilities to nephrolithiasis.
2008,
Pubmed
,
Xenbase
Comelli,
Biomarkers of human gastrointestinal tract regions.
2009,
Pubmed
Cornaglia,
Dysplastic histogenesis of cartilage growth plate by alteration of sulphation pathway: a transgenic model.
2009,
Pubmed
Dawson,
Urolithiasis and hepatotoxicity are linked to the anion transporter Sat1 in mice.
2010,
Pubmed
Deplancke,
Gastrointestinal and microbial responses to sulfate-supplemented drinking water in mice.
2003,
Pubmed
Dorwart,
The solute carrier 26 family of proteins in epithelial ion transport.
2008,
Pubmed
Everett,
Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS).
1997,
Pubmed
Forlino,
A diastrophic dysplasia sulfate transporter (SLC26A2) mutant mouse: morphological and biochemical characterization of the resulting chondrodysplasia phenotype.
2005,
Pubmed
Freel,
Ileal oxalate absorption and urinary oxalate excretion are enhanced in Slc26a6 null mice.
2006,
Pubmed
Freel,
Parsing apical oxalate exchange in Caco-2BBe1 monolayers: siRNA knockdown of SLC26A6 reveals the role and properties of PAT-1.
2009,
Pubmed
Fuster,
Steady-state function of the ubiquitous mammalian Na/H exchanger (NHE1) in relation to dimer coupling models with 2Na/2H stoichiometry.
2008,
Pubmed
Galamb,
Diagnostic mRNA expression patterns of inflamed, benign, and malignant colorectal biopsy specimen and their correlation with peripheral blood results.
2008,
Pubmed
Gomez,
High levels of inorganic sulfate cause diarrhea in neonatal piglets.
1995,
Pubmed
Haila,
SLC26A2 (diastrophic dysplasia sulfate transporter) is expressed in developing and mature cartilage but also in other tissues and cell types.
2001,
Pubmed
Hassan,
Regulation of anion exchanger Slc26a6 by protein kinase C.
2007,
Pubmed
,
Xenbase
Hatch,
Intestinal transport of an obdurate anion: oxalate.
2005,
Pubmed
Holmes,
Contribution of dietary oxalate to urinary oxalate excretion.
2001,
Pubmed
Humphreys,
NH4Cl activates AE2 anion exchanger in Xenopus oocytes at acidic pHi.
1997,
Pubmed
,
Xenbase
Hästbacka,
The diastrophic dysplasia gene encodes a novel sulfate transporter: positional cloning by fine-structure linkage disequilibrium mapping.
1994,
Pubmed
Höglund,
Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea.
1996,
Pubmed
Jiang,
Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6.
2006,
Pubmed
Karniski,
Mutations in the diastrophic dysplasia sulfate transporter (DTDST) gene: correlation between sulfate transport activity and chondrodysplasia phenotype.
2001,
Pubmed
,
Xenbase
Karniski,
Functional expression and cellular distribution of diastrophic dysplasia sulfate transporter (DTDST) gene mutations in HEK cells.
2004,
Pubmed
,
Xenbase
Krick,
Ability of sat-1 to transport sulfate, bicarbonate, or oxalate under physiological conditions.
2009,
Pubmed
,
Xenbase
Kujala,
Expression of ion transport-associated proteins in human efferent and epididymal ducts.
2007,
Pubmed
Kuo,
CT evaluation of multisystem involvement by oxalosis.
2001,
Pubmed
Liu,
Prestin, a cochlear motor protein, is defective in non-syndromic hearing loss.
2003,
Pubmed
Razaq,
Regulation of intracellular pH by bovine intervertebral disc cells.
2000,
Pubmed
Rossi,
Mutations in the diastrophic dysplasia sulfate transporter (DTDST) gene (SLC26A2): 22 novel mutations, mutation review, associated skeletal phenotypes, and diagnostic relevance.
2001,
Pubmed
Sasaki,
Regulation mechanisms of intracellular pH of Xenopus laevis oocyte.
1992,
Pubmed
,
Xenbase
Satoh,
Functional analysis of diastrophic dysplasia sulfate transporter. Its involvement in growth regulation of chondrocytes mediated by sulfated proteoglycans.
1998,
Pubmed
,
Xenbase
Schaechinger,
Nonmammalian orthologs of prestin (SLC26A5) are electrogenic divalent/chloride anion exchangers.
2007,
Pubmed
Stewart,
Regulation of AE2-mediated Cl- transport by intracellular or by extracellular pH requires highly conserved amino acid residues of the AE2 NH2-terminal cytoplasmic domain.
2002,
Pubmed
,
Xenbase
Takenaka,
Widespread cutaneous oxalosis in a patient with primary hyperoxaluria.
2003,
Pubmed
Touré,
The testis anion transporter 1 (Slc26a8) is required for sperm terminal differentiation and male fertility in the mouse.
2007,
Pubmed
Treuhaft,
Synovial fluid pH, lactate, oxygen and carbon dioxide partial pressure in various joint diseases.
1971,
Pubmed
Wang,
Renal and intestinal transport defects in Slc26a6-null mice.
2005,
Pubmed
Xu,
Deletion of the chloride transporter slc26a7 causes distal renal tubular acidosis and impairs gastric acid secretion.
2009,
Pubmed
Xu,
Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach.
2008,
Pubmed
,
Xenbase
von Stein,
Multigene analysis can discriminate between ulcerative colitis, Crohn's disease, and irritable bowel syndrome.
2008,
Pubmed
