ArticleThe Journal of physiology2008
Species differences in Cl- affinity and in electrogenicity of SLC26A6-mediated oxalate/Cl- exchange correlate with the distinct human and mouse susceptibilities to nephrolithiasis.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 83 citations in OpenAlex.
- Autophagy Regulates Putative Anion Transporter 1 Expression in Intestinal Epithelial Cells.Journal of cellular and molecular medicine · 2025Article
- Unity Is Strength: The Mutual Alliance between CFTR and SLC26A6 as Therapeutic Opportunity in Cystic Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The enigmatic SLC26A6 multifunctional anion transporter: recent advances in structure-function relationship, pathophysiological significance and novel pharmacological inhibitors.Frontiers in pharmacology · 2024Review
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Oxalate (dys)Metabolism: Person-to-Person Variability, Kidney and Cardiometabolic Toxicity.Genes · 2023Review
- Structural and functional properties of the transporter SLC26A6 reveal mechanism of coupled anion exchange.eLife · 2023Article
- The anion exchanger PAT-1 (Slc26a6) does not participate in oxalate or chloride transport by mouse large intestine.Pflugers Archiv : European journal of physiology · 2021Article
- Calcium oxalate crystal deposition in the kidney: identification, causes and consequences.Urolithiasis · 2020Review
- Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Whole exome sequencing identified ATP6V1C2 as a novel candidate gene for recessive distal renal tubular acidosis.Kidney international · 2020Article
- Characterization of renal NaCl and oxalate transport in Slc26a6American journal of physiology. Renal physiology · 2019Article
- Article
- Action Potential Shortening and Impairment of Cardiac Function by Ablation ofCirculation. Arrhythmia and electrophysiology · 2017Article
- Bicarbonate-rich fluid secretion predicted by a computational model of guinea-pig pancreatic duct epithelium.The Journal of physiology · 2017Article
- The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man.Urolithiasis · 2017Review
- Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion.Journal of the American Society of Nephrology : JASN · 2017Article
- N-glycosylation critically regulates function of oxalate transporter SLC26A6.American journal of physiology. Cell physiology · 2016Article
- Sulfate and thiosulfate inhibit oxalate transport via a dPrestin (Slc26a6)-dependent mechanism in an insect model of calcium oxalate nephrolithiasis.American journal of physiology. Renal physiology · 2016Article
- Effects of acid-base variables and the role of carbonic anhydrase on oxalate secretion by the mouse intestine in vitro.Physiological reports · 2015Article
- Nephropathy in dietary hyperoxaluria: A potentially preventable acute or chronic kidney disease.World journal of nephrology · 2014Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
The mouse is refractory to lithogenic agents active in rats and humans, and so has been traditionally considered a poor experimental model for nephrolithiasis. However, recent studies have identified slc26a6 as an oxalate nephrolithiasis gene in the mouse. Here we extend our earlier demonstration of different anion selectivities of the orthologous mouse and human SLC26A6 polypeptides to investigate the correlation between species-specific differences in SLC26A6 oxalate/anion exchange properties as expressed in Xenopus oocytes and in reported nephrolithiasis susceptibility. We find that human SLC26A6 mediates minimal rates of Cl(-) exchange for Cl(-), sulphate or formate, but rates of oxalate/Cl(-) exchange roughly equivalent to those of mouse slc2a6. Both transporters exhibit highly cooperative dependence of oxalate efflux rate on extracellular [Cl(-)], but whereas the K(1/2) for extracellular [Cl(-)] is only 8 mM for mouse slc26a6, that for human SLC26A6 is 62 mM. This latter value approximates the reported mean luminal [Cl(-)] of postprandial human jejunal chyme, and reflects contributions from both transmembrane and C-terminal cytoplasmic domains of human SLC26A6. Human SLC26A6 variant V185M exhibits altered [Cl(-)] dependence and reduced rates of oxalate/Cl(-) exchange. Whereas mouse slc26a6 mediates bidirectional electrogenic oxalate/Cl(-) exchange, human SLC26A6-mediated oxalate transport appears to be electroneutral. We hypothesize that the low extracellular Cl(-) affinity and apparent electroneutrality of oxalate efflux characterizing human SLC26A6 may partially explain the high human susceptibility to nephrolithiasis relative to that of mouse. SLC26A6 sequence variant(s) are candidate risk modifiers for nephrolithiasis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.