ArticleUrological research2012
Hyperoxaluric rats do not exhibit alterations in renal expression patterns of Slc26a1 (SAT1) mRNA or protein.
Article in Urological research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Contributions of the anion exchangers SLC26A1, SLC26A2, SLC26A3, and SLC26A6 to intestinal oxalate transport in human Caco2-BBE cells.Physiological reports · 2026Article
- Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Changes of Klotho protein and Klotho mRNA expression in a hydroxy-L-proline induced hyperoxaluric rat model.The Journal of veterinary medical science · 2017Article
- Extracellular Cl(-) regulates human SO4 (2-)/anion exchanger SLC26A1 by altering pH sensitivity of anion transport.Pflugers Archiv : European journal of physiology · 2016Article
- In female rats, ethylene glycol treatment elevates protein expression of hepatic and renal oxalate transporter sat-1 (Slc26a1) without inducing hyperoxaluria.Croatian medical journal · 2015Article
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Abstract
Little is known about oxalate transport in renal epithelia under basal conditions, let alone in hyperoxaluria when the capacity for renal oxalate excretion is increased. Sulfate anion transporter 1 (SAT1, Slc26a1) is considered to be a major basolateral anion-oxalate exchanger in the proximal tubule and we hypothesized its expression may correlate with urinary oxalate excretion. We quantified changes in the renal expression of SAT1 mRNA and protein in two rat models, one with hyperoxaluria (HYP) and one with renal insufficiency (HRF) induced by hyperoxaluria. The hyperoxaluria observed in the HYP group could not simply be ascribed to changes in SAT1 mRNA or protein abundance. However, when hyperoxaluria was accompanied by renal insufficiency, significant reductions in SAT1 mRNA and protein were detected in medullary and papillary tissue. Together, the results indicate that transcriptional modulation of the SAT1 gene is not a significant component of the hyperoxaluria observed in these rat models.
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