The apical membrane Na⁺-sulfate cotransporter NaS1 (SLC13A1) mediates sulfate (re)absorption across renal proximal tubule and small intestinal epithelia. NaS1 is a 595-amino acid (~66 kDa) protein with 13 putative transmembrane domains. Substrate preferences of NaS1 are sodium and sulfate, thiosulfate, and selenite. Its activity is inhibited by molybdate, selenate, tungstate, thiosulfate, succinate, and citrate. NaS1 is primarily expressed in the kidney and intestine. Its expression is down-regulated in the renal cortex by high sulfate diet, hypothyroidism, vitamin D depletion, glucocorticoids, hypokalemia, metabolic acidosis, and NSAIDs and up-regulated by low sulfate diet, thyroid hormone, vitamin D supplementation, growth hormone, chronic renal failure, and during post-natal growth.
|Basic Information of SLC13A1|
|Protein Name||Solute carrier family 13 member 1|
|Aliases||Renal sodium/sulfate cotransporter, Na(+)/sulfate cotransporter, hNaSi-1|
|Organism||Homo sapiens (Human)|
SLC13A1/NaS1 is an important protein regulating sulfate reabsorption in the kidney in human. Disruption of this protein leads to hyposulfatemia and hypersulfaturia, as well as changes in metabolism, growth, fecundity, behavior, gut physiology, and liver detoxification. NaS1 is an important sulfate transporter and its disruption leads to perturbed sulfate homeostasis, which contributes to numerous pathophysiological conditions. It also takes part in sulfate symporter activity and sodium ion transmembrane transporting.
Fig.1 Sulfate transporters in the renal and small intestinal epithelial cell. (Tise, 2016)
This article identifies that NAS1 gene contains 15 exons, spanning over 83 kb in length. These findings will permit the screening of NAS1 mutations in humans with disorders in renal sulfate reabsorption and homeostasis.
Authors in this study reveal that the expression of these two proteins, Slc13a1 and Slc26a1, is dramatically reduced after the transfer of eels from freshwater to seawater.
This article suggests that NaS1 (SLC13A1) and Sat1 (SLC26A1) mediate sulfate (re)absorption across renal proximal tubule and small intestinal epithelia, thereby regulating blood sulfate levels. Disruption of these two genes will lead to hyposulfatemia and hypersulfaturia.
This article shows that disruption of SLC13A1 in the dog similarly causes undersulfation of proteoglycans in the extracellular matrix (ECM), which impacts the conversion of cartilage to bone.
This article suggests that NaS1 is an important sulfate transporter and its disruption leads to perturbed sulfate homeostasis, which contributes to numerous pathophysiological conditions.
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