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Solute carrier family 13 member 1 (SLC13A1, also known as NaS1 or hNaSi-1) is an integral membrane sodium-dependent inorganic sulfate transporter predominantly expressed in the apical membrane of renal proximal tubules and, in rodents, also in the small intestine[1][2][4]. It mediates electrogenic sodium-dependent uptake of sulfate, selenate, and thiosulfate, playing a key role in renal sulfate reabsorption and systemic sulfate homeostasis[1][2]. Defects or mutations in SLC13A1 lead to syndromes of impaired skeletal development (achondrogenesis type Ib, atelosteogenesis) and increased renal sulfate loss[1][2]. SLC13A1 is a pharmacologically relevant transporter potentially impacting the disposition of inorganic anions and homeostasis-regulating drugs[1][2][4]. While there are currently no approved drugs directly targeting SLC13A1 in clinical use, it remains a research target for modulating sulfate and related anion balance, with therapeutic risks mainly stemming from mineral imbalance if transporter function is altered[2][4].
Sodium-coupled symport of sulfate/similar anions across apical renal membrane
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