Target intelligence / Profile preview

Solute carrier family 13 member 1 (SLC13A1)

Target
SLC13A1
Molecular classification
Transporter, Solute carrier (SLC) family, Sodium-coupled symporter, Integral membrane protein
01

Overview

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].

Other names
SLC13A1NaS1hNaSi-1Sodium-dependent sulfate transporterSodium sulfate cotransporter
02

Mechanism of action

Sodium-coupled symport of sulfate/similar anions across apical renal membrane

03

Biological functions

Sulfate homeostasis (renal sulfate reabsorption)Transport of inorganic anions (sulfate, selenate, thiosulfate)Sodium-dependent substrate transport (symport mechanism)
04

Disease associations

Skeletal dysplasias (achondrogenesis, Type Ib and Atelosteogenesis)Growth disordersPotential behavioral and memory disturbances (preclinical model)Other (disturbances in sulfate/selenate metabolism)
05

Safety considerations

Disruption leads to increased renal loss of sulfate and growth/developmental defectsDefective transporter may contribute to disease by impaired sulfate homeostasis; therapeutic modulation must consider risks to mineral balance.
06

Interacting drugs

No clinically approved drugs directly targeting SLC13A1; potential for pharmacological modulation in experimental models

1 more in the full profile.

07

Biomarkers

SLC13A1 mutation status for skeletal dysplasia diagnosisUrinary sulfate concentration (biomarker of transporter function in knockout models)

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