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Sodium-dependent vitamin C transporter 1 (SVCT1) and Sodium-dependent vitamin C transporter 2 (SVCT2) (SVCT1, SVCT2)

Target
SVCT1, SVCT2
Molecular classification
Transporter, Membrane protein, Nucleobase-ascorbate transporter (NAT) family
01

Overview

The **sodium-dependent vitamin C transporters** SVCT1 (SLC23A1) and SVCT2 (SLC23A2) are primary ascorbate transporters in mammals, regulating cellular uptake and distribution of vitamin C. SVCT1 is predominantly expressed in epithelial tissues (notably kidney, mediating renal reabsorption of ascorbate), while SVCT2 is widely expressed in non-epithelial tissues including the brain. These hydrophobic membrane proteins belong to the nucleobase-ascorbate transporter (NAT) family and operate via a sodium-dependent symport mechanism, coupling the movement of ascorbate against its concentration gradient to the inward flow of sodium ions generated by the Na+/K+ ATPase. They are critical for maintaining the high intracellular concentrations of ascorbate required for antioxidant defense, modulation of oxidative stress, and overall physiological health. Loss of function of SVCT transporters is incompatible with survival in model organisms, and their dysfunction may contribute to neurological, cardiovascular, and other diseases associated with vitamin C deficiency[3][4][7].

Other names
Sodium-dependent vitamin C transporter 1SVCT1Sodium-dependent vitamin C transporter 2SVCT2Solute carrier family 23 member 1 (SLC23A1)Solute carrier family 23 member 2 (SLC23A2)Ascorbate transporter
02

Mechanism of action

Sodium gradient-driven co-transport of ascorbate across cell membranes Coupling inward movement of ascorbate with sodium ions

03

Biological functions

Cellular uptake of vitamin C (ascorbic acid)Maintenance of intracellular ascorbate concentrationsAntioxidant defense (through vitamin C uptake)Regulation of oxidative stress response
04

Disease associations

Neurodegenerative diseaseCancerCardiovascular diseaseOther (vitamin C deficiency disorders, e.g., scurvy)
05

Safety considerations

Genetic knockout leads to early lethality in mice, indicating necessity for survival[3]Potential for impaired absorption or transport in genetic variants or pharmacological inhibition
06

Interacting drugs

Ascorbic acid (vitamin C)

1 more in the full profile.

07

Biomarkers

Tissue or cellular expression levels of SVCT1/SVCT2 for vitamin C uptake capacity

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