Solute carrier family 23 member 1 is a protein that in humans is encoded by the SLC23A1 gene. The SLC23A1 gene is 16096 bp long, contains 15 exons and maps to human chromosome 5q31.2-31.3. Analysis of the SLC23A1 genomic structure reveals the presence of classical CAAT and TATA 1 boxes, together with two AP-1 and one GATA1 binding sites. Human SLC23A1 lacks a seven amino acid fragment in the N-terminus, thus resulting in a protein of 598 amino acids.
|Basic Information of SLC23A1|
|Protein Name||Solute carrier family 23 member 1|
|Aliases||Na(+)/L-ascorbic acid transporter 1, Sodium-dependent vitamin C transporter 1, hSVCT1, Yolk sac permease-like molecule 3|
|Organism||Homo sapiens (Human)|
SLC23 proteins are surface glycoproteins encoded by two different genes, which are very similar in structure. They show distinct tissue distribution and functional characteristics, which indicate different physiological roles. SLC23A1 is involved in whole-body homeostasis of vitamin C, while SLC23A2 protects metabolically active cells against oxidative stress. SLC23A1, expressed on the apical membrane, transports vitamin C across the intestinal barrier, while SLC23A2 is located at the basolateral surface, where it should be involved in vitamin C transport from blood into enterocytes. Immunohistochemistry analysis shows that SLC23A1 is expressed in medullary rays and the brush border of proximal tubules. SLC23s functions are obligatorily dependent on sodium ions. Replacement of Na+ with K+, Li+ or coline almost completely abolishes ascorbate uptake. Distribution and kinetic parameters suggest that the primary role of SLC23A2 is to maintain the homeostasis of vitamin C in the whole-body.
Fig.1 Vitamin C transporters (SLC23A1 and SLC23A2) and their transport mechanisms in the skin.
Authors find that there is no evidence showing a relation between the variation rs33972313 of SLC23A1 gene and cardiometabolic outcomes.
SNP rs6596473 of SLC23A1 is suggested to be associated with AgP. These results supplement previous reports that vitamin C plays a role in the pathogenesis of periodontitis.
This article reveals that SLC23A1 variations can modulate the risk of CD, which has implications for understanding ascorbate transport in CD patients and provides a novel opportunity toward individualized nutritional therapy for patients carrying the disease-associated genotype.
Common variants in SLC23A1 and SLC23A2 may influence plasma vitamin C concentration independent of dietary intake.
Authors successfully express the human vitamin C transporter-1 in Xenopus laevis oocytes and isolate highly pure protein in microgram amounts. Recombinant hSVCT1 is functional when expressed in oocytes and glycosylated.
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