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Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes.
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consensus site for HNF1 that is crucial for the regulation of the human SVCT1 promoter is present in the SVCT1 rat promoter but has no effect on its transcriptional activity
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SNP rs6596473 of SLC23A1 is suggested to be associated with AgP. results add to previous reports vitamin C plays a role in pathogenesis of periodontitis.
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Data from observational/genetic association studies in Europe suggest an SNP in SLC23A1 (rs33972313) is associated with up-regulation of circulating L-ascorbic acid but not with any cardiometabolic/cardiovascular outcome investigated. [META-ANALYSIS]
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The SVCT1 was induced and localized to the apical membrane of tubular epithelial cells.
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polymorphisms in SLC23A1/2 genes influenced ascorbate concentration in aqueous humor and lens nucleus.
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A genetic variant in the SLC23A1 ascorbate transporter locus was identified and is associated with an increased risk of Crohn disease in a white Canadian inflammatory bowel diseases cohort.
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Data show that the mRNA level of svct2 was approximately 600- to 900-fold higher than that of svct1 indicating SVCT2 is a main isoform in fibroblast OUMS-36 cells, and no significant difference in svct2 mRNA and protein between young and old cells.
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Data suggest that N-terminal and C-terminal sorting signals interact, directly or indirectly, within each gene family (here, SVCT1 and SVCT2) in basolateral targeting of transmembrane proteins to basolateral cell membrane.
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SVCT1 directly interacts with GRHPR.
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These findings show a role for Rab8a in the physiological function of SVCT1 in intestinal epithelia.
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glutathione depletion failed to affect ascorbic acid transport, and SVCT1 and SVCT2 expression in hepatoma cells. Therefore, our data indicate an essential role for glutathione in controlling vitamin C metabolism in rat hepatocytes and rat hepatoma cells
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In patients with hepatocellular cholestasis, primary biliary cirrhosis, haemochromatosis and non-alcoholic steatohepatitis, using real-time RT-PCR, an enhanced hepatic expression of both SLC23A1 and SLC23A2 was found.
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hSVCT1 and 2 promoters establish that ascorbic acid uptake by human liver epithelial cells is adaptively regulated and show that transcriptional mechanisms via HNF-1 in the hSVCT1 promoter may, in part, be involved in this regulation.
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A genetic variant (rs33972313) in the SLC23A1 vitamin C active transporter locus was identified that is reliably associated with circulating concentrations of L-ascorbic acid in the general population.
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SVCT1 is the transporter that allows vectorial uptake of ascorbic acid in differentiated CaCo-2 cells
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Results provide the first direct resolution of functional hSVCT1 expression at the apical cell surface of polarized epithelia and define an apical targeting signal of relevance to transporters of diverse substrate specificity.
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Functionally, SVCT1 expression led to more transport activity from the apical membrane, while SVCT2 expression only increased the uptake under the condition when basolateral membrane was exposed.
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Findings link genetic variants in the vitamin C transporter gene SLC23A1 to spontaneous preterm birth.
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C uptake is increased in UVB-irradiated keratinocytes through the translocation of SVCT-1 and regulates inflammatory response in the skin via the downregulation of IL-8 and MCP-1 production
