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anti-Human SLC23A2 Antibodies:
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These data suggest that both fruit intake and genetic marker in SLC23A2 may play an independent role in chronic lymphocytic leukemia biology.
Ascorbic acid kills cholangiocarcinoma cells via DNA damage, ATP depletion, and inhibition of mTOR (show FRAP1 Antibodies) pathway in a SVCT-2 dependent manner.
Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 (show SVCT1 Antibodies) 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.
Significant methylation changes in the SLC23A2 and NCOR2 regulatory regions.
Vitamin C supplementation significantly increases skeletal muscle SVCT2 protein expression.
ascorbic acid uptake mechanism, kinetics, and regulation by sodium dependent vitamin C transporter (SVCT2) in MDA-MB231, T47D and ZR-75-1 cells.
Together, these data clarify previous inconsistencies in the literature andimplicate SVCT2 as the pericyte ascorbate transporter.
The functional expression of SVCT2 was detected in HEK293 cells.The kinetic analysis suggested that an ascorbate-dependent mechanism accounts for targeted SVCT2 expression in the developing kidney during medullary epithelial cell differentiation.
We propose that the mitochondrial localization of SVCT2 is a property shared across cells, tissues, and species.
Demonstrate that the expression of SVCT2 transporter is significantly down-regulated in human grade 3 osteoarthritic tissues.
Our studies demonstrate that the active SVCT2 is expressed in IVD (show IVD Antibodies) cells and that the expression of this transporter is regulated by growth factors IGF-1 (show IGF1 Antibodies) and dexamethasone
Study shows that SVCT2 is regulated at the post-transcriptional level by miR (show MLXIP Antibodies)-141 and miR (show MLXIP Antibodies)-200a during osteogenic differentiation of bone marrow stromal cells.
Results indicate that both the SVCT2 transporter and oxidative stress play a vital role in BMSC attachment, migration and cytoskeletal re-arrangement.
Increased expression of SVCT2 in a new mouse model raises ascorbic acid in tissues and protects against oxidative stress.
the expression and transport activity of SVCT2 in brain capillary endothelial cells after transient ischemia
Expression of various collagen types is reduced in sciatic nerves of SVCT2(+/-) heterozygous mice compared to wild-type.
The results suggest that expression of the SVCT2 is differentially regulated during embryonic development and in adulthood.
Evidence of increased apoptosis in SVCT2(-/-) mice and disruption of the basement membrane in fetal brain.
By using primary cultured hepatocytes from SMP30/GNL (show RGN Antibodies) KO mice, we found that SVCT1 (show SVCT1 Antibodies) and SVCT2 mRNA expression levels and AA uptake ability were significantly enhanced in the hepatocytes of ascorbic acid-depleted SMP30/GNL (show RGN Antibodies) KO mice.
These results provide evidence for the first time that uptake of ascorbic acid in the peripheral nervous system is crucially dependent on the expression and activity of SVCT2.
The absorption of vitamin C into the body and its distribution to organs requires two sodium-dependent vitamin C transporters. This gene encodes one of the two required transporters and the encoded protein accounts for tissue-specific uptake of vitamin C. Previously, this gene had an official symbol of SLC23A1.
Na(+)/L-ascorbic acid transporter 2
, nucleobase transporter-like 1 protein
, sodium-dependent vitamin C transporter-2
, solute carrier family 23 (nucleobase transporters), member 1
, solute carrier family 23 (nucleobase transporters), member 2
, solute carrier family 23 member 2
, yolk sac permease-like molecule 2
, sodium-coupled ascorbic acid transporter 2
, sodium-dependent vitamin C transporter 2
, sodium-coupled ascorbic acid transporter SVCT2