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Gene Review

Slc23a2  -  solute carrier family 23 (nucleobase...

Mus musculus

Synonyms: AI844736, Kiaa0238, NBTL1, Na(+)/L-ascorbic acid transporter 2, SVCT-2, ...
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Disease relevance of Slc23a2


High impact information on Slc23a2


Biological context of Slc23a2

  • Slc23a2+/- and Slc23a2+/+ mice were fed an ascorbate-free diet for 10-12 wk, and then segregated according to gender and genome, and were placed in groups of 3-4 in metabolic cages for 24-h urine collection [6].
  • Our previous studies suggested that Zn-induced osteoblast differentiation and Ca2+-, PO4(3-)-stimulated osteopontin (OPN) expression might result from their up-regulation effect on SVCT2 expression and AA uptake [7].
  • These findings suggested that Ca(2+) and PO(4)(3-) regulate osteoblastic phenotype by entering into cells to stimulate SVCT2 and OPN expression [8].
  • We found that the SVCT2 helps to maintain high intracellular ascorbate levels, normal ascorbate transport kinetics, and activity-dependent ascorbate recycling [9].
  • On the ultrastructural level, adrenal chromaffin cells in SVCT2 null mice showed depletion of catecholamine storage vesicles, increased amounts of rough endoplasmic reticulum, signs of apoptosis, and increased glycogen storage [10].

Anatomical context of Slc23a2


Associations of Slc23a2 with chemical compounds

  • SVCT2 contributed to a gender effect in spleen because males had higher spleen ascorbate concentration than females in wild-type but not in Slc23a2+/- mice [6].
  • These findings suggest that AA and SVCT2 mediate Zn-induced OPN and OCN expression and partly regulate Zn-induced osteoblastic differentiation [12].
  • In addition, the L-type calcium channel blocker, nifedipine (5 to 20 micro M) and the phosphate transporter inhibitor, foscarnet (0.15 to 0.6 mM), dose-dependently abolished Ca(2+)- and PO(4)(3-)-induced SVCT2, OPN expression and OPN promoter activity [8].
  • Finally, hippocampal cultures from SVCT2-deficient mice showed increased susceptibility to oxidative damage and N-methyl-D-aspartate-induced excitotoxicity [9].
  • In the absence of SVCT2, hippocampal neurons exhibited stunted neurite outgrowth, less glutamate receptor clustering, and reduced spontaneous neuronal activity [9].
  • Together, these results suggest that PGE2-induced SVCT2 plasma membrane translocation through EP4 receptor and subsequent phosphorylation of SVCT2 at Ser402 and Ser639 sites by PKA results in an increase of AA uptake and consequent promotion of osteoblast-like differentiation in MC3T3-E1 cells [13].

Other interactions of Slc23a2

  • Additionally, lower ascorbate excretion in females may elevate the vitamin's concentrations in plasma and tissues expressing SVCT1 that, unlike SVCT2, is not saturated by plasma ascorbate concentrations [6].

Analytical, diagnostic and therapeutic context of Slc23a2

  • Western blotting and kinetic assays showed that Zn increased functional SVCT2 protein levels and AA transport [12].
  • HPLC analysis, performed on HRPE cells, confirmed the SVCT2 mediated transport for the BrAA-conjugate of nipecotic acid, whereas kynurenic acids conjugates although interacting with the transporter did not enter the cells [14].


  1. Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. Sotiriou, S., Gispert, S., Cheng, J., Wang, Y., Chen, A., Hoogstraten-Miller, S., Miller, G.F., Kwon, O., Levine, M., Guttentag, S.H., Nussbaum, R.L. Nat. Med. (2002) [Pubmed]
  2. Relative suppression of the sodium-dependent Vitamin C transport in mouse versus human lens epithelial cells. Obrenovich, M.E., Fan, X., Satake, M., Jarvis, S.M., Reneker, L., Reddan, J.R., Monnier, V.M. Mol. Cell. Biochem. (2006) [Pubmed]
  3. Vitamin C homeostasis in skeletal muscle cells. Savini, I., Catani, M.V., Duranti, G., Ceci, R., Sabatini, S., Avigliano, L. Free Radic. Biol. Med. (2005) [Pubmed]
  4. Macrophage uptake and recycling of ascorbic acid: response to activation by lipopolysaccharide. May, J.M., Huang, J., Qu, Z.C. Free Radic. Biol. Med. (2005) [Pubmed]
  5. Sodium vitamin C cotransporter SVCT2 is expressed in hypothalamic glial cells. García, M.d.e. .L., Salazar, K., Millán, C., Rodríguez, F., Montecinos, H., Caprile, T., Silva, C., Cortes, C., Reinicke, K., Vera, J.C., Aguayo, L.G., Olate, J., Molina, B., Nualart, F. Glia (2005) [Pubmed]
  6. Gender and sodium-ascorbate transporter isoforms determine ascorbate concentrations in mice. Kuo, S.M., MacLean, M.E., McCormick, K., Wilson, J.X. J. Nutr. (2004) [Pubmed]
  7. Stimulation of differentiation in sodium-dependent vitamin C transporter 2 overexpressing MC3T3-E1 osteoblasts. Wu, X., Itoh, N., Taniguchi, T., Hirano, J., Nakanishi, T., Tanaka, K. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  8. Requirement of calcium and phosphate ions in expression of sodium-dependent vitamin C transporter 2 and osteopontin in MC3T3-E1 osteoblastic cells. Wu, X., Itoh, N., Taniguchi, T., Nakanishi, T., Tanaka, K. Biochim. Biophys. Acta (2003) [Pubmed]
  9. Ascorbate transport by primary cultured neurons and its role in neuronal function and protection against excitotoxicity. Qiu, S., Li, L., Weeber, E.J., May, J.M. J. Neurosci. Res. (2007) [Pubmed]
  10. Impaired adrenal catecholamine system function in mice with deficiency of the ascorbic acid transporter (SVCT2). Bornstein, S.R., Yoshida-Hiroi, M., Sotiriou, S., Levine, M., Hartwig, H.G., Nussbaum, R.L., Eisenhofer, G. FASEB J. (2003) [Pubmed]
  11. High-affinity sodium-vitamin C co-transporters (SVCT) expression in embryonic mouse neurons. Castro, M., Caprile, T., Astuya, A., Millán, C., Reinicke, K., Vera, J.C., Vásquez, O., Aguayo, L.G., Nualart, F. J. Neurochem. (2001) [Pubmed]
  12. Zinc-induced sodium-dependent vitamin C transporter 2 expression: potent roles in osteoblast differentiation. Wu, X., Itoh, N., Taniguchi, T., Nakanishi, T., Tatsu, Y., Yumoto, N., Tanaka, K. Arch. Biochem. Biophys. (2003) [Pubmed]
  13. Activation of PKA and phosphorylation of sodium-dependent vitamin C transporter 2 by prostaglandin E2 promote osteoblast-like differentiation in MC3T3-E1 cells. Wu, X., Zeng, L.H., Taniguchi, T., Xie, Q.M. Cell Death Differ. (2007) [Pubmed]
  14. Ascorbic and 6-Br-ascorbic acid conjugates as a tool to increase the therapeutic effects of potentially central active drugs. Dalpiaz, A., Pavan, B., Vertuani, S., Vitali, F., Scaglianti, M., Bortolotti, F., Biondi, C., Scatturin, A., Tanganelli, S., Ferraro, L., Marzola, G., Prasad, P., Manfredini, S. European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences. (2005) [Pubmed]
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