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Gene Review

Slc35a2  -  solute carrier family 35 (UDP-galactose...

Mus musculus

Synonyms: AI327289, Had-1, Had1, Sfc8, Solute carrier family 35 member A2, ...
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Disease relevance of Slc35a2

  • 125I-Labeled Newcastle disease virus bound only poorly to gangliosides extracted from either FM3A or Had-1 cells on a high performance thin-layer chromatography plate [1].
  • These results suggest two possibilities by which UGT may mediate TMEV entry and infection [2].
  • These results further indicate that, with UGT deficiencies, HPPH potentially is a potent mediator of phenytoin-initiated genotoxicity and embryopathy, which may be relevant to teratogenesis and other adverse effects of phenytoin [3].
  • Phenytoin-initiated micronucleus formation was increased about 4-fold in both +/j (P = .006) and j/j (P = .009) UGT-deficient cells vs. +/+ UGT-normal cells, providing the first evidence that the bioactivation and oxidative toxicity of phenytoin itself may be avoided by direct N-glucuronidation, which was confirmed by tandem mass spectrometry [3].
  • CLO, PB, and PCN induced histological liver hypertrophy, increases in liver weights, in microsomal protein and cytochrome P450 contents as well as increases in specific UGT activities [4].

High impact information on Slc35a2


Biological context of Slc35a2

  • They were tested for genetic complementation in pairs by cell fusion and shown to fall into a single recessive complementation group, which was designated as Had-1 [6].
  • Reverse transcription polymerase chain reaction with primers that span the UGT open reading frame showed that three Lec8 mutants express a full-length open reading frame, while six Lec8 mutants predominantly express truncated UGT gene transcripts [7].
  • Thus, identifying point mutations that inactivate UGT in Lec8 mutants resulted in the discovery of amino acids that are critical to the activity of both UGT and CST, the two most divergent mammalian NSTs [7].
  • Now we have characterized its isoform, hUGT2, that is most likely generated through the alternative splicing of a transcript derived from the UGT genomic gene, that also codes for hUGT1 [8].
  • The glucuronidation kinetics of the prototypic substrates 4-methylumbelliferone (4MU) and 1-naphthol (1NP) by human UDP-glucuronosyltransferases (UGT) 1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B7, 2B15, and 2B17 were investigated [9].

Anatomical context of Slc35a2


Associations of Slc35a2 with chemical compounds

  • The Had-1 mutant was resistant to wheat germ agglutinin, but sensitive to a Griffonia simplicifolia lectin, GS-II, which recognizes terminal N-acetylglucosamine residues [6].
  • Recent studies have demonstrated that UDP-galactose (UDP-Gal) is the substrate for the ER resident ceramide-galactosyltransferase (cer-GalT) and cells expressing cer-GalT are able to retain the UDP-Gal transporter (UGT) by physical contacts formed between the two proteins [11].
  • Among all UGT isoforms identified to date, it is the only relevant bilirubin-glucuronidating enzyme in human [14].
  • Phenytoin (80 microM) enhanced micronucleus formation 1.7-, 4.4- and 3.8-fold in +/+ cells (P = .03) and +/j and j/j UGT-deficient cells (P = .0001), respectively [3].
  • Exposure to BSO for 24 h produced a 75-85% depletion of GSH levels, proportional to the inhibition of GCS activity, as well as small increases in the UDP-glucuronosyltransferase (UGT, 60%) and glutathione transferase (GST, 30%) enzyme activities in Hepa-1 wild-type (wt) cells [15].

Other interactions of Slc35a2


Analytical, diagnostic and therapeutic context of Slc35a2

  • Molecular cloning and characterization of a novel isoform of the human UDP-galactose transporter, and of related complementary DNAs belonging to the nucleotide-sugar transporter gene family [8].
  • RNA from 14 tissues was isolated from male and female C57BL/6 mice and UGT expression was determined by the branched DNA signal amplification assay [17].
  • Despite this, no significant changes in T4-UGT and T3-UGT activities occurred after treatment by any of these compounds [4].
  • These studies led us to develop a simple procedure, based on Percoll density gradient centrifugation, for preparing functional Golgi vesicles from the hUGT1-transformed Had-1 cells, that will facilitate future biochemical analyses of the UDP-galactose transporter for the elucidation of its structure-function relationship [18].


  1. Had-1, a uridine 5'-diphosphogalactose transport-defective mutant of mouse mammary tumor cell FM3A: composition of glycolipids, cell growth inhibition by lactosylceramide, and loss of tumorigenicity. Taki, T., Ogura, K., Rokukawa, C., Hara, T., Kawakita, M., Endo, T., Kobata, A., Handa, S. Cancer Res. (1991) [Pubmed]
  2. UDP-galactose transporter is required for Theiler's virus entry into mammalian cells. Hertzler, S., Kallio, P., Lipton, H.L. Virology (2001) [Pubmed]
  3. UDP-glucuronosyltransferase-mediated protection against in vitro DNA oxidation and micronucleus formation initiated by phenytoin and its embryotoxic metabolite 5-(p-hydroxyphenyl)-5-phenylhydantoin. Kim, P.M., Winn, L.M., Parman, T., Wells, P.G. J. Pharmacol. Exp. Ther. (1997) [Pubmed]
  4. Phenobarbital, beta-naphthoflavone, clofibrate, and pregnenolone-16alpha-carbonitrile do not affect hepatic thyroid hormone UDP-glucuronosyl transferase activity, and thyroid gland function in mice. Viollon-Abadie, C., Lassere, D., Debruyne, E., Nicod, L., Carmichael, N., Richert, L. Toxicol. Appl. Pharmacol. (1999) [Pubmed]
  5. Persistent glycoprotein misfolding activates the glucosidase II/UGT1-driven calnexin cycle to delay aggregation and loss of folding competence. Molinari, M., Galli, C., Vanoni, O., Arnold, S.M., Kaufman, R.J. Mol. Cell (2005) [Pubmed]
  6. Isolation and characterization of mouse FM3A cell mutants which are devoid of Newcastle disease virus receptors. Hara, T., Hattori, S., Kawakita, M. J. Virol. (1989) [Pubmed]
  7. Point mutations identified in Lec8 Chinese hamster ovary glycosylation mutants that inactivate both the UDP-galactose and CMP-sialic acid transporters. Oelmann, S., Stanley, P., Gerardy-Schahn, R. J. Biol. Chem. (2001) [Pubmed]
  8. Molecular cloning and characterization of a novel isoform of the human UDP-galactose transporter, and of related complementary DNAs belonging to the nucleotide-sugar transporter gene family. Ishida, N., Miura, N., Yoshioka, S., Kawakita, M. J. Biochem. (1996) [Pubmed]
  9. Human udp-glucuronosyltransferases: isoform selectivity and kinetics of 4-methylumbelliferone and 1-naphthol glucuronidation, effects of organic solvents, and inhibition by diclofenac and probenecid. Uchaipichat, V., Mackenzie, P.I., Guo, X.H., Gardner-Stephen, D., Galetin, A., Houston, J.B., Miners, J.O. Drug Metab. Dispos. (2004) [Pubmed]
  10. Indispensability of transmembrane domains of Golgi UDP-galactose transporter as revealed by analysis of genetic defects in UDP-galactose transporter-deficient murine had-1 mutant cell lines and construction of deletion mutants. Ishida, N., Yoshioka, S., Iida, M., Sudo, K., Miura, N., Aoki, K., Kawakita, M. J. Biochem. (1999) [Pubmed]
  11. Endoplasmic reticulum retention of the large splice variant of the UDP-galactose transporter is caused by a dilysine motif. Kabuss, R., Ashikov, A., Oelmann, S., Gerardy-Schahn, R., Bakker, H. Glycobiology (2005) [Pubmed]
  12. Induction of NAD(P)H quinone: oxidoreductase1 inhibits carcinogen-induced aberrant crypt foci in colons of Sprague-Dawley rats. Begleiter, A., Sivananthan, K., Curphey, T.J., Bird, R.P. Cancer Epidemiol. Biomarkers Prev. (2003) [Pubmed]
  13. Nuclear receptor, pregname X receptor, is required for induction of UDP-glucuronosyltranferases in mouse liver by pregnenolone-16 alpha-carbonitrile. Chen, C., Staudinger, J.L., Klaassen, C.D. Drug Metab. Dispos. (2003) [Pubmed]
  14. Activation of the mouse TATA-less and human TATA-containing UDP-glucuronosyltransferase 1A1 promoters by hepatocyte nuclear factor 1. Bernard, P., Goudonnet, H., Artur, Y., Desvergne, B., Wahli, W. Mol. Pharmacol. (1999) [Pubmed]
  15. Enzyme induction by L-buthionine (S,R)-sulfoximine in cultured mouse hepatoma cells. Shertzer, H.G., Vasiliou, V., Liu, R.M., Tabor, M.W., Nebert, D.W. Chem. Res. Toxicol. (1995) [Pubmed]
  16. Elucidation of the phenotypic change on the surface of Had-1 cell, a mutant cell line of mouse FM3A carcinoma cells selected by resistance to Newcastle disease virus infection. Hara, T., Endo, T., Furukawa, K., Kawakita, M., Kobata, A. J. Biochem. (1989) [Pubmed]
  17. Tissue- and Gender-Specific mRNA Expression of UDP-Glucuronosyltransferases (UGTs) in Mice. Buckley, D.B., Klaassen, C.D. Drug Metab. Dispos. (2007) [Pubmed]
  18. Expression of the human UDP-galactose transporter in the Golgi membranes of murine Had-1 cells that lack the endogenous transporter. Yoshioka, S., Sun-Wada, G.H., Ishida, N., Kawakita, M. J. Biochem. (1997) [Pubmed]
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