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Gene Review

Slc37a4  -  solute carrier family 37 (glucose-6...

Mus musculus

Synonyms: 100043178, G6PT, G6pt1, GSD-1b, mG6PT
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Disease relevance of Slc37a4


High impact information on Slc37a4

  • The bone and spleen of G6PT-/- mice are developmentally delayed and accompanied by marked hypocellularity of the bone marrow, elevation of myeloid progenitor cell frequencies in both organs and a corresponding dramatic increase in granulocyte colony stimulating factor levels in both GSD-Ib mice and humans [1].
  • Both encode transmembrane proteins sharing 93-95% sequence homology to the human GSD-1b protein [2].
  • The gene responsible for GSD-1b maps to human chromosome 11q23 and a candidate human GSD-1b cDNA that encodes a microsomal transmembrane protein has been identified [2].
  • In this study, we show that this cDNA maps to chromosome 11q23; thus it is a strong candidate for GSD-1b [2].
  • GSD-1a and GSD-1b, the two major subgroups, have been confirmed at the molecular genetic level [2].

Chemical compound and disease context of Slc37a4


Anatomical context of Slc37a4

  • Interestingly, although the G6Pase mRNA is expressed primarily in the liver, kidney, and intestine, the GSD-1b mRNA is expressed in numerous tissues, including human neutrophils/monocytes [2].
  • Ad-hG6PT infusion restores significant levels of G6PT mRNA expression in the liver, bone marrow and spleen, and corrects metabolic as well as myeloid abnormalities in G6PT(-/-) mice [5].

Associations of Slc37a4 with chemical compounds


Physical interactions of Slc37a4

  • Mutually exclusive mutations in the G6Pase gene and the G6P transport gene establish GSD la and GSD 1b as independent molecular processes and are consistent with a multicomponent translocase catalytic model [4].


  1. Impaired glucose homeostasis, neutrophil trafficking and function in mice lacking the glucose-6-phosphate transporter. Chen, L.Y., Shieh, J.J., Lin, B., Pan, C.J., Gao, J.L., Murphy, P.M., Roe, T.F., Moses, S., Ward, J.M., Lee, E.J., Westphal, H., Mansfield, B.C., Chou, J.Y. Hum. Mol. Genet. (2003) [Pubmed]
  2. Cloning and characterization of cDNAs encoding a candidate glycogen storage disease type 1b protein in rodents. Lin, B., Annabi, B., Hiraiwa, H., Pan, C.J., Chou, J.Y. J. Biol. Chem. (1998) [Pubmed]
  3. The molecular basis of type 1 glycogen storage diseases. Chou, J.Y. Curr. Mol. Med. (2001) [Pubmed]
  4. Glucose-6-phosphatase mutation G188R confers an atypical glycogen storage disease type 1b phenotype. Weston, B.W., Lin, J.L., Muenzer, J., Cameron, H.S., Arnold, R.R., Seydewitz, H.H., Mayatepek, E., Van Schaftingen, E., Veiga-da-Cunha, M., Matern, D., Chen, Y.T. Pediatr. Res. (2000) [Pubmed]
  5. Glucose-6-phosphate transporter gene therapy corrects metabolic and myeloid abnormalities in glycogen storage disease type Ib mice. Yiu, W.H., Pan, C.J., Allamarvdasht, M., Kim, S.Y., Chou, J.Y. Gene Ther. (2007) [Pubmed]
  6. Discriminant responses of the catalytic unit and glucose 6-phosphate transporter components of the hepatic glucose-6-phosphatase system in Ehrlich ascites-tumor-bearing mice. Foster, J.D., Wiedemann, J.M., Pan, C.J., Chou, J.Y., Nordlie, R.C. Arch. Biochem. Biophys. (2001) [Pubmed]
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