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Gene Review

Slc2a4  -  solute carrier family 2 (facilitated...

Mus musculus

Synonyms: GLUT-4, GT2, Glucose transporter type 4, insulin-responsive, Glut-4, Glut4, ...
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Disease relevance of Slc2a4

  • We used adenovirus to overexpress the cytosolic domain of these syntaxin's and studied their effects on Glut4 traffic [1].
  • We conclude that HIV protease inhibitors as a class are capable of selectively inhibiting the transport function of Glut4 and that this effect may be responsible for a major iatrogenic complication frequently observed in HIV patients [2].
  • From insulin receptor signalling to Glut 4 translocation abnormalities in obesity and insulin resistance [3].
  • In epididymal fat of L-Scap- mice, phosphorylated Akt, Glut-4 mRNA, and glucose uptake are also increased, indicating insulin hypersensitivity [4].

Psychiatry related information on Slc2a4

  • However, the Glut4-selective abundance in cerebral motor areas supports its suggested role in providing the energy needed for the control of the motor activity [5].

High impact information on Slc2a4


Biological context of Slc2a4


Anatomical context of Slc2a4

  • Moreover, we observed that T0901317 produced in itself a significant increase over basal glucose uptake consistent with an increase of SLC2A4 protein content in plasma membrane, attributable to the activation of protein kinase zeta and/or the increase of Slc2a4 expression [15].
  • In this study, we have quantified the absolute levels of expression of these proteins in murine 3T3-L1 adipocytes, with the objective of determining the stoichiometry of these proteins both relative to each other and also in comparison with previous estimates of Glut4 levels within these cells [16].
  • Glut4 is targeted to specific vesicles in adipocytes of transgenic mice overexpressing Glut4 selectively in adipose tissue [17].
  • Glut4-containing intracellular membranes from both cell types have a specific and narrow distribution in these gradients, i.e. behave as homogeneous vesicles with identical sedimentation coefficients and different buoyant densities [17].
  • To study compartmentalization of intracellular Glut4 in these cells, we fractionated light microsomes prepared from transgenic and normal adipocytes in velocity and density sucrose gradients [17].

Associations of Slc2a4 with chemical compounds

  • Neomycin prevents the wortmannin inhibition of insulin-stimulated Glut4 translocation and glucose transport in 3T3-L1 adipocytes [18].
  • Soleus muscles from male Glut 4-null mice took up twice more deoxyglucose in the absence of insulin than control muscles, but did not respond to insulin [8].
  • To determine whether indinavir may be directly affecting the intrinsic transport activity of glucose transporters, the Glut1 and Glut4 isoforms were heterologously expressed and analyzed in Xenopus laevis oocytes [2].
  • Subcellular fractionation experiments demonstrated that reduction in insulin-stimulated 2-deoxyglucose uptake by glucosamine was due to an inhibition of translocation of both Glut 1 and Glut 4 from the low density microsomes (LDM) to the plasma membrane [12].
  • Increase of triglyceride content over culture time and mRNA expression of other adipocyte genes, such as PPARgamma and Glut-4, were found to be similar [19].
  • Taken together, these data show that insulin signaling accelerates the transition from docking of GLUT4-containing vesicles to their fusion with the plasma membrane and promotes GLUT4 accumulation in clathrin-based endocytic structures on the plasma membrane [20].
  • S21A-C/EBPalpha had impaired ability to activate the Glut4 promoter specifically, and S21A-C/EBPalpha expression resulted in diminished GLUT4 and adiponectin expression, as well as reduced insulin-stimulated glucose uptake [21].

Physical interactions of Slc2a4

  • The mechanisms underlying insulin and insulin-like growth factor-I (IGF-I) action on glucose transport share similar processes leading to Glut 4 translocation after respective receptor activation [22].

Regulatory relationships of Slc2a4


Other interactions of Slc2a4


Analytical, diagnostic and therapeutic context of Slc2a4


  1. Syntaxin 6 regulates Glut4 trafficking in 3T3-L1 adipocytes. Perera, H.K., Clarke, M., Morris, N.J., Hong, W., Chamberlain, L.H., Gould, G.W. Mol. Biol. Cell (2003) [Pubmed]
  2. The mechanism of insulin resistance caused by HIV protease inhibitor therapy. Murata, H., Hruz, P.W., Mueckler, M. J. Biol. Chem. (2000) [Pubmed]
  3. From insulin receptor signalling to Glut 4 translocation abnormalities in obesity and insulin resistance. Le Marchand-Brustel, Y., Tanti, J.F., Cormont, M., Ricort, J.M., Grémeaux, T., Grillo, S. J. Recept. Signal Transduct. Res. (1999) [Pubmed]
  4. Compensatory increase in fatty acid synthesis in adipose tissue of mice with conditional deficiency of SCAP in liver. Kuriyama, H., Liang, G., Engelking, L.J., Horton, J.D., Goldstein, J.L., Brown, M.S. Cell metabolism. (2005) [Pubmed]
  5. Immunohistochemical localization and quantification of glucose transporters in the mouse brain. Choeiri, C., Staines, W., Messier, C. Neuroscience (2002) [Pubmed]
  6. The exocyst complex is required for targeting of Glut4 to the plasma membrane by insulin. Inoue, M., Chang, L., Hwang, J., Chiang, S.H., Saltiel, A.R. Nature (2003) [Pubmed]
  7. Insulin resistance and the disruption of Glut4 trafficking in skeletal muscle. Mueckler, M. J. Clin. Invest. (2001) [Pubmed]
  8. Diverse effects of Glut 4 ablation on glucose uptake and glycogen synthesis in red and white skeletal muscle. Stenbit, A.E., Burcelin, R., Katz, E.B., Tsao, T.S., Gautier, N., Charron, M.J., Le Marchand-Brustel, Y. J. Clin. Invest. (1996) [Pubmed]
  9. Overexpression of Glut4 protein in muscle increases basal and insulin-stimulated whole body glucose disposal in conscious mice. Ren, J.M., Marshall, B.A., Mueckler, M.M., McCaleb, M., Amatruda, J.M., Shulman, G.I. J. Clin. Invest. (1995) [Pubmed]
  10. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes. Yang, Q., Graham, T.E., Mody, N., Preitner, F., Peroni, O.D., Zabolotny, J.M., Kotani, K., Quadro, L., Kahn, B.B. Nature (2005) [Pubmed]
  11. Sequence, tissue distribution, and differential expression of mRNA for a putative insulin-responsive glucose transporter in mouse 3T3-L1 adipocytes. Kaestner, K.H., Christy, R.J., McLenithan, J.C., Braiterman, L.T., Cornelius, P., Pekala, P.H., Lane, M.D. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  12. Glucosamine-induced insulin resistance in 3T3-L1 adipocytes is caused by depletion of intracellular ATP. Hresko, R.C., Heimberg, H., Chi, M.M., Mueckler, M. J. Biol. Chem. (1998) [Pubmed]
  13. Skeletal muscle glucose transport and metabolism are enhanced in transgenic mice overexpressing the Glut4 glucose transporter. Hansen, P.A., Gulve, E.A., Marshall, B.A., Gao, J., Pessin, J.E., Holloszy, J.O., Mueckler, M. J. Biol. Chem. (1995) [Pubmed]
  14. Age-dependent changes in phenotypes and candidate gene analysis in a polygenic animal model of Type II diabetes mellitus; NSY mouse. Ueda, H., Ikegami, H., Kawaguchi, Y., Fujisawa, T., Nojima, K., Babaya, N., Yamada, K., Shibata, M., Yamato, E., Ogihara, T. Diabetologia (2000) [Pubmed]
  15. Liver X receptor agonists ameliorate TNFalpha-induced insulin resistance in murine brown adipocytes by downregulating protein tyrosine phosphatase-1B gene expression. Fern??ndez-Veledo, S., Nieto-Vazquez, I., Rondinone, C.M., Lorenzo, M. Diabetologia (2006) [Pubmed]
  16. Quantification of SNARE protein levels in 3T3-L1 adipocytes: implications for insulin-stimulated glucose transport. Hickson, G.R., Chamberlain, L.H., Maier, V.H., Gould, G.W. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  17. Glut4 is targeted to specific vesicles in adipocytes of transgenic mice overexpressing Glut4 selectively in adipose tissue. Tozzo, E., Kahn, B.B., Pilch, P.F., Kandror, K.V. J. Biol. Chem. (1996) [Pubmed]
  18. Neomycin prevents the wortmannin inhibition of insulin-stimulated Glut4 translocation and glucose transport in 3T3-L1 adipocytes. James, D.J., Salaün, C., Brandie, F.M., Connell, J.M., Chamberlain, L.H. J. Biol. Chem. (2004) [Pubmed]
  19. Generation of mature fat pads in vitro and in vivo utilizing 3-D long-term culture of 3T3-L1 preadipocytes. Fischbach, C., Spruss, T., Weiser, B., Neubauer, M., Becker, C., Hacker, M., Göpferich, A., Blunk, T. Exp. Cell Res. (2004) [Pubmed]
  20. Insulin stimulates membrane fusion and GLUT4 accumulation in clathrin coats on adipocyte plasma membranes. Huang, S., Lifshitz, L.M., Jones, C., Bellve, K.D., Standley, C., Fonseca, S., Corvera, S., Fogarty, K.E., Czech, M.P. Mol. Cell. Biol. (2007) [Pubmed]
  21. Phosphorylation of CCAAT/enhancer-binding protein alpha regulates GLUT4 expression and glucose transport in adipocytes. Cha, H.C., Oak, N.R., Kang, S., Tran, T.A., Kobayashi, S., Chiang, S.H., Tenen, D.G., MacDougald, O.A. J. Biol. Chem. (2008) [Pubmed]
  22. Effected of insulin and insulin-like growth factor-I on glucose transport and its transporters in soleus muscle of lean and obese mice. Le Marchand-Brustel, Y., Heydrick, S.J., Jullien, D., Gautier, N., Van Obberghen, E. Metab. Clin. Exp. (1995) [Pubmed]
  23. Insulin-stimulated plasma membrane fusion of Glut4 glucose transporter-containing vesicles is regulated by phospholipase D1. Huang, P., Altshuller, Y.M., Hou, J.C., Pessin, J.E., Frohman, M.A. Mol. Biol. Cell (2005) [Pubmed]
  24. Glut4 storage vesicles without Glut4: transcriptional regulation of insulin-dependent vesicular traffic. Gross, D.N., Farmer, S.R., Pilch, P.F. Mol. Cell. Biol. (2004) [Pubmed]
  25. Essential role of insulin receptor substrate-2 in insulin stimulation of Glut4 translocation and glucose uptake in brown adipocytes. Fasshauer, M., Klein, J., Ueki, K., Kriauciunas, K.M., Benito, M., White, M.F., Kahn, C.R. J. Biol. Chem. (2000) [Pubmed]
  26. Rab10, a target of the AS160 Rab GAP, is required for insulin-stimulated translocation of GLUT4 to the adipocyte plasma membrane. Sano, H., Eguez, L., Teruel, M.N., Fukuda, M., Chuang, T.D., Chavez, J.A., Lienhard, G.E., McGraw, T.E. Cell Metab. (2007) [Pubmed]
  27. Insulin regulates fusion of GLUT4 vesicles independent of Exo70-mediated tethering. Lizunov, V.A., Lisinski, I., Stenkula, K., Zimmerberg, J., Cushman, S.W. J. Biol. Chem. (2009) [Pubmed]
  28. Insulin unmasks a COOH-terminal Glut4 epitope and increases glucose transport across T-tubules in skeletal muscle. Wang, W., Hansen, P.A., Marshall, B.A., Holloszy, J.O., Mueckler, M. J. Cell Biol. (1996) [Pubmed]
  29. Characterization of the insulin-regulated membrane aminopeptidase in 3T3-L1 adipocytes. Ross, S.A., Scott, H.M., Morris, N.J., Leung, W.Y., Mao, F., Lienhard, G.E., Keller, S.R. J. Biol. Chem. (1996) [Pubmed]
  30. The amino terminus of insulin-responsive aminopeptidase causes Glut4 translocation in 3T3-L1 adipocytes. Waters, S.B., D'Auria, M., Martin, S.S., Nguyen, C., Kozma, L.M., Luskey, K.L. J. Biol. Chem. (1997) [Pubmed]
  31. Runx2 deficiency in chondrocytes causes adipogenic changes in vitro. Enomoto, H., Furuichi, T., Zanma, A., Yamana, K., Yoshida, C., Sumitani, S., Yamamoto, H., Enomoto-Iwamoto, M., Iwamoto, M., Komori, T. J. Cell. Sci. (2004) [Pubmed]
  32. Effect of cold acclimation on the expression of glucose transporter Glut 4. Olichon-Berthe, C., Van Obberghen, E., Le Marchand-Brustel, Y. Mol. Cell. Endocrinol. (1992) [Pubmed]
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