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Gene Review

SLC2A1  -  solute carrier family 2 (facilitated...

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Disease relevance of SLC2A1

  • Hypoxia (0.5% O2, 5% CO2, and 94.5% N2) stimulated GLUT1 mRNA expression in BRECs in a time-dependent manner with an 8.9 +/- 1.5-fold (P < 0.01) increase observed after 12 h [1].
  • Transfection of C6 glioma cells with pGL2 (containing nucleotides 2,100-2,300 of the bovine GLUT1 3'-UTR inserted at the Pfl MI site within the luciferase 3'-UTR) results in a fivefold increase in luciferase gene expression [2].
  • The absence of neuroglucopenia symptoms in chronic hypoglycemia may be due to up-regulation of the blood-brain barrier glucose transporter type 1 (GLUT1) [3].

High impact information on SLC2A1

  • The transport of glucose across the mammalian blood-brain barrier is mediated by the GLUT1 glucose transporter, which is concentrated in the endothelial cells of the cerebral microvessels [4].
  • Several studies supported an asymmetric distribution of GLUT1 protein between the luminal and abluminal membranes (1:4) with a significant proportion of intracellular transporters [4].
  • Western blot analysis with antibodies raised against either the intracellular loop of GLUT1 or the purified erythrocyte protein exhibited luminal:abluminal ratios of 1:1 [4].
  • These data suggest that hypoxia in BRECs upregulates glucose transport activity through an increase of GLUT1 expression that is partially mediated by adenosine, A2R, and the cAMP-PKA pathway [1].
  • The adenosine A2a receptor antagonist 8-(3-chlorostyryl)caffeine (CSC) (Kd = 100 nmol/l for A2R) inhibited hypoxia-stimulated GLUT1 mRNA expression by 40 +/- 8% at 100 nmo/l. Hypoxia upregulated GLUT1 protein expression by 3.0 +/- 0.3-fold after 12 h (P < 0.01), but this response was attenuated by CSC (P < 0.05) [1].

Chemical compound and disease context of SLC2A1


Biological context of SLC2A1

  • An impaired expression of Glut leads to an increase in apoptosis at the blastocyst stage and involves Bax [5].
  • Glucose deprivation causes posttranscriptional enhancement of brain capillary endothelial glucose transporter gene expression via GLUT1 mRNA stabilization [3].
  • Taken together, these findings show that hyperglycaemia increases the production rate of 12-HETE, which in turn mediates the down-regulation of GLUT-1 expression and the glucose-transport system in vascular endothelial and smooth-muscle cells [6].
  • Deletion of nucleotides 2,181-2,190 of the bovine GLUT1 3'-UTR, i.e., the putative binding site of the 80-kDa protein, completely eliminated the enhancement of luciferase activity in the transfected cells [2].
  • These putative cis/trans interactions were examined in the present studies with RNase T1 protection assays using 32P-labeled GLUT1 3'-UTR prepared from transcription plasmids and cytosolic proteins from C6 rat glioma cells [7].

Anatomical context of SLC2A1


Associations of SLC2A1 with chemical compounds


Physical interactions of SLC2A1

  • An enhanced glucose transport in response to IGF-I appears to be coupled to activation of IGF receptor type 1 and GLUT1 translocation [13].
  • PURPOSE: To investigate effects of vascular endothelial growth factor (VEGF) on glucose transport and GLUT1 glucose transporter expression in primary bovine retinal endothelial cell (BREC) cultures [14].
  • Using RNA mobility shift, UV cross-linking, and in vitro degradation assays, followed by mass-spectrometric analysis, we identified calreticulin as a specific destabilizing trans-acting factor that binds to a 10-nucleotide cis-acting element (CAE(2181-2190)) in the 3'-untranslated region of GLUT-1 mRNA [15].

Regulatory relationships of SLC2A1


Other interactions of SLC2A1

  • GLUT 1 mRNA quantity decreased whereas GLUT 2 increased with age [18].
  • Dc II, Glut-1, and Glut-4 were more abundant in the TE than in ICM [19].
  • As part of the validation of this technique, we determined that there was no nonspecific amplification of bovine GLUTs by rhodopsin primers, that there were no differences in amplification due to different regions of the Glut gene amplified, and that there were no secondary structure effects on amplification [18].
  • CONCLUSIONS: The present study demonstrates VEGF-mediated enhancement of retinal endothelial cell glucose transport and suggests that this increase is due to PKC beta-mediated translocation of cytosolic GLUT1 to the plasma membrane surface [14].
  • Notably, the currents were desensitized, reduced in a glucose concentration-dependent manner, and markedly inhibited by either a second application of glucose or the addition of glucose to the patch electrode filling solution; they were potentiated, however, by treatment with cytochalasin B, a GLUT1 to GLUT5 inhibitor [20].

Analytical, diagnostic and therapeutic context of SLC2A1


  1. Hypoxia upregulates glucose transport activity through an adenosine-mediated increase of GLUT1 expression in retinal capillary endothelial cells. Takagi, H., King, G.L., Aiello, L.P. Diabetes (1998) [Pubmed]
  2. Site-directed deletion of a 10-nucleotide domain of the 3'-untranslated region of the GLUT1 glucose transporter mRNA eliminates cytosolic protein binding in human brain tumors and induction of reporter gene expression. Tsukamoto, H., Boado, R.J., Pardridge, W.M. J. Neurochem. (1997) [Pubmed]
  3. Glucose deprivation causes posttranscriptional enhancement of brain capillary endothelial glucose transporter gene expression via GLUT1 mRNA stabilization. Boado, R.J., Pardridge, W.M. J. Neurochem. (1993) [Pubmed]
  4. Glucose transporter asymmetries in the bovine blood-brain barrier. Simpson, I.A., Vannucci, S.J., DeJoseph, M.R., Hawkins, R.A. J. Biol. Chem. (2001) [Pubmed]
  5. Mitogenic and anti-apoptotic activity of insulin on bovine embryos produced in vitro. Augustin, R., Pocar, P., Wrenzycki, C., Niemann, H., Fischer, B. Reproduction (2003) [Pubmed]
  6. A natural protective mechanism against hyperglycaemia in vascular endothelial and smooth-muscle cells: role of glucose and 12-hydroxyeicosatetraenoic acid. Alpert, E., Gruzman, A., Totary, H., Kaiser, N., Reich, R., Sasson, S. Biochem. J. (2002) [Pubmed]
  7. Cis-element/cytoplasmic protein interaction within the 3'-untranslated region of the GLUT1 glucose transporter mRNA. Dwyer, K.J., Boado, R.J., Pardridge, W.M. J. Neurochem. (1996) [Pubmed]
  8. Distinct regulation of glucose transport and GLUT1/GLUT3 transporters by glucose deprivation and IGF-I in chromaffin cells. Fladeby, C., Skar, R., Serck-Hanssen, G. Biochim. Biophys. Acta (2003) [Pubmed]
  9. Regulation of hexose transport in aortic endothelial cells by vascular permeability factor and tumor necrosis factor-alpha, but not by insulin. Pekala, P., Marlow, M., Heuvelman, D., Connolly, D. J. Biol. Chem. (1990) [Pubmed]
  10. High glucose downregulates glucose transport activity in retinal capillary pericytes but not endothelial cells. Mandarino, L.J., Finlayson, J., Hassell, J.R. Invest. Ophthalmol. Vis. Sci. (1994) [Pubmed]
  11. A sodium- and energy-dependent glucose transporter with similarities to SGLT1-2 is expressed in bovine cortical vessels. Nishizaki, T., Kammesheidt, A., Sumikawa, K., Asada, T., Okada, Y. Neurosci. Res. (1995) [Pubmed]
  12. Captopril inhibits glucose accumulation in retinal cells in diabetes. Zhang, J.Z., Gao, L., Widness, M., Xi, X., Kern, T.S. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  13. GLUT1-mediated glucose transport and its regulation by IGF-I in cultured bovine chromaffin cells. Fladeby, C., Bjønness, B., Serck-Hanssen, G. J. Cell. Physiol. (1996) [Pubmed]
  14. Enhancement of glucose transport by vascular endothelial growth factor in retinal endothelial cells. Sone, H., Deo, B.K., Kumagai, A.K. Invest. Ophthalmol. Vis. Sci. (2000) [Pubmed]
  15. Calreticulin destabilizes glucose transporter-1 mRNA in vascular endothelial and smooth muscle cells under high-glucose conditions. Totary-Jain, H., Naveh-Many, T., Riahi, Y., Kaiser, N., Eckel, J., Sasson, S. Circ. Res. (2005) [Pubmed]
  16. Molecular cloning and mRNA expression of the bovine insulin-responsive glucose transporter (GLUT4). Abe, H., Morimatsu, M., Nikami, H., Miyashige, T., Saito, M. J. Anim. Sci. (1997) [Pubmed]
  17. Regulation of glucose transporter 1 (GLUT1) gene expression by epidermal growth factor in bovine corneal endothelial cells. Ishida, K., Yamashita, H., Katagiri, H., Oka, Y. Jpn. J. Ophthalmol. (1995) [Pubmed]
  18. Measurement of GLUT mRNA in liver of fetal and neonatal rats using a novel method of quantitative polymerase chain reaction. Lane, R.H., Flozak, A.S., Simmons, R.A. Biochem. Mol. Med. (1996) [Pubmed]
  19. Timing of blastocyst expansion affects spatial messenger RNA expression patterns of genes in bovine blastocysts produced in vitro. Wrenzycki, C., Herrmann, D., Niemann, H. Biol. Reprod. (2003) [Pubmed]
  20. Low glucose enhances Na+/glucose transport in bovine brain artery endothelial cells. Nishizaki, T., Matsuoka, T. Stroke (1998) [Pubmed]
  21. Characterization of glucose transporter in cultured human retinal pigment epithelial cells: gene expression and effect of growth factors. Takagi, H., Tanihara, H., Seino, Y., Yoshimura, N. Invest. Ophthalmol. Vis. Sci. (1994) [Pubmed]
  22. The insulin-dependent glucose transporter isoform 4 is expressed in bovine blastocysts. Navarrete Santos, A., Augustin, R., Lazzari, G., Galli, C., Sreenan, J.M., Fischer, B. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  23. Enhanced GLUT1 glucose transporter and cytoskeleton gene expression in cultured bovine brain capillary endothelial cells after treatment with phorbol esters and serum. Farrell, C.R., Boado, R.J., Pardridge, W.M. Brain Res. Mol. Brain Res. (1992) [Pubmed]
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