Disease relevance of SLC2A1

• We used this system in a functional cDNA screening to isolate and confirm that the glucose transporter protein 1 (GLUT-1) is a receptor for HTLV-1 [1].
• Neurons were identified by the presence of polysialogangliosides recognized by tetanus toxin (GD1b, GT1) or by the monoclonal antibody Q211 directed against polysialogangliosides containing four, five and six sialic acid residues [2].
• In acute hypoglycemia, induced by a single dose of tolbutamide (100 mg/kg body mass), HKII, PFK-1 and GS mRNA levels remained unchanged; however, levels of HKI mRNA and glucose transporter 1 (GLUT1) were significantly increased 4 h after administration [3].
• We investigated the effects on the avian ALAS-1 gene promoter of a phenobarbital-like chemical, Glut (glutethimide), and a haem synthesis inhibitor, DHA (4,6-dioxoheptanoic acid), using a reporter gene assay in transiently transfected LMH (Leghorn male hepatoma) hepatoma cells [4].

High impact information on SLC2A1

• Cloning and sequencing of chicken GLUT1 cDNA showed that it shares 95% amino acid sequence similarity to mammalian GLUT1s [5].
• Nevertheless, unlike mammalian GLUT1 mRNA, it was not induced by v-src, serum addition, or treatment with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate in chicken embryo fibroblasts [5].
• Overexpression of GLUT1 increased 3-O-methylglucose uptake, but did not alter either glucose utilization or glucose-stimulated insulin secretion [6].
• In embryonic skeletal muscle, the levels of Glut1 and Glut3 proteins and mRNA were highest very early, and declined severely by mid-development [7].
• The inhibitory effect of a constant amount of GT1 ganglioside was higher at low concentrations of membrane preparation, but the inhibition was similar at different concentrations of the substrates GM3 or UDP-N-acetylgalactosamine and at all incubation times studied [8].

Biological context of SLC2A1

• GLUT1 gene expression was identified in all tissues examined and shares 88% homology with chicken and 84% homology with human GLUT1 [9].
• The results demonstrate the utilization of cell surface GLUT-1 in HTLV-1 infection of CD4(+) T lymphocytes and implicate a critical role for the ECL1 region in viral tropism [1].
• The patterns of Glut1 and Glut3 glucose transporter protein and mRNA expression were assessed during embryogenesis of chicken brain and skeletal muscle, Glut4 protein levels were also evaluated in skeletal muscle and heart, and Glut1 was examined in the developing heart and liver [7].
• This is associated with transcriptional activation of the GLUT1 gene [10].
• In contrast, chicken GLUT1 transcription is completely uninducible, suggesting either avian signal transduction events are different or the chicken GLUT1 gene lacks these transcriptional control elements [10].

Anatomical context of SLC2A1

• Compared to the rat control, GLUT1 immunostaining of sparrow extensor digitorum communis muscle was weak and appeared to be localized to blood vessels whereas immunostaining of gastrocnemius muscles was comparable to rat muscle controls [9].
• GLUT-1 is a ubiquitously expressed plasma membrane glycoprotein with 12 transmembrane domains and 6 extracellular loops (ECL) [1].
• Even after treatment with anti-inflammatory agents, however, astrocyte graft vasculature fails to express high levels of a barrier marker, the GLUT-1 isoform of the glucose transporter [11].
• Transplantation of avascular embryonic spinal cord, that induces robust vessel ingrowth and GLUT-1 expression in intra-embryonic vessels, was unable to elicit the ingrowth of more than a few vessels from the chorioallantoic membrane vasculature, and none of these expressed glucose transporter [11].
• Commitment to the erythrocyte lineage alters expression of specific genes: TFR mRNA level increases while expression decreases for GLUT1 and GLUT3 glucose transporter mRNAs and GAD mRNA [12].

Associations of SLC2A1 with chemical compounds

• In our analysis of glucose transporter (GLUT) isoform expression, the level of GLUT1 mRNA increased with follicle development while GLUT2, GLUT3 and GLUT8 mRNA levels were unaffected by follicle development [13].
• The overall increase in GLUT-1 may reflect a deregulation of the transporter induced by ethanol exposure [14].

Analytical, diagnostic and therapeutic context of SLC2A1

• By Western blotting analysis, ethanol exposure caused a mean 7- to 10-fold increase in total GLUT-1 and a 2-fold increase in total GLUT-3 [14].

References