Disease relevance of Slc2a1

• Hypoxia inducible factor (HIF)-1alpha and Glucose Transporter 1 (Glut-1) levels were determined by Western blot [1].
• In vivo hyperglycemia and its effect on Glut-1 expression in the embryonic heart [2].
• This increase in glucose transport was not associated with a change in transporter affinity for glucose, but increased Glut-1 expression was observed indicating a 'heat stress' effect that overrode the effects attributable to oncogene loss [3].
• The GT1 strain (inducing 100% mortality at day 9) also gave the fastest response in terms of weight loss (onset by day 8) and increase in serum haptoglobin (onset by day 6), which occurred 1-2 days before these parameters were affected in the other low-dose groups [4].

High impact information on Slc2a1

• Whether this is due to a change in Glut 1 intrinsic activity or targeting and/or to the appearance of another glucose transporter remains to be determined [5].
• An improved immunogold labeling procedure was used to examine the subcellular distribution of glucose transporters in Lowricryl HM20-embedded skeletal muscle from transgenic mice overexpressing either Glut1 or Glut4 [6].
• Glut1 was highly enriched in the sarcolemma, both in the basal state and after insulin treatment [6].
• Here we demonstrate that the glutamate receptor agonist, N-methyl-D-aspartic acid (NMDA), nitric oxide (NO) and cGMP each repress expression of the gonadotropin-releasing hormone (GnRH) gene in the hypothalamic cell line, GT1 [7].
• Activation of this pathway specifically represses expression of a reporter gene containing the regulatory region of the GnRH gene in transfected GT1 cells, indicating that repression occurs at the transcriptional level [7].

Biological context of Slc2a1

• The levels of the Glut-1 mRNA declined about 3-fold between days 7.5 and 12.5 of gestation [8].
• Nucleotide sequence analysis revealed that each of these clones was a different member of the family of facilitative glucose transporters (Glut genes) [8].
• To investigate the transcriptional activation of Glut1 gene, transient transfection of cells with luciferase reporter construct driven by Glut1 promoter was performed [9].
• GT2 cDNA encodes a protein with 63% amino acid sequence identity and a similar structural organization to GT1 [10].
• To test the role of glucose uptake and phosphorylation in growth factor-independent survival, cells were transfected with Glut1 and hexokinase 1 (Glut1/HK1) cells [11].

Anatomical context of Slc2a1

• While both transporters were expressed in the amnion and chorion, only Glut-1 was expressed in the ectoplacental cone [8].
• METHODS: The rate of 2-deoxyglucose uptake was measured in Xenopus laevis oocytes heterologously expressing mammalian Glut isoforms [12].
• GT1 mRNA is most abundant in mouse brain and is expressed in both 3T3-L1 preadipocytes and adipocytes [10].
• One of these cDNAs encodes the murine homolog of the human hepG2/erythrocyte glucose transporter, termed GT1 [10].
• In addition, our data indicate that the restriction of Glut 1 expression to the intraneural capillaries reflects the onset of bbb function in the mouse embryo [13].

Associations of Slc2a1 with chemical compounds

• HIF-1alpha and Glut-1 levels are increased following APAP poisoning, implying that HIF-1alpha is functional during the pathogenic response to APAP poisoning [1].
• Nevertheless, expression of Glut1 and HK1 promoted increased cytosolic NADH and NADPH levels relative to those of the control cells upon growth factor withdrawal, prevented activation of Bax, and promoted growth factor-independent survival [11].
• Glut-1 and HKI, but not GRP78, are likely involved in tolbutamide-induced cardiac dysmorphogenesis [14].
• Reduction of intracellular ATP using azide inhibited Glut 1 and Glut 4 translocation from the LDM to the plasma membrane, insulin receptor autophosphorylation, and IRS-1 tyrosine phosphorylation [15].
• 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 [15].

Other interactions of Slc2a1

• The differentially expressed cDNA clones represent mouse Glut-1 and Glut-3 [8].
• We found that Glut1 transcription was also increased by ET-1 and cAMP in a synergistic fashion [9].
• Glut-1 expression was increased in WT and eNOS KO mice [1].
• Furthermore, PMA was found to act synergistically with 8-bromo cAMP to induce Glut1 transcription and ET-1 was shown to activate novel PKCdelta and PKC [9].
• Glut1/HK1 cells accumulated Glut1 on the cell surface and had high glucose uptake capacity similar to that of cells with constitutively active Akt (mAkt) [11].

Analytical, diagnostic and therapeutic context of Slc2a1

• Glut 1 immunofluorescence staining was done on cryosections using a rabbit polyclonal antiserum to purified human erythrocyte glucose transporter [13].
• Glut-1, HKI, and GRP78 protein levels were determined by Western analysis, and Glut-1 mRNA was measured by RT-PCR [14].
• Embryos were examined for morphology and total cardiac protein, and embryonic hearts were evaluated for Glut-1 protein and mRNA expression immediately after treatment (GD 9.75, GD 10.0), as well as on GD 10.5 and GD 12 [2].

References