Affinage

Showing SLC2A1GLUT1 is a alias.

SLC2A1

Solute carrier family 2, facilitated glucose transporter member 1 · UniProt P11166

Length
492 aa
Mass
54.1 kDa
Annotated
2026-06-10
100 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC2A1/GLUT-1 is the constitutive facilitative glucose transporter that delivers glucose across the plasma membrane to fuel cellular metabolism, and it is the obligate hexose transporter of the blood-brain barrier (PMID:10980529, PMID:16497725). Its substrate selectivity and cation impermeability are determined by individual transmembrane residues, with isoleucine deletions in the transmembrane domain both abrogating glucose transport and creating a cation-leaky channel (PMID:22492876). Transport activity is set not only by surface abundance but by direct protein-protein modulation: stomatin binds the GLUT-1 C-terminal 42-residue segment and suppresses intrinsic transport activity without changing membrane content, and GLUT-1 functions within a multiprotein erythrocyte membrane complex with stomatin, band 3/SLC4A1, and aquaporin-1 (PMID:11287341, PMID:23219802). Surface delivery is governed by trafficking: N-glycosylation-dependent folding under calnexin/calreticulin in the ER (PMID:8662691), PI3-kinase-dependent insulin/TSH-induced translocation (PMID:11089547), ATM-mediated phosphorylation at S490 that drives GIPC1-dependent recycling endosome surface localization (PMID:23776597), and RAB21/retromer-dependent endosomal recycling that prevents lysosomal mis-sorting and thereby restrains AMPK-ULK1 autophagy (PMID:35993307). GLUT-1 transcription is driven by Sp1 in developing cardiomyocytes (PMID:10364200) and by HIF-1α under hypoxia (PMID:34983574), while its mRNA is stabilized by osmotic and metabolic stress (PMID:11546675, PMID:2100513) and repressed post-transcriptionally by microRNAs targeting its 3'-UTR (PMID:29374351, PMID:28440026). Functionally, GLUT-1-mediated glucose uptake fuels macrophage glycolysis required for phagocytosis and inflammatory metabolic programming (PMID:30659108), drives feed-forward extracellular matrix production in mesangial cells (PMID:11249857), and protects against hypoxic apoptosis upstream of JNK stress signaling (PMID:10780954). Heterozygous loss-of-function mutations cause GLUT-1 Deficiency Syndrome with hypoglycorrhachia, seizures, and microcephaly, and allelic mutations cause paroxysmal exercise-induced dyskinesia (DYT9/DYT18) (PMID:10980529, PMID:21832227). GLUT-1 also serves as the functional receptor for HTLV-1 and HTLV-2 (PMID:14622599).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1990 Medium

    Established that GLUT-1 expression is regulated post-transcriptionally, addressing whether transporter abundance is controlled beyond transcription.

    Evidence Vanadate-induced mRNA half-life measurement by actinomycin D chase and Northern blot in NIH3T3 fibroblasts

    PMID:2100513

    Open questions at the time
    • The trans-acting factor or 3'-UTR element mediating stabilization was not identified
    • Single stimulus and single cell type
  2. 1994 High

    Showed that glucose transporter isoform identity, not just transport capacity, shapes whole-body insulin responsiveness, distinguishing GLUT-1 from insulin-responsive GLUT-4.

    Evidence Euglycemic hyperinsulinemic clamp in transgenic mice overexpressing GLUT-1 versus GLUT-4 in skeletal muscle

    PMID:7977725

    Open questions at the time
    • Mechanism for paradoxical reduction in insulin-stimulated disposal and hyperketonemia not resolved
    • Does not address endogenous GLUT-1 physiology
  3. 1996 High

    Defined the biogenesis route of GLUT-1, showing glycosylation-dependent ER chaperone engagement governs folding before surface delivery.

    Evidence In vitro translation with pancreatic microsomes, anti-calnexin Co-IP, UV cross-linking, and a non-glycosylated AGGT155 mutant

    PMID:8662691

    Open questions at the time
    • Downstream quality-control fate of misfolded GLUT-1 not characterized
    • In vitro reconstitution only
  4. 1999 High

    Identified Sp1 as the transcriptional driver of GLUT-1 in heart and linked perinatal Sp1 loss to developmental repression of the gene.

    Evidence Reporter assays, EMSA with Sp1 site mutagenesis, and developmental Western blot in cardiomyocytes

    PMID:10364200

    Open questions at the time
    • Cofactors at the Sp1 site not defined
    • Restricted to cardiac/skeletal muscle context
  5. 1999 Medium

    Resolved the signaling route for stimulus-induced GLUT-1 surface translocation, showing it is PI3-kinase-dependent and PKA-independent.

    Evidence Pharmacological dissection with wortmannin, LY294002, H89, and tunicamycin plus subcellular fractionation in FRTL-5 thyroid cells

    PMID:11089547

    Open questions at the time
    • Vesicle machinery downstream of PI3K not identified
    • Pharmacological inhibitors lack target specificity
  6. 2000 High

    Confirmed in vivo that single-allele GLUT-1 mutations are sufficient to impair CNS glucose delivery, establishing GLUT-1 as the essential blood-brain barrier hexose transporter and defining GLUT-1 Deficiency Syndrome.

    Evidence Mutation screening across multiple patients correlated with erythrocyte glucose transport assays

    PMID:10980529

    Open questions at the time
    • Genotype-phenotype severity correlation not fully resolved
    • Does not address tissue-specific dosage thresholds
  7. 2000 Medium

    Placed GLUT-1-dependent glucose uptake upstream of the JNK stress-kinase apoptosis pathway, linking the transporter to cell survival under hypoxia.

    Evidence GLUT-1 overexpression with hypoxia/rotenone challenge, JNK activity assay, and dominant-negative MEKK1 epistasis in vascular smooth muscle cells

    PMID:10780954

    Open questions at the time
    • Metabolic signal connecting glucose uptake to JNK suppression not defined
    • Overexpression rather than endogenous regulation
  8. 2001 High

    Demonstrated direct protein-protein modulation of GLUT-1 transport activity by stomatin, independent of surface abundance.

    Evidence Co-IP, GST pulldown mapping to the GLUT-1 C-terminal 42 residues, and glucose transport assay in transfected cells

    PMID:11287341

    Open questions at the time
    • Structural basis of the C-terminal interaction not solved
    • Mechanism by which binding lowers intrinsic activity unknown
  9. 2001 Medium

    Showed GLUT-1-mediated glucose uptake drives a feed-forward loop promoting extracellular matrix production, linking the transporter to diabetic glomerular pathology.

    Evidence Antisense GLUT-1 knockdown with fibronectin readout and metabolic substrate substitution in mesangial cells

    PMID:11249857

    Open questions at the time
    • Metabolic signal coupling glucose flux to fibronectin transcription not identified
    • Single cell type
  10. 2001 Medium

    Defined a biphasic GLUT-1 response to osmotic stress combining transcriptional induction and mRNA stabilization, mapping a 44-bp proximal promoter element.

    Evidence mRNA stability assay, promoter deletion reporters, transport assay, and membrane fractionation under hyperosmolarity

    PMID:11546675

    Open questions at the time
    • The factor mediating mRNA stabilization not identified
    • Early phase mechanism (non-transcriptional, non-translocation) unexplained
  11. 2003 High

    Identified GLUT-1 as the obligate functional receptor for HTLV-1 and HTLV-2, with envelope binding directly inhibiting glucose transport.

    Evidence siRNA knockdown, ectopic GLUT-1 versus GLUT-3 rescue, glucose transport inhibition, and infection assays

    PMID:14622599

    Open questions at the time
    • The GLUT-1 binding interface for envelope glycoprotein not mapped
    • Whether transport inhibition is mechanistically required for entry not resolved
  12. 2006 High

    Recapitulated GLUT-1 Deficiency Syndrome in vivo, directly demonstrating that GLUT-1 haploinsufficiency reduces brain glucose uptake and causes the seizure/microcephaly phenotype.

    Evidence Heterozygous GLUT-1 knockout mouse with PET, EEG, CSF glucose, Western blot, and behavioral assays

    PMID:16497725

    Open questions at the time
    • Cellular site of critical dosage sensitivity (endothelium vs glia vs neuron) not isolated
    • Developmental timing of irreversible injury not defined
  13. 2010 Medium

    Established a developmental and structural role for GLUT-1 in blood-brain barrier formation beyond simple glucose delivery, showing it is required for cerebral endothelial integrity.

    Evidence Morpholino Glut1 knockdown in zebrafish with junction protein immunostaining and BBB permeability assays

    PMID:21194153

    Open questions at the time
    • Whether the vascular defect is secondary to metabolic deficit or a distinct function unclear
    • Morpholino off-target effects not fully excluded
  14. 2011 High

    Expanded the GLUT-1 deficiency phenotypic spectrum to paroxysmal dyskinesia, showing DYT9 is allelic with DYT18 and that the mutations reduce glucose uptake.

    Evidence SLC2A1 sequencing, cosegregation, control screening, and glucose uptake functional assays in two pedigrees

    PMID:21832227

    Open questions at the time
    • Why partial loss yields paroxysmal rather than constant phenotype not explained
    • Genotype-phenotype determinants across the spectrum unresolved
  15. 2012 High

    Defined the native GLUT-1 membrane complex partners in erythrocytes, situating the transporter within a multiprotein assembly.

    Evidence In situ chemical cross-linking, immunoaffinity purification, and mass spectrometry of erythrocyte membranes

    PMID:23219802

    Open questions at the time
    • Functional consequence of band 3 and aquaporin-1 association not tested
    • Stoichiometry and architecture of the complex unknown
  16. 2012 Medium

    Showed that single transmembrane residues govern both glucose selectivity and cation impermeability, as an isoleucine deletion creates a cation-leaky GLUT-1.

    Evidence SLC2A1 sequencing with red cell cation content and temperature-dependent K+ loss assays

    PMID:22492876

    Open questions at the time
    • Single family; structural mechanism of the cation leak not modeled
    • Relationship between leak and clinical phenotype not fully defined
  17. 2013 High

    Identified ATM-mediated S490 phosphorylation as a regulatory switch driving GLUT-1 surface localization through GIPC1-dependent recycling.

    Evidence S490A/S490D mutants, pharmacological ATM modulation, GLUT-1/GIPC1 Co-IP, and transport assays in cells and mouse muscle

    PMID:23776597

    Open questions at the time
    • Physiological signal activating ATM-GLUT-1 phosphorylation in muscle not defined
    • How GIPC1 engagement directs recycling mechanistically unclear
  18. 2017 Medium

    Demonstrated microRNA control of GLUT-1, with miR-148b directly targeting the 3'-UTR to limit glycolysis in cancer cells.

    Evidence Luciferase 3'-UTR reporter, Western blot, siRNA, GLUT1 overexpression rescue, and glucose/lactate assays in gastric cancer cells

    PMID:28440026

    Open questions at the time
    • In vivo relevance of the miR-148b axis not established
    • Single cancer context
  19. 2017 Medium

    Established GLUT-1-mediated retinal glucose transport as a causal driver of diabetic inflammatory microangiopathy.

    Evidence Intravitreal GLUT-1 siRNA in diabetic mice with retinal glucose, ICAM-1/TNF-α, leukostasis, and vascular permeability readouts

    PMID:28785055

    Open questions at the time
    • Cell type within retina mediating the effect not isolated
    • Single lab in vivo model
  20. 2018 Medium

    Added a second microRNA, miR-328, directly repressing GLUT1 via its 3'-UTR to reduce glycolysis in colon cancer.

    Evidence Luciferase reporter with SLC2A1 3'-UTR, Western blot, and miR-328 overexpression in colon cancer cell lines

    PMID:29374351

    Open questions at the time
    • Functional metabolic rescue not shown as definitively as for miR-148b
    • No in vivo validation
  21. 2019 High

    Defined GLUT1 as the essential fuel source for macrophage glycolysis, required for phagocytosis and inflammatory metabolic programming.

    Evidence Myeloid-specific Slc2a1 knockout with Seahorse flux, metabolite profiling, flow cytometry, phagocytosis, and atherosclerosis modeling

    PMID:30659108

    Open questions at the time
    • Whether glycolytic versus non-metabolic functions drive the phenotype not fully separated
    • Compensatory glutamine/oleate pathways not therapeutically tested
  22. 2022 Medium

    Identified RAB21-controlled retromer recycling as essential for keeping GLUT-1 at the surface, with disruption mis-sorting it to lysosomes and activating autophagy.

    Evidence RAB21 siRNA, microscopy of GLUT-1 and SNX27 retromer, glucose uptake, AMPK-ULK1 analysis, and tumor xenograft

    PMID:35993307

    Open questions at the time
    • Direct RAB21-GLUT-1 versus indirect retromer effect not separated
    • Single lab
  23. 2022 Medium

    Established HIF-1α as the transcriptional driver of GLUT-1 induction in blood-brain barrier endothelium under hypoxia.

    Evidence Hypoxia and desferrioxamine HIF-1α stabilization in brain capillary endothelial cells with glucose uptake, qPCR, and Western blot

    PMID:34983574

    Open questions at the time
    • Direct HIF-1α occupancy of the SLC2A1 promoter not shown here
    • Primary culture model only
  24. 2022 Medium

    Linked CDK6 to GLUT1 enhancer activity, showing CDK6 maintains active histone marks that drive GLUT1 transcription in hepatocellular carcinoma.

    Evidence Isoginkgetin-induced CDK6 degradation, thermal shift binding, CDK6 rescue, ChIP of enhancer histone marks, glucose uptake, and xenograft

    PMID:36048765

    Open questions at the time
    • How CDK6 mechanistically promotes enhancer acetylation/methylation not defined
    • Restricted to HCC context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the diverse transcriptional (Sp1, HIF-1α, CDK6), post-transcriptional (mRNA stabilization, microRNAs), and trafficking (calnexin, PI3K, ATM/GIPC1, RAB21/retromer, stomatin) regulatory layers are integrated to set GLUT-1 surface activity in a given tissue remains unresolved.
  • No unified model connecting trafficking control to transcriptional control
  • Structural basis of substrate selectivity and cation gating not resolved in the corpus
  • Tissue-specific dosage thresholds underlying disease severity not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0001618 virus receptor activity 1 GO:0005198 structural molecule activity 1
Localization
GO:0005886 plasma membrane 3 GO:0005768 endosome 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-382551 Transport of small molecules 3 R-HSA-1430728 Metabolism 2 R-HSA-9612973 Autophagy 2
Complex memberships
erythrocyte GLUT-1/stomatin/band 3/aquaporin-1 membrane complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 GLUT-1 (SLC2A1) is a functional receptor for both HTLV-1 and HTLV-2. The receptor-binding domains of HTLV-1 and HTLV-2 envelope glycoproteins interact with GLUT-1 and inhibit glucose transport. siRNA knockdown of GLUT-1 abrogated HTLV infection, and ectopic expression of GLUT-1 (but not the related GLUT-3) restored infection in GLUT-1-depleted cells. siRNA knockdown, ectopic overexpression, glucose transport inhibition assay, HTLV envelope-driven infection assay Cell High 14622599
2001 Stomatin (band 7.2b) physically associates with GLUT-1 at the C-terminal 42-amino acid segment of GLUT-1, and overexpression of stomatin reduces GLUT-1 intrinsic transport activity by 35–70% without altering GLUT-1 plasma membrane content, demonstrating that stomatin modulates GLUT-1 activity via protein–protein interaction. Co-immunoprecipitation, GST pulldown with GLUT-1 C-terminal fusion protein, stable transfection, glucose transport assay American Journal of Physiology. Cell Physiology High 11287341
2012 In human erythrocyte membranes, in situ chemical cross-linking followed by immunoaffinity purification and mass spectrometry identified stomatin, band 3/SLC4A1, and aquaporin-1 as direct interaction partners of GLUT-1, establishing GLUT-1 as a component of a multiprotein membrane complex. In situ chemical cross-linking, immunoaffinity chromatography, mass spectrometry Biochimica et Biophysica Acta High 23219802
1996 GLUT-1 interacts with the ER chaperone calnexin (and its soluble homologue calreticulin) in a glycosylation-dependent manner during folding in the endoplasmic reticulum; a non-glycosylated GLUT-1 mutant (AGGT155) failed to associate with either calnexin or calreticulin. In vitro translation in rabbit reticulocyte lysate with canine pancreatic microsomes, co-immunoprecipitation with anti-calnexin antiserum, UV cross-linking, glycosylation mutant analysis The Journal of Biological Chemistry High 8662691
2013 ATM kinase phosphorylates GLUT-1 at serine 490 (S490), and this phosphorylation promotes cell-surface localization of GLUT-1, its interaction with GIPC1 (a recycling endosome protein), and GLUT-1-mediated glucose and dehydroascorbic acid transport in skeletal muscle cells. S490A mutation decreased transport and surface GLUT-1, while S490D mutation increased both. ATM inhibitor treatment, doxorubicin-mediated ATM activation, S490A and S490D point mutants, cell-surface GLUT-1 measurement, glucose and DHA transport assays, Co-IP of GLUT-1/GIPC1, mouse skeletal muscle ex vivo transport assay PloS One High 23776597
2022 RAB21 GTPase regulates retromer-mediated recycling of GLUT-1/SLC2A1: RAB21 depletion mis-sorts GLUT-1 to lysosomes, reducing glucose uptake and thereby activating the AMPK-ULK1 autophagy pathway. RAB21 depletion also caused accumulation of the SNX27-containing retromer complex on enlarged endosomes, indicating RAB21 regulates endosomal tubule fission during GLUT-1 recycling. siRNA knockdown of RAB21, subcellular localization by microscopy, glucose uptake assay, AMPK-ULK1 pathway analysis, immunofluorescence of retromer/SNX27, in vivo tumor xenograft Autophagy Medium 35993307
1999 Insulin- and TSH-induced translocation of GLUT-1 from intracellular compartments to the plasma membrane in FRTL-5 thyroid cells is dependent on PI3-kinase activity (blocked by wortmannin and LY294002). TSH/cAMP-driven translocation occurs via a PKA-independent, PI3-kinase-dependent pathway. N-glycosylation of GLUT-1 is required for full transport activity but not for its translocation to the plasma membrane. PI3-kinase inhibitors (wortmannin, LY294002), PKA inhibitor (H89), tunicamycin (N-glycosylation inhibitor), subcellular fractionation, glucose uptake assay Endocrinology Medium 11089547
2001 In mesangial cells, GLUT-1 transcription is stimulated by high D-glucose in a manner dependent on glucose metabolism (not the hexose monophosphate shunt). Antisense-mediated reduction of GLUT-1 expression blocks high-glucose-induced upregulation of GLUT-1 and fibronectin expression, demonstrating that GLUT-1-mediated glucose uptake drives a feed-forward loop promoting extracellular matrix production. Stable antisense GLUT-1 transfection, radiolabeled glucose uptake, GLUT-1 transcription assay, fibronectin mRNA and protein measurement, metabolic substrate substitution experiments American Journal of Physiology. Renal Physiology Medium 11249857
1999 The transcription factor Sp1 binds the −102/−82 region of the GLUT-1 promoter and is essential for high transcriptional activity in fetal/neonatal cardiomyocytes; Sp1 is markedly downregulated perinatally in heart and skeletal muscle, explaining the developmental repression of GLUT-1 transcription. Transient transfection reporter assays, electrophoretic mobility shift assay (EMSA), Sp1 site mutagenesis, developmental Western blot The Journal of Biological Chemistry High 10364200
2001 Hyperosmolarity (600 mosmol/L) induces a biphasic increase in GLUT-1-mediated glucose transport: an early phase (0–6 h) independent of changes in GLUT-1 mRNA or protein, and a late phase (12–24 h) driven by increased GLUT-1 mRNA (via both enhanced transcription and mRNA stabilization, half-life increasing from ~2 h to ~8 h) and increased GLUT-1 protein. A 44-bp proximal promoter region is required for basal and hyperosmolarity-induced transcription. mRNA stability assay, promoter deletion/reporter assay, glucose transport assay, Western blot, GLUT-1 plasma membrane fractionation American Journal of Physiology. Cell Physiology Medium 11546675
1990 Vanadate increases GLUT-1 mRNA expression 4–5-fold in NIH3T3 fibroblasts partly through mRNA stabilization (half-life increased from ~0.5–1 h to ~1.5–2 h), indicating a post-transcriptional regulatory mechanism for GLUT-1 expression. Northern blot, mRNA half-life determination with actinomycin D chase, glucose transporter functional assay Endocrinology Medium 2100513
2000 Heterozygous missense, deletion, insertion, splice-site, and nonsense mutations in GLUT-1/SLC2A1 cause Glut-1 Deficiency Syndrome, characterized by reduced erythrocyte glucose transport activity and hypoglycorrhachia, confirming that GLUT-1 is the essential blood-brain barrier hexose transporter and that single-allele loss is sufficient to impair CNS glucose delivery. FISH, PCR, SSCP, DNA sequencing, erythrocyte glucose transport activity assay Human Mutation High 10980529
2006 Heterozygous targeted disruption of the mouse GLUT-1 gene produces haploinsufficiency phenotype: 66% reduction in brain GLUT-1 protein, reduced brain glucose uptake by PET, hypoglycorrhachia, microencephaly, epileptiform EEG discharges, and impaired motor activity — directly demonstrating that GLUT-1 is the critical blood-brain barrier glucose transporter in vivo. Targeted gene disruption (homologous recombination), PET imaging, EEG, Western blot, behavioral assays, CSF glucose measurement Human Molecular Genetics High 16497725
2010 In vivo knockdown of Glut1 in zebrafish causes loss of cerebral endothelial cells, downregulation of adherens and tight junction proteins, impaired cerebral circulation, and vasogenic brain edema, demonstrating that Glut1 is required for blood-brain barrier development and maintenance of cerebrovascular integrity. Morpholino-based Glut1 knockdown in zebrafish, live fluorescence imaging, junction protein immunostaining, BBB permeability assay Annals of Neurology Medium 21194153
2011 Mutations in SLC2A1 cause paroxysmal choreoathetosis/spasticity (DYT9), and DYT9 is allelic with DYT18 (paroxysmal exercise-induced dyskinesia); identified mutations reduce glucose uptake in functional assays, confirming causality and expanding the clinical spectrum of GLUT-1 deficiency. SLC2A1 sequencing, glucose uptake functional assay, cosegregation analysis, absence from 400 control chromosomes Neurology High 21832227
2019 Myeloid-specific deletion of Slc2a1 (GLUT1) in macrophages blocks glucose uptake and glycolysis, forces metabolic compensation via glutamine and oleate oxidation, blunts maximal respiratory capacity, reduces proinflammatory metabolites, elevates alternative-activation markers (ornithine, polyamines, CD206), and impairs phagocytic capacity — demonstrating that GLUT1 fuels macrophage glycolysis and is required for normal phagocytosis and inflammatory metabolic programming. Myeloid-specific Cre-lox Slc2a1 knockout, glucose uptake assay, Seahorse metabolic flux analysis, flow cytometry, cytokine measurement, phagocytosis assay, atherosclerosis model Journal of Immunology High 30659108
2000 GLUT-1 overexpression in vascular smooth muscle cells reduces hypoxia-induced apoptosis and markedly attenuates hypoxia- and rotenone-induced JNK kinase activation; a catalytically inactive MEKK1 mutant partially phenocopied this protection, placing GLUT-1-dependent glucose uptake upstream of the JNK stress-kinase apoptosis pathway. Stable GLUT-1 overexpression, hypoxia and rotenone treatment, apoptosis morphology quantification, JNK activity assay, dominant-negative MEKK1 transfection American Journal of Physiology. Endocrinology and Metabolism Medium 10780954
2022 GLUT-1/SLC2A1 expression is upregulated by hypoxia via HIF-1α stabilization in brain capillary endothelial cells, accompanied by increased [3H]-glucose uptake; stabilizing HIF-1α pharmacologically with desferrioxamine under normoxia mimics this effect, establishing HIF-1α as the transcriptional regulator of GLUT-1 upregulation in BBB endothelium under hypoxia. Primary bovine brain capillary endothelial cell culture under hypoxia, HIF-1α immunocytochemistry/confocal imaging, qPCR, Western blot, [3H]-glucose uptake assay, desferrioxamine (DFO) pharmacological HIF-1α stabilization Fluids and Barriers of the CNS Medium 34983574
2018 miR-328 directly targets the 3′-UTR of SLC2A1/GLUT1 mRNA (confirmed by luciferase reporter assay) and suppresses GLUT1 protein expression in colon cancer cells, reducing glycolysis. Luciferase reporter assay with SLC2A1 3′-UTR, Western blot, miR-328 overexpression in colon cancer cell lines Clinical & Translational Oncology Medium 29374351
2017 miR-148b directly targets SLC2A1/GLUT1 3′-UTR (luciferase assay), suppresses GLUT1 protein, and limits glycolysis (glucose consumption, lactate production) in gastric cancer cells; GLUT1 overexpression rescued glycolysis suppressed by miR-148b, establishing direct miR-148b → GLUT1 → glycolysis regulation. Luciferase 3′-UTR reporter assay, Western blot, siRNA, GLUT1 overexpression rescue, glucose/lactate metabolic assays Cancer Medicine Medium 28440026
2022 Isoginkgetin (ISO) suppresses SLC2A1/GLUT1 enhancer activity (reducing H3K27ac, H4K8ac, and H3K4me1 marks on the GLUT1 enhancer) by binding to and promoting degradation of CDK6; CDK6 overexpression rescued GLUT1 transcription and autophagy suppression, placing CDK6 upstream of GLUT1 enhancer activity in HCC. Molecular docking, thermal shift analysis, CDK6 overexpression rescue, ChIP for histone marks at SLC2A1 enhancer, glucose uptake assay, AMPK-ULK1 pathway analysis, xenograft Autophagy Medium 36048765
1994 Transgenic overexpression of GLUT-1 in skeletal muscle paradoxically reduces insulin-stimulated whole-body glucose disposal (GIR 54% of controls) and induces marked hyperketonemia, whereas GLUT-4 overexpression enhances insulin-stimulated glucose disposal — demonstrating that the identity (not merely level) of glucose transporter isoform critically shapes whole-body insulin responsiveness. Euglycemic hyperinsulinemic clamp in transgenic mice overexpressing GLUT-1 or GLUT-4, glucose infusion rate measurement, β-hydroxybutyrate measurement The American Journal of Physiology High 7977725
2012 SLC2A1 trinucleotide deletion (deleting isoleucine 435 or 436) causes a cation-leaky GLUT-1 variant that constitutively allows monovalent cation (Na+/K+) permeation across the red cell membrane, in addition to abrogating glucose transport — demonstrating that single residues in the GLUT-1 transmembrane domain determine both substrate selectivity and cation permeability. SLC2A1 sequencing, red cell cation content measurement, temperature-dependent K+ loss assay, clinical phenotyping The Journal of Clinical Endocrinology and Metabolism Medium 22492876
2017 GLUT-1/SLC2A1 siRNA intravitreal injection in diabetic mice reduces retinal glucose concentration, ICAM-1 and TNF-α expression, leukostasis, and vascular leakage — establishing that GLUT-1-mediated glucose transport into the retina is a causal driver of the inflammatory microangiopathy of diabetic retinopathy. Intravitreal siRNA injection in streptozotocin-diabetic mice, retinal glucose assay, ERG, immunoblotting for ICAM-1/TNF-α, leukostasis assay, Evans blue vascular permeability assay Scientific Reports Medium 28785055

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 The SLC2 (GLUT) family of membrane transporters. Molecular aspects of medicine 975 23506862
2005 Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer. Journal of cellular physiology 960 15389572
2003 Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins. The British journal of nutrition 613 12568659
2003 The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV. Cell 328 14622599
2003 GLUT-1 and CAIX as intrinsic markers of hypoxia in carcinoma of the cervix: relationship to pimonidazole binding. International journal of cancer 187 12532423
1997 GLUT-1 expression in the cerebra of patients with Alzheimer's disease. Neurobiology of aging 167 9390772
2019 Glut 1 in Cancer Cells and the Inhibitory Action of Resveratrol as A Potential Therapeutic Strategy. International journal of molecular sciences 160 31324056
2006 A mouse model for Glut-1 haploinsufficiency. Human molecular genetics 156 16497725
2001 GLUT-1 expression in ovarian carcinoma: association with survival and response to chemotherapy. Cancer 146 11571727
2000 Correlation of Glut-1 glucose transporter expression with [(18)F]FDG uptake in non-small cell lung cancer. European journal of nuclear medicine 146 24578007
1998 FDG uptake, GLUT-1 glucose transporter and cellularity in human pancreatic tumors. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 138 9776278
1999 Placental glucose transport and GLUT 1 expression in insulin-dependent diabetes. American journal of obstetrics and gynecology 122 9914598
2002 Expression of hexokinase II and Glut-1 in untreated human breast cancer. Nuclear medicine and biology 119 12031879
2000 Mutational analysis of GLUT1 (SLC2A1) in Glut-1 deficiency syndrome. Human mutation 115 10980529
2019 Myeloid Slc2a1-Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1. Journal of immunology (Baltimore, Md. : 1950) 110 30659108
2010 Glut1/SLC2A1 is crucial for the development of the blood-brain barrier in vivo. Annals of neurology 97 21194153
1999 GLUT-4myc ectopic expression in L6 myoblasts generates a GLUT-4-specific pool conferring insulin sensitivity. The American journal of physiology 92 10484371
2001 Overexpression of stomatin depresses GLUT-1 glucose transporter activity. American journal of physiology. Cell physiology 91 11287341
2005 The differential expression of VEGF, VEGFR-2, and GLUT-1 proteins in disease subtypes of systemic sclerosis. Human pathology 88 16426919
2014 Increased glucose and placental GLUT-1 in large infants of obese nondiabetic mothers. American journal of obstetrics and gynecology 82 25132463
2012 Cellular distribution of Glut-1 and Glut-5 in benign and malignant human prostate tissue. Journal of cellular biochemistry 82 21938742
2020 Long noncoding RNA SLC2A1-AS1 regulates aerobic glycolysis and progression in hepatocellular carcinoma via inhibiting the STAT3/FOXM1/GLUT1 pathway. Molecular oncology 80 32174012
2020 GLUT-1: An Effective Target To Deliver Brain-Derived Neurotrophic Factor Gene Across the Blood Brain Barrier. ACS chemical neuroscience 77 32352752
1992 Expression and function of GLUT-1 and GLUT-2 glucose transporter isoforms in cells of cultured rat pancreatic islets. The Journal of biological chemistry 76 1512261
2005 Oxygen-regulated expression of GLUT-1, GLUT-3, and VEGF in the mouse blastocyst. Molecular reproduction and development 74 15515055
2000 GLUT-1 reduces hypoxia-induced apoptosis and JNK pathway activation. American journal of physiology. Endocrinology and metabolism 74 10780954
2011 Glut-1 Expression Correlates with Basal-like Breast Cancer. Translational oncology 73 22190995
2019 Synthesis of Indomorphan Pseudo-Natural Product Inhibitors of Glucose Transporters GLUT-1 and -3. Angewandte Chemie (International ed. in English) 72 31469221
2012 GLUT4, GLUT1, and GLUT8 are the dominant GLUT transcripts expressed in the murine left ventricle. Cardiovascular diabetology 70 22681646
2004 Expression of glucose transporter 1 (Glut-1) in cell lines and clinical specimens from human prostate adenocarcinoma. Anticancer research 70 15517916
2011 Paroxysmal choreoathetosis/spasticity (DYT9) is caused by a GLUT1 defect. Neurology 69 21832227
2003 GLUT-1 overexpression: Link between hemodynamic and metabolic factors in glomerular injury? Hypertension (Dallas, Tex. : 1979) 69 12771048
2012 Stomatin interacts with GLUT1/SLC2A1, band 3/SLC4A1, and aquaporin-1 in human erythrocyte membrane domains. Biochimica et biophysica acta 68 23219802
2008 GLUT-1 expression in mesenchymal tumors: an immunohistochemical study of 247 soft tissue and bone neoplasms. Human pathology 65 18620729
1999 Functional electrical stimulation exercise increases GLUT-1 and GLUT-4 in paralyzed skeletal muscle. Metabolism: clinical and experimental 64 10582549
1996 Increments in skeletal muscle GLUT-1 and GLUT-4 after endurance training in humans. The American journal of physiology 62 8638693
1994 Differential effects of GLUT-1 or GLUT-4 overexpression on insulin responsiveness in transgenic mice. The American journal of physiology 62 7977725
1998 Distinct localization of GLUT-1, -3, and -5 in human monocyte-derived macrophages: effects of cell activation. The American journal of physiology 61 9530136
2000 Expression of GLUT-1 glucose transporter in borderline and malignant epithelial tumors of the ovary. Gynecologic oncology 58 11006027
2005 Expression of HIF-1alpha and Glut-1 in human bladder cancer. Oncology reports 57 16142350
2017 Placental glucose transporter (GLUT)-1 is down-regulated in preeclampsia. Placenta 56 28623979
2000 Glut-1 translocation in FRTL-5 thyroid cells: role of phosphatidylinositol 3-kinase and N-glycosylation. Endocrinology 55 11089547
2015 Inhibiting GLUT-1 expression and PI3K/Akt signaling using apigenin improves the radiosensitivity of laryngeal carcinoma in vivo. Oncology reports 53 26238658
2022 Isoginkgetin, a potential CDK6 inhibitor, suppresses SLC2A1/GLUT1 enhancer activity to induce AMPK-ULK1-mediated cytotoxic autophagy in hepatocellular carcinoma. Autophagy 49 36048765
2014 Apigenin suppresses GLUT-1 and p-AKT expression to enhance the chemosensitivity to cisplatin of laryngeal carcinoma Hep-2 cells: an in vitro study. International journal of clinical and experimental pathology 49 25120770
2009 Usefulness of EMA, GLUT-1, and XIAP for the cytologic diagnosis of malignant mesothelioma in body cavity fluids. American journal of clinical pathology 44 19289587
2019 Roles of GLUT-1 and HK-II expression in the biological behavior of head and neck cancer. Oncotarget 43 31105886
2013 IMP3 and GLUT-1 immunohistochemistry for distinguishing benign from malignant mesothelial proliferations. The American journal of surgical pathology 43 23108021
1996 The glut 1 glucose transporter interacts with calnexin and calreticulin. The Journal of biological chemistry 43 8662691
2022 Hypoxia increases expression of selected blood-brain barrier transporters GLUT-1, P-gp, SLC7A5 and TFRC, while maintaining barrier integrity, in brain capillary endothelial monolayers. Fluids and barriers of the CNS 41 34983574
2017 Suppression of diabetic retinopathy with GLUT1 siRNA. Scientific reports 41 28785055
1999 Factors involved in GLUT-1 glucose transporter gene transcription in cardiac muscle. The Journal of biological chemistry 41 10364200
2020 Steroids Regulate SLC2A1 and SLC2A3 to Deliver Glucose Into Trophectoderm for Metabolism via Glycolysis. Endocrinology 40 32556218
2018 miR-328 mediates a metabolic shift in colon cancer cells by targeting SLC2A1/GLUT1. Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 40 29374351
2018 Inhibition of GLUT-1 expression and the PI3K/Akt pathway to enhance the chemosensitivity of laryngeal carcinoma cells in vitro. OncoTargets and therapy 39 30464533
2017 miR-148b inhibits glycolysis in gastric cancer through targeting SLC2A1. Cancer medicine 38 28440026
2001 Antisense GLUT-1 protects mesangial cells from glucose induction of GLUT-1 and fibronectin expression. American journal of physiology. Renal physiology 38 11249857
1996 Regulation of glucose transporters (GLUT-1 and GLUT-3) in human retinal endothelial cells. The Biochemical journal 38 8761487
2015 Inhibition of glucose-transporter 1 (GLUT-1) expression reversed Warburg effect in gastric cancer cell MKN45. International journal of clinical and experimental medicine 37 25932183
2013 ATM and GLUT1-S490 phosphorylation regulate GLUT1 mediated transport in skeletal muscle. PloS one 36 23776597
2022 RAB21 controls autophagy and cellular energy homeostasis by regulating retromer-mediated recycling of SLC2A1/GLUT1. Autophagy 35 35993307
2021 GLUT-1 Enhances Glycolysis, Oxidative Stress, and Fibroblast Proliferation in Keloid. Life (Basel, Switzerland) 35 34070830
2015 GLUT-1 immunoexpression in oral epithelial dysplasia, oral squamous cell carcinoma, and verrucous carcinoma. Journal of oral science 35 26062860
2018 Individualizing Treatment Approaches for Epileptic Patients with Glucose Transporter Type1 (GLUT-1) Deficiency. International journal of molecular sciences 34 29303961
2014 Upregulation of Claudin-4, CAIX and GLUT-1 in distant breast cancer metastases. BMC cancer 34 25417118
2009 GLUT-1 expression and response to chemoradiotherapy in rectal cancer. International journal of cancer 34 19569052
2003 Glucose transporter type1 (GLUT-1) deficiency. Brain & development 33 13129590
2001 Stimulation of GLUT-1 glucose transporter expression in response to hyperosmolarity. American journal of physiology. Cell physiology 32 11546675
2018 Significance of Glucose Transporter Type 1 (GLUT-1) Expression in the Therapeutic Strategy for Pancreatic Ductal Adenocarcinoma. Annals of surgical oncology 31 29404819
2018 Glucose transporter-1 (GLUT-1) expression in psoriasis: correlation with disease severity. International journal of dermatology 30 29797802
2013 Anticancer mechanism of apigenin and the implications of GLUT-1 expression in head and neck cancers. Future oncology (London, England) 30 23980682
2012 An infant with pseudohyperkalemia, hemolysis, and seizures: cation-leaky GLUT1-deficiency syndrome due to a SLC2A1 mutation. The Journal of clinical endocrinology and metabolism 30 22492876
2006 Identification of a novel SEREX antigen, SLC2A1/GLUT1, in esophageal squamous cell carcinoma. International journal of oncology 30 16391802
2009 INI1 and GLUT-1 expression in epithelioid sarcoma and its cutaneous neoplastic and nonneoplastic mimics. The American Journal of dermatopathology 29 19318800
2002 Assessment of Glut-1 expression in cholangiocarcinoma, benign biliary lesions and hepatocellular carcinoma. Oncology reports 29 12066193
2022 Effect of Glut-1 and HIF-1α double knockout by CRISPR/CAS9 on radiosensitivity in laryngeal carcinoma via the PI3K/Akt/mTOR pathway. Journal of cellular and molecular medicine 28 35415942
2022 Therapeutic implications of glucose transporters (GLUT) in cerebral ischemia. Neurochemical research 28 35596882
2021 Placental expression of glucose transporters GLUT-1, GLUT-3, GLUT-8 and GLUT-12 in pregnancies complicated by gestational and type 1 diabetes mellitus. Journal of diabetes investigation 28 34555239
2013 The many faces of Glut1 deficiency syndrome. Journal of child neurology 28 23340081
2006 Role for GLUT1 in diabetic glomerulosclerosis. Expert reviews in molecular medicine 28 16515729
1995 Regulation of glucose transport and GLUT-1 expression by iron chelators in muscle cells in culture. The American journal of physiology 28 8572196
2022 Dihydroartemisinin inhibited the Warburg effect through YAP1/SLC2A1 pathway in hepatocellular carcinoma. Journal of natural medicines 27 36068393
2021 Oxidative Stress-Induced Sirtuin1 Downregulation Correlates to HIF-1α, GLUT-1, and VEGF-A Upregulation in Th1 Autoimmune Hashimoto's Thyroiditis. International journal of molecular sciences 27 33916948
2018 Membrane-enriched solute carrier family 2 member 1 (SLC2A1/GLUT1) in psoriatic keratinocytes confers sensitivity to 2-deoxy-D-glucose (2-DG) treatment. Experimental dermatology 26 30480843
1990 Vanadate regulates glucose transporter (Glut-1) expression in NIH3T3 mouse fibroblasts. Endocrinology 26 2100513
2023 Characterization of the effect of the GLUT-1 inhibitor BAY-876 on T cells and macrophages. European journal of pharmacology 25 36739076
2022 GLUT-1 Expression in Breast Cancer. Turk patoloji dergisi 25 34580846
2021 TFAP2A-induced SLC2A1-AS1 promotes cancer cell proliferation. Biological chemistry 25 33580997
2021 Long non-coding RNA SLC2A1-AS1 induced by GLI3 promotes aerobic glycolysis and progression in esophageal squamous cell carcinoma by sponging miR-378a-3p to enhance Glut1 expression. Journal of experimental & clinical cancer research : CR 25 34517880
2016 Immunohistochemical Expression of GLUT-1 and HIF-1α in Tooth Germ, Ameloblastoma, and Ameloblastic Carcinoma. International journal of surgical pathology 23 27020375
2014 A novel SLC2A1 mutation linking hemiplegic migraine with alternating hemiplegia of childhood. Cephalalgia : an international journal of headache 23 24824604
2000 Correlation of Glut-1 glucose transporter expression with. European journal of nuclear medicine 23 11189940
2023 Metabolic Effects of New Glucose Transporter (GLUT-1) and Lactate Dehydrogenase-A (LDH-A) Inhibitors against Chemoresistant Malignant Mesothelioma. International journal of molecular sciences 22 37175477
2016 Correlation of Glut-1 and Glut-3 expression with F-18 FDG uptake in pulmonary inflammatory lesions. Medicine 21 27902598
2015 GLUT-1 Expression in Cutaneous Basal and Squamous Cell Carcinomas. International journal of surgical pathology 21 26092229
2017 GLUT 1 receptor expression and circulating levels of fasting glucose in high grade serous ovarian cancer. Journal of cellular physiology 20 28542798
2017 Expression of Glut-1 in Malignant Melanoma and Melanocytic Nevi: an Immunohistochemical Study of 400 Cases. Pathology oncology research : POR 20 29128957
2006 GLUT-1 is preferentially expressed in atypical endometrial hyperplasia and endometrial adenocarcinoma. Applied immunohistochemistry & molecular morphology : AIMM 20 16785788
2022 Antihyperglycemic effect of an anthocyanin, cyanidin-3-O-glucoside, is achieved by regulating GLUT-1 via the Wnt/β-catenin-WISP1 signaling pathway. Food & function 19 35357376
2020 Gene and immunohistochemical expression of HIF-1α, GLUT-1, FASN, and adipophilin in carcinoma ex pleomorphic adenoma development. Oral diseases 19 32180291

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