Affinage

SLC2A1

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

Round 2 corrected
Length
492 aa
Mass
54.1 kDa
Annotated
2026-04-28
130 papers in source corpus 36 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC2A1 (GLUT1) is a ubiquitously expressed, 12-transmembrane-domain facilitated glucose uniporter of the major facilitator superfamily that mediates basal glucose uptake across the plasma membrane and also transports dehydroascorbic acid (PMID:3839598, PMID:24847886, PMID:9228080). Its surface abundance is dynamically regulated by TXNIP-driven clathrin-mediated internalization (relieved by AMPK-dependent TXNIP degradation), SNX27–retromer–RAB21-mediated endosomal recycling back to the plasma membrane, and GIPC1 binding to a C-terminal PDZ motif that protects internalized GLUT1 from lysosomal degradation; ATM phosphorylation of Ser490 promotes GIPC1 association and surface retention, while stomatin binding to the C-terminal tail inhibits intrinsic transport activity without altering surface levels (PMID:23453806, PMID:23563491, PMID:35993307, PMID:19016655, PMID:23776597, PMID:11287341). GLUT1 is the predominant glucose transporter at the blood–brain barrier and in erythrocytes, and heterozygous loss-of-function mutations cause GLUT1 deficiency syndrome, characterized by hypoglycorrhachia, seizures, and developmental delay (PMID:2211679, PMID:1714544, PMID:10980529). GLUT1 also serves as the obligate receptor for HTLV-1 and HTLV-2 entry, and its differential expression programs distinct metabolic fates in effector versus regulatory T cells (PMID:14622599, PMID:21317389).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1985 High

    Determination of the full primary structure of human GLUT1 from cDNA sequencing established the protein as a ~500 amino acid, 12-transmembrane-domain transporter, providing the molecular framework for all subsequent functional studies.

    Evidence cDNA cloning/sequencing with biochemical validation of purified erythrocyte transporter

    PMID:3839598

    Open questions at the time
    • No three-dimensional structure available
    • Transport mechanism inferred from topology only
    • Post-translational regulation unknown
  2. 1990 High

    Quantitative protein and ligand-binding analyses demonstrated that GLUT1 accounts for essentially all glucose transporter activity at the blood–brain barrier, establishing its physiological centrality for cerebral glucose supply.

    Evidence Quantitative Western blotting, [3H]cytochalasin B binding, and in situ hybridization on bovine brain cortex

    PMID:2211679

    Open questions at the time
    • Contribution of other GLUT isoforms under pathological conditions not addressed
    • Human BBB confirmation needed
  3. 1991 High

    Clinical and functional characterization of patients with persistent hypoglycorrhachia, seizures, and developmental delay linked these phenotypes to defective erythrocyte glucose transport, defining GLUT1 deficiency syndrome as a haploinsufficiency disorder.

    Evidence Clinical phenotyping combined with erythrocyte glucose transport assays and CSF glucose measurements

    PMID:1714544

    Open questions at the time
    • Causative mutations not yet molecularly identified at the DNA level in this initial report
    • Genotype–phenotype correlations not established
  4. 1991 High

    Discovery that glucose deprivation redistributes GLUT1 from intracellular pools to the plasma membrane, and that GLUT1 mRNA is stress-inducible (like GRP-78), established that GLUT1 surface abundance and expression are dynamically regulated by metabolic stress rather than being constitutive.

    Evidence Subcellular fractionation, immunofluorescence, Northern blots under glucose deprivation, calcium ionophore, tunicamycin, and reductant stress in multiple cell lines

    PMID:1706526 PMID:2017192

    Open questions at the time
    • Signaling pathways mediating stress-induced translocation unknown
    • Whether intrinsic activity also changes during stress not resolved
  5. 1993 High

    Glycosylation scanning mutagenesis in Xenopus oocytes experimentally verified the 12-transmembrane-helix topology with cytoplasmic N- and C-termini and a large central cytoplasmic loop, resolving the membrane orientation predicted from the sequence.

    Evidence Systematic glycosylation site insertion mutagenesis in Xenopus oocytes and reticulocyte lysate with 2-deoxyglucose uptake readout

    PMID:8051147

    Open questions at the time
    • No atomic-resolution structure
    • Helix packing and substrate translocation path unknown
  6. 1993 High

    Inhibition of oxidative phosphorylation was shown to stimulate glucose transport primarily by activating pre-existing plasma membrane GLUT1 rather than recruiting intracellular transporters, revealing that intrinsic transporter activity is a regulated parameter distinct from surface abundance.

    Evidence Four orthogonal approaches (immunofluorescence, differential centrifugation, surface biotinylation, cytochalasin B binding) in Clone 9 cells treated with azide

    PMID:8349608

    Open questions at the time
    • Molecular basis of intrinsic activity modulation unknown
    • Kinase or signaling intermediate responsible not identified
  7. 1997 High

    Reconstitution in Xenopus oocytes demonstrated that GLUT1 transports dehydroascorbic acid (Km ~1.1 mM) via the same pathway as glucose, expanding the substrate repertoire beyond hexoses and establishing GLUT1 as the molecular basis for cellular vitamin C acquisition via its oxidized form.

    Evidence Xenopus oocyte expression, radiolabeled uptake, HPLC product identification, CHO overexpression, inhibitor competition

    PMID:9228080

    Open questions at the time
    • Structural basis for DHA recognition versus glucose not defined
    • Physiological relevance of DHA transport versus sodium-dependent ascorbate transporters not quantified in vivo
  8. 1999 High

    Identification of Sp1 binding to the −102/−82 promoter element, with postnatal Sp1 downregulation in heart, provided the first transcription-factor-level explanation for the developmental switch from high to low GLUT1 expression in cardiac and skeletal muscle.

    Evidence EMSA, site-directed mutagenesis of Sp1 site, reporter assays, Western blot of Sp1 during heart development

    PMID:10364200

    Open questions at the time
    • Other transcription factors contributing to developmental regulation not mapped
    • Mechanism of postnatal Sp1 downregulation unknown
  9. 2001 High

    Stomatin was identified as a direct negative regulator of GLUT1 intrinsic activity that binds the C-terminal 42-amino-acid segment without altering surface expression, providing a molecular mechanism for modulation of transport kinetics independent of trafficking.

    Evidence Co-immunoprecipitation, GST pulldown domain mapping, functional glucose transport in stomatin-overexpressing cells

    PMID:11287341

    Open questions at the time
    • Stoichiometry and structural basis of the stomatin–GLUT1 interaction unknown
    • Physiological contexts where stomatin regulation is rate-limiting not defined
  10. 2003 High

    GLUT1 was established as the receptor for HTLV-1 and HTLV-2 through siRNA knockdown, ectopic rescue, and pharmacological inhibition, linking glucose transporter biology to retroviral entry and explaining HTLV tropism.

    Evidence siRNA knockdown, GLUT1/GLUT3 ectopic expression, cytochalasin B inhibition, HTLV infection assays

    PMID:14622599

    Open questions at the time
    • Structural interface between HTLV envelope and GLUT1 not defined
    • Whether HTLV binding alters glucose transport in infected cells in vivo not resolved
  11. 2009 High

    Discovery that a C-terminal PDZ-binding motif recruits GIPC1 to protect internalized GLUT1 from lysosomal degradation, and that disruption of this motif reduces surface GLUT1, established the first post-endocytic sorting mechanism controlling GLUT1 fate.

    Evidence PDZ motif deletion/mutation, co-immunoprecipitation of GIPC–GLUT1, surface GLUT1 quantification, lysosomal inhibitor rescue, glucose uptake in GIPC-deficient cells

    PMID:19016655

    Open questions at the time
    • Upstream signals controlling GIPC–GLUT1 interaction not defined
    • Relationship to retromer-mediated recycling not yet established
  12. 2013 High

    Three converging studies defined the GLUT1 surface-abundance regulatory circuit: TXNIP directly binds GLUT1 and promotes clathrin-mediated internalization (relieved by AMPK-dependent TXNIP phosphorylation/degradation); ATM phosphorylates GLUT1-S490 to promote GIPC1 binding and surface retention; and SNX27–retromer recycles internalized GLUT1 from endosomes, preventing lysosomal degradation.

    Evidence Co-IP of TXNIP–GLUT1 with clathrin inhibitor experiments, AMPK-TXNIP phospho-mutants, ATM inhibitor/activator with S490A/D mutants and ex vivo muscle, quantitative proteomics of SNX27 interactome and surface proteome in retromer-depleted cells

    PMID:23453806 PMID:23563491 PMID:23776597

    Open questions at the time
    • Relative quantitative contribution of each pathway to steady-state GLUT1 surface levels unknown
    • Whether TXNIP, ATM, and SNX27–retromer act in series or in parallel not resolved
    • Structural basis of TXNIP–GLUT1 interaction not determined
  13. 2014 High

    The 3.2 Å crystal structure of human GLUT1 in an inward-open conformation revealed the canonical MFS fold and enabled structural mapping of disease-causing mutations onto the transport pathway, providing the atomic framework for understanding alternating-access transport and pathogenic mechanism.

    Evidence X-ray crystallography at 3.2 Å, structural comparison with bacterial homologue XylE, mutation mapping

    PMID:24847886

    Open questions at the time
    • Outward-open and occluded conformations not captured
    • Dynamics of the alternating-access cycle not resolved
    • No structure with bound glucose substrate
  14. 2019 High

    Myeloid-specific GLUT1 deletion demonstrated that GLUT1 is essential for macrophage glucose uptake, glycolysis, pentose phosphate pathway activity, and phagocytic capacity, directly linking GLUT1-dependent metabolism to innate immune function and atherosclerotic plaque stability.

    Evidence Conditional Slc2a1 knockout in myeloid cells, metabolic flux analysis, phagocytosis assays, Ldlr−/− atherosclerosis model

    PMID:30659108

    Open questions at the time
    • Whether GLUT3 or other transporters can compensate over longer time frames not tested
    • Contribution of GLUT1-dependent glycolysis to other macrophage effector functions (cytokine secretion, antigen presentation) not fully explored
  15. 2022 High

    RAB21 was identified as the GTPase controlling fission of SNX27–retromer-decorated endosomal tubules for GLUT1 recycling; RAB21 depletion diverts GLUT1 to lysosomes, reduces glucose uptake, and triggers AMPK–ULK1 autophagy, closing the loop between endosomal sorting and metabolic signaling.

    Evidence RAB21 siRNA/shRNA, GLUT1 subcellular imaging, glucose uptake assays, AMPK-ULK1 pathway analysis, in vivo tumor growth

    PMID:35993307

    Open questions at the time
    • Whether RAB21 directly contacts GLUT1 or acts only on the retromer tubule not determined
    • GEF and GAP for RAB21 in this context not identified
    • Integration with TXNIP- and ATM-dependent regulation not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • A complete structural view of the GLUT1 transport cycle (outward-open, occluded, substrate-bound states), the quantitative integration of TXNIP, ATM–GIPC1, and SNX27–retromer–RAB21 trafficking arms into a unified regulatory model, and the structural basis of the stomatin inhibitory interaction remain unresolved.
  • No outward-open or occluded-state human GLUT1 structure
  • Relative flux contributions of each trafficking pathway to surface GLUT1 not quantified in any single system
  • Structural basis of stomatin-mediated intrinsic activity inhibition unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 7 GO:0001618 virus receptor activity 1
Localization
GO:0005886 plasma membrane 7 GO:0005768 endosome 2 GO:0031410 cytoplasmic vesicle 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-382551 Transport of small molecules 6 R-HSA-1643685 Disease 4 R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-168256 Immune System 2 R-HSA-9612973 Autophagy 1
Partners
BSGCALNEXINCALRETICULINGIPC1RAB21SNX27STOMATINTXNIP

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1985 The primary structure of human GLUT1 (SLC2A1) was deduced from cDNA sequencing, revealing a ~500 amino acid protein with 12 predicted membrane-spanning domains, with the amino terminus, carboxyl terminus, and a central hydrophilic domain all predicted to lie on the cytoplasmic face. cDNA cloning and sequencing, structural analysis by fast atom bombardment mapping and gas phase Edman degradation of purified erythrocyte transporter Science High 3839598
1987 The human GLUT1 gene (designated GLUT) was mapped to chromosome 1p31.3–p35 (most likely 1p33), and a two-allele XbaI restriction-fragment-length polymorphism was identified. Somatic cell hybrid panel hybridization and in situ hybridization to metaphase chromosomes Diabetes High 3028891
1990 GLUT1 is selectively and highly expressed at the blood-brain barrier (cerebral capillary endothelium); essentially 100% of glucose transporter binding sites at the BBB can be accounted for by the GLUT1 isoform. Quantitative Western blotting with purified erythrocyte GLUT1 standard, [3H]cytochalasin B binding assay, and in situ hybridization on bovine brain cortex The Journal of biological chemistry High 2211679
1991 GLUT1 deficiency syndrome was established as a disease caused by defective glucose transport across the blood-brain barrier, resulting in persistent hypoglycorrhachia, seizures, and developmental delay. Clinical characterization combined with erythrocyte glucose transport assays and CSF glucose measurements The New England journal of medicine High 1714544
1991 GLUT1 expression is regulated as a stress-response gene: glucose starvation, calcium ionophore A23187, 2-mercaptoethanol, and tunicamycin all increase GLUT1 mRNA (50–300%) similarly to GRP-78, classifying GLUT1 as a member of the glucose-regulated protein (GRP) family of stress proteins. Northern blot analysis of GLUT1 and GRP-78 mRNA in L8 myocytes and NIH 3T3 fibroblasts under multiple stress conditions; glucose uptake assays Proceedings of the National Academy of Sciences of the United States of America High 1706526
1991 Glucose deprivation induces selective accumulation of glycosylated GLUT1 (55 kDa) in the plasma membrane of NRK cells, increasing hexose transport; under glucose-fed conditions GLUT1 resides predominantly in intracellular membrane fractions. Subcellular fractionation, [3H]cytochalasin B binding, immunofluorescence microscopy, Western blotting Molecular endocrinology High 2017192
1992 Glucose autoregulates its own transport in L8 myocytes by modulating GLUT1 trafficking: decreased glucose concentration increases plasma membrane GLUT1 and transport activity with parallel reductions in intracellular GLUT1, without apparent changes in intrinsic transporter activity. [3H]cytochalasin B binding, Western blotting of subcellular fractions, 2-deoxy-D-[3H]glucose uptake assays The Biochemical journal High 1520263
1993 Inhibition of oxidative phosphorylation (azide treatment) causes rapid ~7.5-fold stimulation of GLUT1-mediated glucose transport in Clone 9 cells primarily through activation of pre-existing plasma membrane GLUT1, not translocation from intracellular pools. Immunofluorescence microscopy, differential centrifugation + Western blot, cell surface biotinylation, [3H]cytochalasin B binding The Journal of biological chemistry High 8349608
1993 GLUT1 topology was experimentally determined: the protein contains 12 membrane-spanning domains with cytoplasmic N- and C-termini and a large central cytoplasmic loop, consistent with the predicted model; insertion of an exofacial epitope into various loops confirmed this topology in vivo. Glycosylation scanning mutagenesis expressed in Xenopus oocytes (in vivo) and rabbit reticulocyte lysate (in vitro); 2-deoxyglucose uptake assays The Journal of biological chemistry High 8051147
1993 Transfection of GLUT1 (but not GLUT2) into AtT-20ins cells increases glucose transport affinity (Km ~4 mM vs 2 mM for untransfected cells) but does not confer glucose-stimulated insulin release, demonstrating that GLUT1 kinetics are insufficient to act as a glucose sensor in beta-cells. Stable transfection, 3-O-methyl glucose uptake kinetics, static incubation and perifusion insulin secretion assays, [5-3H]glucose usage The Journal of biological chemistry High 8325893
1993 During glucose deprivation of 3T3-L1 adipocytes, a lower molecular weight (37 kDa) underglycosylated isoform of GLUT1 appears; the 10-fold increase in transport activity requires new protein synthesis but involves only a small transient increase in GLUT1 mRNA, suggesting post-translational regulation and trafficking changes dominate. Glucose transport assays, Northern blot, Western blot with glycoforms, mannose/analog competition experiments The Journal of biological chemistry Medium 7678253
1994 GLUT1 topology confirmed in vivo as 12 transmembrane helices; insertion into the NH2 terminus, large central loop, or exofacial loops 2, 3, and 5 had little effect on transport activity, whereas insertion into other soluble domains abolished or significantly reduced transport. Glycosylation scanning mutagenesis in Xenopus oocytes with 2-deoxyglucose uptake functional readout The Journal of biological chemistry High 8051147
1995 Exposure to calcium ionophore A-23187 stimulates GLUT1 gene expression via both enhanced transcription (1.5–1.7-fold by nuclear run-on) and mRNA stabilization (half-life increased from 1.5 h to 5.5 h), resulting in increased GLUT1 protein and glucose transport. Nuclear run-on transcription assays, actinomycin D mRNA decay experiments, Northern blot, Western blot, 3-O-methyl-D-glucose transport assays The American journal of physiology High 7491913
1996 GLUT1 interacts with the ER chaperones calnexin and calreticulin in a glycosylation-dependent manner; non-glycosylated GLUT1 mutants fail to associate with either chaperone, indicating that the N-linked oligosaccharide is essential for this interaction during GLUT1 folding in the ER. Cross-linking studies, co-immunoprecipitation with anti-calnexin antibody, in vitro translation in the presence of microsomal membranes using a truncated GLUT1 construct The Journal of biological chemistry High 8662691
1996 Increased cytosolic calcium does not mediate the induction of GLUT1 mRNA in response to inhibition of oxidative phosphorylation by azide; although ionomycin raises [Ca2+]i and induces GLUT1 mRNA, BAPTA chelation of Ca2+ does not prevent azide-induced GLUT1 mRNA induction, demonstrating distinct signaling pathways. BAPTA chelation, ionomycin dose-response, ionomycin vs. azide kinetic comparisons, [Ca2+]i measurements, actinomycin D mRNA decay, Northern blot The American journal of physiology High 8772449
1996 Glycogen in 3T3-L1 adipocytes serves as a carbohydrate buffer for GLUT1 glycosylation during glucose deprivation; glycogen-depleted cells show more rapid alteration of GLUT1 glycosylation upon glucose removal, linking cellular glycogen stores to GLUT1 glycosylation fidelity. Glycogen quantification, glycogen depletion experiments, glycoform analysis by Western blot comparing adipocytes vs. CHO cells The American journal of physiology Medium 8928771
1996 Both thyroid hormone (T3) and insulin stimulate glucose transport in Clone 9 cells (which express only GLUT1) primarily through activation of plasma membrane-resident GLUT1, not solely by increasing surface GLUT1 abundance, as transport stimulation exceeds the increase in surface GLUT1 detected by biotinylation. Cell surface biotinylation, Western blot of plasma membrane fractions, 3-O-methyl-D-glucose transport assays Biochimica et biophysica acta Medium 8972727
1997 GLUT1 and GLUT3 transport dehydroascorbic acid (DHA) with apparent Km values of 1.1 mM and 1.7 mM, respectively; DHA transport is inhibited by glucose analogs and cytochalasin B but not by L-glucose or fructose; GLUT2, GLUT5, and SGLT1 do not transport DHA; none transport ascorbic acid. Xenopus laevis oocyte expression system, radiolabeled sugar uptake, HPLC confirmation of intracellular reduction of DHA to AA, CHO cell overexpression, competition assays with inhibitors The Journal of biological chemistry High 9228080
1997 The C-terminal tail of GLUT2 contributes to glucose transport kinetics (Km for 2-deoxyglucose), while the N-terminal region of GLUT1/GLUT2 determines substrate specificity for alternative substrates (fructose, arabinose, streptozotocin); structural domains for substrate specificity are distinct from those governing kinetic function. GLUT1/GLUT2 chimeras and N62Q mutant expressed via recombinant adenovirus in CV-1 cells; 2-deoxyglucose Km/Vmax kinetics; fructose, arabinose, streptozotocin uptake assays Biochemistry High 9154929
1999 Sp1 binds to the −102/−82 region of the GLUT1 promoter during fetal cardiac development but not during adulthood; Sp1 site mutation abolishes high transcriptional activity in cardiomyocytes; Sp1 is downregulated postnatally in heart and skeletal muscle, establishing Sp1 as a key transcriptional activator of GLUT1 in the perinatal heart. Transient transfection assays (reporter gene), electrophoretic mobility shift assays (EMSA), site-directed mutagenesis of Sp1 binding site, Western blot of Sp1 in heart/muscle development The Journal of biological chemistry High 10364200
2000 Fifteen novel heterozygous GLUT1 mutations (including large deletion, missense, nonsense, deletions, insertions, and splice site mutations) cause GLUT1 deficiency syndrome; these mutations correlate with hypoglycorrhachia and reduced erythrocyte glucose transport activity. FISH, PCR, SSCP, DNA sequencing; erythrocyte glucose transport functional assay Human mutation High 10980529
2001 Overexpression of stomatin reduces basal GLUT1-mediated glucose transport by 35–50% without altering plasma membrane GLUT1 content, through protein–protein interaction; stomatin binds specifically to the C-terminal 42-amino acid segment of GLUT1 but not to its central loop, decreasing intrinsic transporter activity. Stable transfection of stomatin, glucose transport assays, co-immunoprecipitation, GST-fusion protein pulldown with GLUT1 C-terminal and central loop domains, Western blot of plasma membrane fractions American journal of physiology. Cell physiology High 11287341
2001 Hyperosmolarity stimulates GLUT1 expression in a biphasic manner: early phase (0–6 h) involves activation of pre-existing plasma membrane GLUT1 without change in GLUT1 mRNA/protein; late phase (12–24 h) involves ~7.5-fold increase in GLUT1 mRNA mediated by both enhanced transcription and mRNA stabilization (t½ increased from 2 to 8 h), requiring a 44-bp proximal promoter element. Glucose transport assays, Northern blot with actinomycin D mRNA half-life measurements, promoter deletion analysis by transient transfection, GLUT1 protein quantification American journal of physiology. Cell physiology High 11546675
2001 A GLUT1 R126H missense mutation causes autosomal dominant GLUT1 deficiency syndrome; in Xenopus oocyte expression, the mutant shows high membrane expression but significantly reduced Vmax for 3-O-methyl-D-glucose and dehydroascorbic acid transport, demonstrating that R126 is critical for transport function. Xenopus oocyte expression and transport kinetics, SSCP/sequencing of family members, erythrocyte glucose transport, immunoblot Annals of neurology High 11603379
2003 GLUT1 serves as a receptor for both HTLV-1 and HTLV-2; HTLV envelope receptor-binding domains inhibit glucose transport by interacting with GLUT1; HTLV infection is selectively blocked by cytochalasin B, GLUT1 siRNA knockdown, or competing HTLV envelope glycoproteins; ectopic GLUT1 (but not GLUT3) rescues infection in GLUT1-depleted cells. siRNA knockdown, ectopic expression of GLUT1/GLUT3, cytochalasin B inhibition, HTLV infection assays, glucose transport inhibition assays Cell High 14622599
2003 N-glycosylation of GLUT1 at its sole N-linked glycosylation site contributes to transporter affinity for glucose: tunicamycin treatment produces a 2–2.5-fold decrease in Km without change in Vmax, and inhibition of N-glycan processing (deoxymannojirimycin, swainsonine) does not affect GLUT1 trafficking or activity in thyroid anaplastic carcinoma cells; O-glycosylation also contributes to transport activity. Tunicamycin, deoxymannojirimycin, swainsonine inhibitor studies; 2-deoxyglucose uptake; Western blot of glycoforms; jacalin lectin binding; benzyl-GalNAc O-glycosylation inhibition Biochimica et biophysica acta Medium 12667615
2006 Targeted disruption of the promoter and exon 1 of mouse Glut1 in heterozygous mice recapitulates GLUT1 deficiency syndrome: GLUT1+/- mice show epileptiform EEG discharges, impaired motor activity, hypoglycorrhachia, microencephaly, decreased brain glucose uptake (by PET), and 66% reduction of brain GLUT1 protein. Targeted gene disruption, EEG, PET brain glucose uptake, Western blot, behavioral testing Human molecular genetics High 16497725
2009 A C-terminal PDZ-binding motif in GLUT1 is critical for growth factor-stimulated cell surface localization and protection from lysosomal degradation; disruption of this motif reduces surface GLUT1 and promotes lysosomal targeting; the PDZ-domain protein GIPC binds GLUT1 via this motif and is required for normal GLUT1 surface levels and glucose uptake. PDZ-motif deletion and point mutation, flow cytometry for surface GLUT1, lysosomal inhibitor experiments, co-immunoprecipitation of GIPC-GLUT1, transferrin receptor recycling comparison, glucose uptake assays in GIPC-deficient cells The Biochemical journal High 19016655
2011 GLUT1 deficiency syndrome-causing mutations in SLC2A1 can produce both loss of glucose transport and a novel cation leak phenotype in erythrocytes (stomatin-deficient cryohydrocytosis), as demonstrated by Xenopus oocyte expression studies of two specific missense mutations. Xenopus oocyte expression, glucose transport assays, cation flux measurements, 3D structural modeling of GLUT1 Blood High 21791420
2011 Effector CD4+ T cells (Th1, Th2, Th17) express high surface GLUT1 and are highly glycolytic, while regulatory T cells express low GLUT1 and rely on lipid oxidation; GLUT1 transgenic mice show selective increase in effector T cells; these distinct metabolic programs can be manipulated in vivo to control T cell subset development. Flow cytometry for surface GLUT1, metabolic flux analysis, GLUT1 transgenic mice, AMPK activator treatment in asthma model Journal of immunology High 21317389
2013 ATM phosphorylates GLUT1 at serine 490 (S490); ATM inhibition decreases surface GLUT1, glucose and DHA transport, and GLUT1 association with GIPC1, while ATM activation (doxorubicin) increases these parameters; S490A mutation phenocopies ATM inhibition and S490D mutation phenocopies ATM activation, establishing S490 as a functional phosphorylation site regulating GLUT1 trafficking. ATM inhibitor (KU55933) and activator (doxorubicin) experiments, S490A/D point mutants, cell surface GLUT1 quantification, 2-deoxyglucose and DHA transport assays, co-immunoprecipitation of GLUT1/GIPC1, ex vivo skeletal muscle transport PloS one High 23776597
2013 TXNIP suppresses glucose uptake by directly binding to GLUT1 and inducing GLUT1 internalization through clathrin-coated pits; AMPK-dependent phosphorylation of TXNIP leads to its rapid degradation, releasing GLUT1 inhibition and acutely increasing GLUT1-mediated glucose influx; long-term adaptation also involves TXNIP-dependent regulation of GLUT1 mRNA levels. Co-immunoprecipitation of TXNIP-GLUT1, clathrin-coated pit inhibition, AMPK activation/inhibition, TXNIP phosphorylation mutants, glucose uptake assays, GLUT1 surface quantification, mRNA measurements Molecular cell High 23453806
2013 The SNX27-retromer complex maintains GLUT1 surface levels by recycling internalized GLUT1 from endosomes back to the plasma membrane, preventing lysosomal degradation; SNX27 or retromer suppression reduces surface GLUT1 abundance. Quantitative proteomics of SNX27 interactome, quantification of surface proteome in SNX27/retromer-suppressed cells by quantitative mass spectrometry, direct PDZ domain-VPS26 interaction characterization Nature cell biology High 23563491
2014 The crystal structure of human GLUT1 was determined at 3.2 Å resolution; the protein adopts a canonical major facilitator superfamily fold captured in an inward-open conformation with 12 transmembrane helices; structural comparison with the bacterial homologue XylE enabled mechanistic interpretation of the alternating access transport mechanism and mapping of disease-associated mutations. X-ray crystallography at 3.2 Å resolution, structure-based mutagenesis analysis, structural comparison with XylE Nature High 24847886
2015 RdCVF (rod-derived cone viability factor) promotes cone survival by binding to Basigin-1 (BSG1), which then associates with GLUT1, resulting in increased glucose entry into cones and stimulation of aerobic glycolysis; a missense mutation abolishing RdCVF–BSG1 binding prevents glucose uptake stimulation and cone protection. Co-immunoprecipitation of RdCVF-BSG1 and BSG1-GLUT1, glucose uptake assays, RdCVF missense mutant, in vivo retinitis pigmentosa model, cone survival quantification Cell High 25957687
2019 Myeloid-specific GLUT1 deletion in mice abolishes glucose uptake and reduces glycolysis and pentose phosphate pathway activity in macrophages; GLUT1-deficient macrophages show reduced phagocytic capacity contributing to unstable atherosclerotic lesion formation in Ldlr-/- mice, while compensatory glutamine and oleate oxidation occurs but maximal respiratory capacity is blunted. Myeloid-specific Slc2a1 conditional knockout, bone marrow-derived macrophage glucose uptake assays, extracellular flux analysis, flow cytometry for activation markers, phagocytosis assays, atherosclerosis model Journal of immunology High 30659108
2022 RAB21 regulates retromer-mediated recycling of GLUT1/SLC2A1; RAB21 depletion mis-sorts GLUT1 to lysosomes, reduces glucose uptake, and activates AMPK-ULK1 autophagy; RAB21 controls fission of retromer-decorated SNX27-containing endosomal tubules, selectively affecting GLUT1 recycling without overtly disrupting retrograde transport of IGF2R or WLS. RAB21 siRNA/shRNA depletion, GLUT1 subcellular localization by imaging, glucose uptake assays, AMPK-ULK1 pathway analysis, autophagic flux measurement, retromer complex localization, in vivo tumor growth assays Autophagy High 35993307

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets. Journal of immunology (Baltimore, Md. : 1950) 1722 21317389
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2019 Blood-Brain Barrier: From Physiology to Disease and Back. Physiological reviews 1645 30280653
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1985 Sequence and structure of a human glucose transporter. Science (New York, N.Y.) 1396 3839598
2015 Establishment and Dysfunction of the Blood-Brain Barrier. Cell 1304 26590417
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2013 The SLC2 (GLUT) family of membrane transporters. Molecular aspects of medicine 961 23506862
2005 Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer. Journal of cellular physiology 958 15389572
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2003 Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins. The British journal of nutrition 611 12568659
2014 Crystal structure of the human glucose transporter GLUT1. Nature 599 24847886
1991 Defective glucose transport across the blood-brain barrier as a cause of persistent hypoglycorrhachia, seizures, and developmental delay. The New England journal of medicine 550 1714544
2013 AMPK-dependent degradation of TXNIP upon energy stress leads to enhanced glucose uptake via GLUT1. Molecular cell 543 23453806
1990 Brain-type glucose transporter (GLUT-1) is selectively localized to the blood-brain barrier. Studies with quantitative western blotting and in situ hybridization. The Journal of biological chemistry 521 2211679
1993 Overexpression of Glut-1 glucose transporter in human breast cancer. An immunohistochemical study. Cancer 485 8221565
2015 Widespread macromolecular interaction perturbations in human genetic disorders. Cell 454 25910212
2013 A global analysis of SNX27-retromer assembly and cargo specificity reveals a function in glucose and metal ion transport. Nature cell biology 443 23563491
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
1989 Cloning and characterization of the major insulin-responsive glucose transporter expressed in human skeletal muscle and other insulin-responsive tissues. The Journal of biological chemistry 432 2656669
2004 Dissection of the mammalian midbody proteome reveals conserved cytokinesis mechanisms. Science (New York, N.Y.) 417 15166316
1988 Evidence for a family of human glucose transporter-like proteins. Sequence and gene localization of a protein expressed in fetal skeletal muscle and other tissues. The Journal of biological chemistry 413 3170580
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1997 Glucose transporter isoforms GLUT1 and GLUT3 transport dehydroascorbic acid. The Journal of biological chemistry 380 9228080
2018 DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity. Cell 379 29656893
1996 Structure, function, and regulation of the mammalian facilitative glucose transporter gene family. Annual review of nutrition 348 8839927
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2015 Rod-derived cone viability factor promotes cone survival by stimulating aerobic glycolysis. Cell 334 25957687
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