Affinage

SLC2A4

Solute carrier family 2, facilitated glucose transporter member 4 · UniProt P14672

Round 2 corrected
Length
509 aa
Mass
54.8 kDa
Annotated
2026-04-28
130 papers in source corpus 47 papers cited in narrative 47 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC2A4/GLUT4 is the principal insulin-responsive facilitative glucose transporter in adipose tissue, skeletal muscle, and heart, mediating the acute increase in glucose uptake triggered by insulin and muscle contraction (PMID:2649253, PMID:2656669). In unstimulated cells, GLUT4 is sequestered in specialized GLUT4 storage vesicles (GSVs) whose biogenesis requires sortilin, retromer-mediated retrieval from lysosomal degradation, and CHC22 clathrin-dependent trafficking from the ERGIC; intracellular retention is enforced by TUG tethering and AS160/TBC1D4 Rab-GAP activity acting through distinct FQQI and TELEY cytoplasmic motifs (PMID:15992544, PMID:28450454, PMID:31863584, PMID:14562105, PMID:18550797). Insulin signaling through PI3K→Akt phosphorylates AS160, relieving GAP-mediated inhibition and enabling GTP-loading of Rab10 (adipocytes) and Rab8A/Rab13 (muscle) to drive GSV release, tethering, and SNARE-dependent fusion at the plasma membrane, while contraction activates a parallel AMPK/CaMKII→TBC1D1 pathway; palmitoylation at Cys223 by DHHC7 is additionally required for proper GSV sorting (PMID:16213228, PMID:18076383, PMID:21041651, PMID:10330141, PMID:28057756, PMID:24895284). GLUT4 transcription is positively regulated by MEF2/GEF and C/EBPα (the latter induced by ERα/estradiol signaling), is upregulated by exercise via AMPK-mediated HDAC5 nuclear export, and is repressed by NF-κB under inflammatory conditions (PMID:18184930, PMID:15282314, PMID:16423895, PMID:23462193).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1989 High

    Cloning of SLC2A4/GLUT4 established the molecular identity of the insulin-responsive glucose transporter and showed that insulin redistributes it from intracellular microsomes to the plasma membrane, resolving the long-sought molecular basis of insulin-stimulated glucose uptake.

    Evidence cDNA cloning from muscle, functional reconstitution in Xenopus oocytes, and subcellular fractionation of rat adipocytes

    PMID:2649253 PMID:2656669

    Open questions at the time
    • Crystal structure of GLUT4 not yet solved
    • Intracellular compartment identity undefined
    • Signals controlling translocation unknown
  2. 1992 High

    Expression of GLUT4 in L6 myoblasts reconstituted both insulin-stimulated transport and cAMP-mediated inhibition, demonstrating that these regulatory properties are intrinsic to the GLUT4 isoform rather than a general feature of glucose transporters.

    Evidence Stable GLUT4 transfection in L6 myoblasts vs GLUT1-expressing cells with 2-deoxyglucose uptake

    PMID:1314390

    Open questions at the time
    • Mechanism of cAMP-mediated inhibition unresolved
    • Isoform-specific structural determinants not mapped
  3. 1997 High

    Identification of sortilin as a major GSV component and recognition that GSVs are a specialized compartment distinct from general endosomes established the concept of a dedicated GLUT4 storage organelle.

    Evidence Protein sequencing from purified GLUT4 vesicles; subcellular fractionation and vesicle immunoisolation

    PMID:9305862 PMID:9356011

    Open questions at the time
    • Mechanism of GSV biogenesis unknown
    • Signals governing GLUT4 entry into GSVs not identified
  4. 1999 High

    Gain- and loss-of-function experiments placed PKBα/Akt as a required node between insulin receptor activation and GLUT4 translocation, anchoring the signaling cascade.

    Evidence Constitutively active and dominant-negative Akt mutants in L6-GLUT4myc cells with surface GLUT4 readout

    PMID:10330141

    Open questions at the time
    • Direct Akt substrates controlling GLUT4 traffic unknown
    • Whether Akt acts at the vesicle or elsewhere unresolved
  5. 2001 High

    Tissue-specific GLUT4 knockouts revealed that adipose GLUT4 is required for whole-body insulin sensitivity (with secondary effects on muscle and liver), while cardiac GLUT4 loss causes compensated hypertrophy, establishing non-redundant physiological roles in different tissues.

    Evidence Cre/loxP adipose-specific and cardiac-specific GLUT4 KO mice; hyperinsulinemic-euglycemic clamp; echocardiography

    PMID:10606624 PMID:11217863

    Open questions at the time
    • Adipose-derived signal mediating secondary insulin resistance not identified
    • Mechanism of cardiac hypertrophy from GLUT4 loss unclear
  6. 2003 High

    Discovery of TUG as a GLUT4 tether and elucidation of the dynamic endosome–GSV cycling pathway showed that intracellular GLUT4 retention is an active process involving vesicle budding/fusion with endosomes, syntaxin 6/16-positive perinuclear compartments, and microtubule-dependent transport, rather than simple static sequestration.

    Evidence Functional screen identifying TUG with Co-IP and dominant-negative validation; kinetic trafficking studies with nocodazole; syntaxin 6/16 colocalization and vesicle immunoisolation

    PMID:12631717 PMID:12857877 PMID:14562105 PMID:14595108

    Open questions at the time
    • Insulin-dependent mechanism of TUG release unknown
    • Identity of kinase/protease acting on TUG unresolved
  7. 2005 High

    Identification of AS160/TBC1D4 as a Rab-GAP whose activity retains GLUT4 basally, and demonstration that sortilin is necessary and sufficient for GSV biogenesis, provided the two key molecular determinants of GLUT4 intracellular sequestration.

    Evidence AS160 siRNA plus GAP-mutant rescue in adipocytes; sortilin knockdown/overexpression/reconstitution with GLUT4 for GSV formation

    PMID:15992544 PMID:16213228

    Open questions at the time
    • Which Rab GTPase(s) are direct AS160 substrates in each tissue not yet resolved
    • Structural basis of sortilin–GLUT4 interaction unknown
  8. 2008 High

    Systematic analysis identified Rab10 as the principal AS160 substrate in adipocytes, mapped three distinct GLUT4 cytoplasmic motifs (FQQI, TELEY, LL) to separate retention cycles, and established the AMPK→HDAC5 phosphorylation→MEF2 de-repression axis for exercise-induced GLUT4 transcription, unifying trafficking and transcriptional control.

    Evidence siRNA of individual Rabs in adipocytes; systematic GLUT4 motif mutagenesis with AS160/AP-1 epistasis; in vitro AMPK kinase assay, HDAC5 mutagenesis, ChIP on GLUT4 promoter in human myotubes

    PMID:18076383 PMID:18184930 PMID:18216015 PMID:18550797

    Open questions at the time
    • Rab substrate identity in muscle cells remained unresolved
    • How FQQI and TELEY motifs recruit distinct sorting machinery structurally unknown
  9. 2010 High

    Identification of Rab13 and Rab8A as insulin-activated, AS160-regulated GTPases in muscle cells extended the Rab-GAP model to skeletal muscle and demonstrated tissue-specific Rab utilization for GLUT4 exocytosis.

    Evidence GTP-loading assay, siRNA knockdown and rescue with Rab orthologs in L6-GLUT4myc cells

    PMID:21041651

    Open questions at the time
    • Effectors downstream of Rab13/Rab8A not identified
    • Whether Rab10 and Rab13/8A act redundantly or in series unknown
  10. 2015 Medium

    Discovery that palmitoylation at Cys223 is required for GLUT4 sorting into insulin-responsive vesicles introduced a lipid-modification checkpoint for GSV biogenesis.

    Evidence C223S mutagenesis abolishes insulin-dependent GLUT4 translocation and GSV localization in adipocytes

    PMID:25824042

    Open questions at the time
    • Palmitoyl acyltransferase identity not yet identified in this study
    • Reversibility and regulation of GLUT4 palmitoylation unknown
  11. 2017 High

    DHHC7 was identified as the principal GLUT4 palmitoyl acyltransferase, and retromer was shown to cooperate with sortilin to retrieve GLUT4 from lysosomal degradation for GSV biogenesis, integrating lipid modification and retrograde trafficking into a coherent GSV formation model.

    Evidence Systematic screen of 23 DHHC proteins plus DHHC7 KO mice with glucose intolerance; sortilin–GLUT4 luminal domain Co-IP, retromer siRNA with fractionation and glucose uptake

    PMID:28057756 PMID:28450454

    Open questions at the time
    • Whether DHHC7 activity itself is insulin-regulated unknown
    • Structural basis of sortilin luminal loop–GLUT4 interaction not resolved
  12. 2020 High

    CHC22 clathrin was shown to initiate GLUT4 pathway biogenesis at the ERGIC by forming a complex with p115, GLUT4, and sortilin, defining the earliest trafficking step in human GSV formation, while RAB10 was localized to a TGN storage domain from which insulin mobilizes GLUT4.

    Evidence CHC22-p115-GLUT4-sortilin Co-IP plus selective siRNA epistasis in human cells; RAB10 knockdown trapping GLUT4 in a TGN compartment

    PMID:31863584 PMID:33175605

    Open questions at the time
    • How CHC22 and retromer pathways are coordinated at the TGN is unclear
    • Whether ERGIC-initiated biogenesis is conserved beyond primates (CHC22 is a pseudogene in mice) is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the atomic structure of GLUT4, the precise mechanism by which insulin triggers TUG cleavage/release, the identity of effectors downstream of Rab13/Rab8A in muscle, whether GLUT4 intrinsic transport activity is regulated by phosphorylation or oxidative modifications in vivo, and how contraction-activated (AMPK/CaMKII) and insulin-activated (Akt/AS160) pathways converge on the same vesicle pool.
  • No high-resolution GLUT4 structure available
  • TUG cleavage mechanism unknown
  • Convergence point of insulin and contraction signals on GLUT4 vesicles unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 3
Localization
GO:0031410 cytoplasmic vesicle 9 GO:0005886 plasma membrane 5 GO:0005768 endosome 3 GO:0005794 Golgi apparatus 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 11 R-HSA-162582 Signal Transduction 8 R-HSA-74160 Gene expression (Transcription) 7 R-HSA-382551 Transport of small molecules 5 R-HSA-392499 Metabolism of proteins 2
Partners
ASPSCR1CHC22DHHC7RAB10RAB13SORT1TBC1D1TBC1D4
Complex memberships
GLUT4 storage vesicle (GSV)

Evidence

Reading pass · 47 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1989 SLC2A4/GLUT4 was molecularly cloned as a novel glucose transporter expressed exclusively in adipose tissue, skeletal muscle, and heart; when expressed in Xenopus oocytes it mediates cytochalasin B-inhibitable 2-deoxyglucose transport; insulin redistributes this transporter from low-density microsomes to the plasma membrane in adipocytes. cDNA cloning from skeletal muscle library, Xenopus oocyte expression assay, subcellular fractionation of rat adipocytes Cell High 2649253
1989 The human SLC2A4/GLUT4 protein (509 amino acids) is the major insulin-regulatable glucose transporter in human skeletal muscle and fat; it is specifically recognized by monoclonal antibody 1F8 that identifies the insulin-responsive transporter in rat muscle, heart, and adipocytes, distinguishing it from GLUT1 and GLUT2. cDNA cloning from human intestine/muscle libraries, RNA blotting, in vitro translation, monoclonal antibody reactivity The Journal of biological chemistry High 2656669
1992 GLUT4 expression confers two hallmark functional properties on L6 myoblasts: (i) a large insulin-stimulated component of glucose transport (5-fold increase) and (ii) cAMP-mediated inhibition of insulin-stimulated transport; neither property is present in GLUT1-only cells, establishing that these regulatory features are intrinsic to the GLUT4 isoform. Stable transfection of GLUT4 cDNA into L6 myoblasts; 2-deoxy[3H]glucose uptake assay; cAMP analog treatment; CHO cell transient expression of GLUT1 vs GLUT4 Proceedings of the National Academy of Sciences of the United States of America High 1314390
1993 Phosphorylation of GLUT4 (induced by parathyroid hormone via cAMP/Ca2+ signaling) inversely correlates with its intrinsic transport activity: phosphorylated GLUT4 at the plasma membrane shows significantly reduced glucose transport activity without affecting its recruitment to the membrane, demonstrating that phosphorylation modulates GLUT4 intrinsic activity independently of translocation. 32P-labeling of rat adipocytes, immunoprecipitation of GLUT4, [14C]2-deoxyglucose uptake in plasma membrane vesicles, in vitro phosphorylation assay, Western blotting The Journal of biological chemistry Medium 8429011
1994 gp160 (IRAP/insulin-regulated aminopeptidase), the major non-GLUT4 protein of GLUT4-containing vesicles, has structural homology to aminopeptidase N and possesses aminopeptidase activity in vitro, establishing it as a functional enzyme co-resident in the GLUT4 storage vesicle. Purification of GLUT4-containing vesicles, sequence homology analysis, in vitro aminopeptidase activity assay The Journal of biological chemistry High 7983006
1995 SHPTP2 (a protein-tyrosine phosphatase) is required for insulin-stimulated GLUT1 expression (via a p21ras-dependent pathway) but is dispensable for insulin-stimulated GLUT4 translocation to the cell surface, demonstrating that the two insulin-regulated glucose transport pathways diverge upstream of SHPTP2. Microinjection of GST-NC-SH2 fusion protein and anti-SHPTP2 antibodies into 3T3-L1 adipocytes; cell-surface GLUT4 quantification The Journal of biological chemistry Medium 7768884
1997 Sortilin (glycoprotein 110) is a major protein component of GLUT4-containing storage vesicles in fat cells, identified by partial protein sequencing and cDNA cloning; it is highly expressed in fat, brain, and lung and dramatically upregulated during adipocyte differentiation. Purification of GLUT4-vesicle protein fraction, partial amino acid sequencing, cDNA cloning, Western blotting The Journal of biological chemistry High 9305862
1997 GLUT4 storage vesicles (GSVs) represent a specialized compartment segregated from the endosomal and biosynthetic pathways, analogous to synaptic vesicles in neurons, and move directly to the plasma membrane in response to insulin. Subcellular fractionation, vesicle immunoisolation, kinetic trafficking studies in muscle and fat cells Diabetes Medium 9356011
1999 PKBα/Akt1 is required for insulin-induced GLUT4 translocation in muscle cells: constitutively active PKBα increases cell-surface GLUT4myc, whereas a dominant-negative kinase-dead/phosphorylation-deficient Akt1 (AAA-PKB) almost completely blocks insulin-stimulated GLUT4myc appearance at the plasma membrane, independently of actin ruffling. L6-GLUT4myc myoblasts; transient transfection of constitutively active and dominant-negative PKB constructs; immunofluorescence of exofacial myc tag in non-permeabilized cells; GFP co-transfection to identify transfected cells Molecular and cellular biology High 10330141
2000 Rab11 is a component of GLUT4-containing vesicles in cardiac muscle; insulin treatment recruits Rab11 from the microsomal fraction to the plasma membrane and increases its abundance in GLUT4 vesicles ~2.2-fold, implicating Rab11 in endosomal recycling and exocytotic movement of GLUT4. Subcellular fractionation, sucrose density gradient, immunoadsorption of GLUT4 vesicles, Western blotting, in vivo insulin treatment Diabetologia Medium 11151761
2001 Adipose-selective knockout of GLUT4 (G4A-/- mice) markedly impairs insulin-stimulated glucose uptake in adipocytes and causes secondary insulin resistance in muscle and liver, manifested by decreased PI3K activation, demonstrating that adipose GLUT4 expression is required for normal whole-body glucose homeostasis and that adipose-derived signals regulate insulin sensitivity in other tissues. Cre/loxP tissue-selective gene knockout; hyperinsulinemic-euglycemic clamp; PI3K activity assay; glucose and insulin tolerance tests Nature High 11217863
2001 Selective deletion of GLUT4 in the heart causes compensated cardiac hypertrophy with increased myocyte size and induction of ANP/BNP, while basal glucose transport is maintained through a 3-fold upregulation of GLUT1; insulin-stimulated glucose uptake in the heart is abolished. Cre/loxP cardiac-selective GLUT4 knockout (G4H-/- mice); glucose transport assay; Western blotting; echocardiography; gene expression analysis The Journal of clinical investigation High 10606624
2001 The N-terminal phenylalanine-based motif (F5) of GLUT4 functions as a binding site for clathrin adaptor medium chains μ1, μ2, and μ3A (identified by yeast two-hybrid), and mutation of F5 substantially increases cell-surface GLUT4 by slowing endocytosis; mutation or deletion of C-terminal sequences alters GLUT4 membrane trafficking, with the C-terminal region required for maximal surface levels. Transient transfection of HA-epitope-tagged GLUT4 mutants in primary rat adipocytes; wortmannin and dominant-negative dynamin treatment; yeast two-hybrid screen Journal of cell science High 11801731
2002 Protein kinase B (Akt) activity at intracellular GLUT4 vesicles is functionally required for insulin-stimulated vesicle translocation: kinase-inactive PKB fused to the N-terminus of GLUT4 (targeted to GLUT4 vesicles) acts as a highly effective dominant-negative inhibitor of IRAP translocation, whereas the same kinase-inactive PKB expressed in the cytoplasm has no effect. Fusion-protein targeting of constitutively active and kinase-inactive PKB to GLUT4 vesicles in 3T3-L1 adipocytes; cell-surface biotinylation of IRAP Journal of cell science Medium 12082147
2002 Insulin activates GLUT4 through two separable pathways: (i) recruitment of transporters to the cell surface (translocation) and (ii) increase in intrinsic transporter activity; the two pathways are differentially sensitive to wortmannin, and p38 MAPK specifically regulates intrinsic GLUT4 activity rather than translocation. 2-deoxy-[3H]glucose uptake in L6 myoblasts/adipocytes; wortmannin and p38 MAPK inhibitor treatment; subcellular fractionation Biochemistry and cell biology Medium 12440698
2003 TUG forms a complex specifically with GLUT4 in unstimulated 3T3-L1 adipocytes; this complex is largely disassembled by insulin. TUG is localized with the insulin-mobilizable GLUT4 pool and is not itself mobilized to the plasma membrane. Dominant-negative TUG inhibits insulin-stimulated GLUT4 redistribution, indicating that TUG tethers endocytosed GLUT4 intracellularly and insulin releases this tether. Functional screen for GLUT4 distribution modulators; co-immunoprecipitation; subcellular localization; dominant-negative overexpression in CHO cells and 3T3-L1 adipocytes Nature High 14562105
2003 GLUT4 is retained in adipocytes by a dynamic cycle of vesicle budding and fusion with endosomes: GLUT4 vesicles are 5× more likely to fuse with endosomes than with the plasma membrane; GLUT4 does not substantially accumulate in the TGN; and an intact microtubule cytoskeleton is required for insulin-stimulated but not basal GLUT4 trafficking. Kinetic trafficking studies in adipocytes; nocodazole disruption of microtubules; fluorescent GLUT4 tracking; subcellular fractionation comparing furin/TGN vs GLUT4 distribution Molecular biology of the cell High 14595108
2003 Syntaxin 6 is found in >85% of GLUT4-containing vesicles and undergoes insulin-stimulated translocation to the plasma membrane; overexpression of its cytosolic domain increases basal GLUT4 at the cell surface and slows GLUT4 re-internalization after insulin withdrawal, implicating Syntaxin 6 in the trafficking step that sequesters GLUT4 into its storage compartment. Adenoviral overexpression of syntaxin cytosolic domains in 3T3-L1 adipocytes; glucose transport assay; cell-surface GLUT4 quantification; subcellular colocalization Molecular biology of the cell Medium 12857877
2003 After endocytosis, GLUT4 rapidly transits through endosomes to a perinuclear compartment enriched in Syntaxins 6 and 16 (but not TGN38); Syntaxins 6 and 16 are upregulated during adipocyte differentiation and translocate to the cell surface with insulin; an acidic targeting motif in the GLUT4 C-terminus regulates its trafficking from endosomes to the TGN subdomain. Epitope-tagged GLUT4 internalization assay; vesicle immunoisolation; confocal colocalization; C-terminal GLUT4 mutant analysis in adipocytes Molecular biology of the cell High 12631717
2004 PKB/Akt phosphorylates PIKfyve at Ser318 in response to insulin (PI3K-dependently), stimulating its PtdIns3P 5-kinase activity; PIKfyve colocalizes with a motile subpopulation of IRAP/GLUT4 vesicles, and overexpression of PIKfyve[S318A] enhances insulin-stimulated GLUT4 vesicle translocation, indicating that PKB-dependent PIKfyve phosphorylation regulates GLUT4 traffic. In vitro Akt kinase assay; phospho-specific antibody; PIKfyve[S318A] mutant overexpression in 3T3-L1 adipocytes; colocalization by immunofluorescence Journal of cell science Medium 15546921
2004 C/EBPα but not PPARγ is required for GLUT4 expression during adipogenesis; PPARγ-differentiated cells form functional insulin-responsive GLUT4 vesicles (containing VAMP2, syntaxin-4, IRAP) and support IRAP translocation and exogenous GLUT4 translocation, demonstrating that the vesicle trafficking machinery is established independently of GLUT4 expression and that C/EBPα's major role is transcriptional regulation of GLUT4. Ectopic expression of C/EBPα and PPARγ in NIH 3T3 fibroblasts; sucrose gradient vesicle analysis; cell-surface biotinylation; reconstitution with GLUT4-myc Molecular and cellular biology High 15282314
2005 AS160 (a Rab-GAP) is a negative regulator of basal GLUT4 exocytosis: AS160 knockdown increases basal surface GLUT4 and GLUT4 exocytosis 3-fold; this effect requires AS160 GAP domain activity since a GAP-mutant AS160 cannot restore normal GLUT4 retention, providing first direct evidence that AS160 GAP activity is required for basal GLUT4 retention. siRNA knockdown of AS160 in 3T3-L1 adipocytes; reexpression of wild-type vs GAP-mutant AS160; GLUT4 exocytosis kinetics; glucose uptake assay Cell metabolism High 16213228
2005 Sortilin is both necessary and sufficient for biogenesis of GLUT4 storage vesicles (GSVs) in 3T3-L1 adipocytes: sortilin is induced on day 2 of adipocyte differentiation coinciding with GSV formation; sortilin knockdown reduces GSV formation and insulin-regulated glucose uptake; overexpression of sortilin increases GSV formation; co-expression of sortilin and GLUT4 in undifferentiated cells reconstitutes functional GSVs. siRNA knockdown; sortilin overexpression; GSV reconstitution by double transfection; subcellular fractionation; glucose uptake assay Developmental cell High 15992544
2005 PKCζ directly interacts with munc18c; this interaction is increased ~3-fold by insulin and requires residues 295–338 of munc18c and the N-terminal region of PKCζ; disruption of this interaction by deletion mutants markedly inhibits insulin-stimulated GLUT4 translocation and glucose uptake, establishing a direct link between the PKCζ insulin-signaling kinase and the GLUT4 vesicle fusion machinery. Yeast two-hybrid screen with munc18c as bait; GST pull-down mapping; endogenous co-immunoprecipitation; GLUT4 translocation assay with deletion mutants Diabetologia Medium 15986239
2006 ERα is a positive transcriptional regulator of GLUT4 in skeletal muscle: ERα−/− mice have severely reduced GLUT4 mRNA and protein at the muscle cell membrane, whereas ERβ acts as a suppressor (ERβ agonist reduces GLUT4 in ArKO mice); both ERα and ERβ are required for optimal caveolin-1 expression and colocalization with GLUT4. ERα−/−, ERβ−/−, and ArKO mouse models; immunohistochemistry; RT-PCR; Western blotting; ERβ agonist (DPN) treatment Proceedings of the National Academy of Sciences of the United States of America High 16423895
2006 Atorvastatin (an HMG-CoA reductase inhibitor) attenuates GLUT4 (SLC2A4) expression and adipocyte maturation in 3T3-L1 cells by inhibiting isoprenoid biosynthesis; these effects are rescued by mevalonate or geranylgeranyl pyrophosphate supplementation, indicating that geranylgeranylation-dependent signaling is required for normal GLUT4 expression. 3T3-L1 adipocyte culture; atorvastatin treatment with mevalonate/GGPP rescue; Western blotting and RT-PCR for SLC2A4; morphological adipocyte differentiation assessment; NSY mouse in vivo model Diabetologia Medium 16685502
2008 AMPK regulates GLUT4 transcription by phosphorylating HDAC5 at Ser259 and Ser498: AMPK phosphorylation causes HDAC5 to associate with 14-3-3 proteins and undergo nuclear export, leading to histone H3 hyperacetylation at the GLUT4 promoter and increased GLUT4 gene expression in human primary myotubes. In vitro AMPK kinase assay; site-directed mutagenesis of HDAC5 phosphosites; phospho-specific antibodies; constitutively active/dominant-negative AMPK in human myotubes; chromatin immunoprecipitation (ChIP); GLUT4 reporter gene assay; AICAR treatment Diabetes High 18184930
2008 Rab10 is present in GLUT4 vesicles (~5% of total Rab10) isolated from 3T3-L1 adipocyte low-density microsomes; siRNA knockdown of Rab10 (but not Rab8A, 8B, or 14) specifically inhibits GLUT4 translocation, implicating Rab10 as the principal AS160 substrate mediating GLUT4 exocytosis in adipocytes. siRNA knockdown of individual Rab GTPases in 3T3-L1 adipocytes; GLUT4 translocation assay; subcellular fractionation; GTP-loading state determination The Biochemical journal High 18076383
2008 Molecular analysis of the GLUT4 promoter identified three cis-acting regulatory elements: a MEF2 binding domain and Domain I that can act as positive or negative regulators; GEF (GLUT4 enhancer factor) dimerizes with hypophosphorylated MEF2A, and MEF2A binding to its cognate site increases GEF DNA-binding activity to Domain I; the transcriptional co-repressor HDAC5 interacts with GEF in the absence of MEF2 to inhibit GLUT4 promoter activity. GEF structural domain mapping; GST pull-down; co-immunoprecipitation; gel shift (EMSA); chromatin immunoprecipitation; GLUT4 reporter gene assay in adipocytes The Journal of biological chemistry Medium 18216015
2008 GLUT4 intracellular retention in adipocytes involves two linked cycles regulated by three distinct cytoplasmic motifs: the FQQI motif targets GLUT4 to an endosome-retention compartment cycle; the TELEY motif targets it to specialized GSV vesicles (under AS160 control); and the LL dileucine motif (with AP-1) controls return to basal retention after insulin withdrawal. Mutagenesis of GLUT4 trafficking motifs in 3T3-L1 adipocytes; AS160 knockdown; AP-1 knockdown; GLUT4 surface level quantification Molecular biology of the cell High 18550797
2008 Contractile activity per se (electrically induced contraction of isolated soleus muscle) rapidly increases SLC2A4/GLUT4 mRNA and protein, and enhances binding of transcription factors MEF2D, HIF-1α, and TRα to the SLC2A4 promoter, as demonstrated by EMSA, supershift, and chromatin immunoprecipitation assays. Electrically induced contraction of isolated rat soleus muscle; EMSA and supershift assay; ChIP; RT-PCR; Western blotting American journal of physiology. Endocrinology and metabolism Medium 18957617
2009 In rat and human skeletal muscle, insulin stimulates GLUT4 exocytosis ~6-fold (rate constants: basal 0.010–0.011 min⁻¹ vs insulin-stimulated 0.067–0.075 min⁻¹), quantitatively accounting for the observed increase in glucose transport; in contrast, AICAR (AMPK activator) does not markedly increase exocytosis, indicating that AMPK-mediated glucose uptake operates through a different mechanism than increased GLUT4 exocytosis rate. Biotinylated photoaffinity labeling of endogenous GLUT4 in isolated rat epitrochlearis and human vastus lateralis muscle; kinetic exocytosis assay Diabetes High 19188436
2010 miR-223 increases GLUT4 protein expression in cardiomyocytes and this upregulation is necessary and sufficient to increase glucose uptake: siRNA knockdown of GLUT4 abolishes the miR-223-induced glucose uptake, and in vivo miR-223 inhibition reduces GLUT4 levels. Adenoviral miR-223 overexpression in neonatal rat cardiomyocytes; siRNA Glut4 knockdown; glucose uptake assay; in vivo miR-223 inhibitor Cardiovascular research Medium 20080987
2010 In L6 skeletal muscle cells, both Rab13 and Rab8A are activated (GTP-loaded) by insulin downstream of AS160 and regulate GLUT4 vesicle traffic: Rab13 siRNA knockdown blocks insulin-induced surface GLUT4 gain and is rescued by a Rab13 ortholog but not Rab8A; constitutively active AS160 lowers surface GLUT4, rescued by overexpressing either Rab8A or Rab13; insulin promotes Rab13 colocalization with GLUT4 at the cell periphery. GTP-loading assay (effector pull-down); siRNA knockdown of Rab13 and Rab8A; rescue experiments; confocal colocalization; L6-GLUT4myc surface quantification Proceedings of the National Academy of Sciences of the United States of America High 21041651
2010 SPARC interacts with AMPKα1 (identified by yeast two-hybrid and confirmed by endogenous co-immunoprecipitation); AMPK activation increases SPARC expression and SPARC knockdown reduces AICAR-stimulated AMPK phosphorylation; SPARC siRNA reduces GLUT4 expression in L6 myocytes, placing SPARC in the AMPK–GLUT4 regulatory axis. Yeast two-hybrid screen; endogenous Co-IP with specific antibodies; siRNA knockdown; Western blotting for GLUT4 Biochemical and biophysical research communications Low 20460104
2013 NF-κB (p50 and p65 subunits) directly binds two κB sites at −134/−113 bp and −83/−62 bp in the mouse Slc2a4 promoter and represses Slc2a4 gene transcription; demonstrated by EMSA, ChIP in adipocytes, and reporter gene transfection experiments. Electrophoretic mobility shift assay (EMSA); chromatin immunoprecipitation (ChIP) in adipocytes; luciferase reporter transfection; computational promoter analysis Molecular and cellular endocrinology Medium 23462193
2014 Insulin regulates GLUT4 trafficking through six distinct quantifiable steps; in adipocytes, sequestration of GLUT4 into GSVs from endosomes is highly regulated (insulin increases kseq 8-fold), and release from GSVs is rate-limiting in basal cells (controlled by AS160); the tethering/docking/fusion step is regulated by an AS160-independent mechanism, and insulin increases the combined rate constant for release and fusion of GSVs 40-fold. Quantitative kinetic trafficking assay of GLUT4, transferrin receptor, and LRP1 in adipocytes and fibroblasts; AS160 knockdown; mathematical modeling of trafficking rate constants The Journal of biological chemistry High 24778187
2015 GLUT4 is palmitoylated at Cys223; mutation of Cys223 to serine (C223S) abolishes insulin-dependent GLUT4 membrane translocation and excludes GLUT4 from tubular-vesicular structures containing insulin-responsive vesicles, demonstrating that palmitoylation at this site is required for GLUT4 sorting into insulin-responsive GSVs. Palmitoylation site mutagenesis (C223S); subcellular localization by imaging; cell-surface GLUT4 translocation assay in adipocytes and CHO-IR cells Biochemical and biophysical research communications Medium 25824042
2015 ZFP407 regulates GLUT4 expression by controlling both Glut4 mRNA transcription and pre-mRNA splicing efficiency; ZFP407 loss reduces GLUT4 mRNA and protein, impairing insulin-stimulated glucose uptake; ZFP407 is required for the PPARγ agonist rosiglitazone to increase Glut4 expression and synergizes with PPARγ to activate a PPARγ reporter. Targeted siRNA screen; Glut4 mRNA/protein quantification; nascent transcription analysis; pre-mRNA splicing assay; transcriptome-wide analysis; co-overexpression reporter assay in adipocytes The Journal of biological chemistry Medium 25596527
2017 DHHC7 is the major palmitoyl acyltransferase (PAT) for GLUT4 at Cys223: among 23 DHHC proteins, DHHC7 overexpression increases GLUT4 palmitoylation while DHHC7 knockdown and DHHC7 KO in adipose tissue/muscle decrease palmitoylation; DHHC7 KO suppresses insulin-dependent GLUT4 membrane translocation and causes hyperglycemia and glucose intolerance in vivo. Ectopic expression of 23 DHHC proteins; siRNA knockdown in 3T3-L1 adipocytes; DHHC7 KO mice; palmitoylation assay; GLUT4 translocation assay; glucose tolerance test The Journal of biological chemistry High 28057756
2017 Sortilin together with retromer retrieves GLUT4 from lysosomal degradation and returns it to the TGN for GSV formation: the luminal Vps10p domain of sortilin interacts with the first luminal loop of GLUT4, and the cytoplasmic tail of sortilin binds to retromer; retromer ablation decreases sortilin and GLUT4 stability, blocks their entry into small vesicular carriers, prevents GLUT4 from reaching the insulin-responsive compartment, and suppresses insulin-stimulated glucose uptake. Co-immunoprecipitation mapping of sortilin-GLUT4 luminal domain interaction; retromer subunit siRNA knockdown; sucrose gradient fractionation; insulin-stimulated glucose uptake assay in 3T3-L1 adipocytes Molecular biology of the cell High 28450454
2018 Tbc1d1 and AS160 cooperatively regulate GLUT4 release: when both are present, Tbc1d1 functionally dominates; AS160 modulates the sensitivity of Tbc1d1-mediated GLUT4 release to Ca2+ and insulin; cooperative activity requires the PTB1 and calmodulin-binding domains of Tbc1d1 and key phosphorylation sites AS160-Thr642 and Tbc1d1-Ser237/Thr596. GLUT4 nanometry; cell-based reconstitution models with variable expression ratios; mutational analysis of domain deletions and phosphorylation site mutations; AICAR, Ca2+, and insulin stimulation The Journal of biological chemistry High 30482843
2019 Estradiol (E2) stimulates Slc2a4/GLUT4 expression via an ESR1 (estrogen receptor α)-dependent and CEBPA-mediated mechanism: ESR1 silencing (~50%) in mature adipocytes abolishes E2-induced nuclear CEBPA accumulation, Slc2a4/GLUT4 expression, and GLUT4 translocation to the plasma membrane. 3T3-L1 adipocyte differentiation; Esr1 siRNA silencing; CEBP/Slc2a4-binding activity; nuclear CEBPA quantification; GLUT4 translocation assay; mRNA and protein quantification Molecular and cellular endocrinology Medium 31100494
2020 TBC1D4-RAB10 signaling module controls GLUT4 mobilization from a trans-Golgi network (TGN) storage compartment: RAB10 knockdown traps GLUT4 in a TGN domain that also stores lysosomal proteins and ATP7A; insulin-mobilized GLUT4 but not ATP7A requires RAB10, demonstrating that insulin acts deep within the cell at the TGN in addition to at the plasma membrane proximal steps. RAB10 siRNA knockdown in adipocytes; confocal microscopy; co-localization with TGN markers, lysosomal cargo, ATP7A; insulin and copper stimulation; GLUT4 translocation assay Molecular biology of the cell High 33175605
2020 CHC22 clathrin mediates GLUT4 pathway biogenesis from the ER-to-Golgi intermediate compartment (ERGIC): CHC22 localizes to the ERGIC and forms a complex with ERGIC tether p115, GLUT4, and sortilin; downregulation of CHC22 or p115 (but not GM130 or sortilin) abolishes insulin-responsive GLUT4 release, defining ERGIC-to-TGN trafficking as the initiation point of human GLUT4 sequestration. Subcellular localization of CHC22 by immunofluorescence; co-immunoprecipitation of CHC22-p115-GLUT4-sortilin complex; siRNA knockdown of CHC22 vs p115 vs GM130 vs sortilin; insulin-stimulated GLUT4 release assay; Legionella replication vacuole formation assay The Journal of cell biology High 31863584
2015 Excessive caloric intake causes oxidative carbonylation of GLUT4 near its glucose transport channel in human adipose tissue, likely reducing GLUT4 activity and contributing to the early onset of insulin resistance; this was associated with oxidative stress but without inflammatory or ER stress. Controlled overfeeding (~6000 kcal/day) in healthy men; adipose tissue proteomics (mass spectrometry); GLUT4 carbonylation site mapping; hyperinsulinemic-euglycemic clamp Science translational medicine Medium 26355033
2014 Ca2+ elevation in L6 muscle cells promotes GLUT4 exocytosis via CaMKIIδ and AMPKα1/α2 activation while simultaneously slowing GLUT4 endocytosis via novel PKC isoforms; siRNA knockdown of CaMKIIδ or AMPKα1/α2 partially reduces ionomycin-induced GLUT4 exocytosis but does not affect reduced endocytosis, whereas novel PKC inhibition specifically reverses the slowing of endocytosis. Ionomycin treatment of L6-GLUT4myc cells; siRNA knockdown of CaMKIIδ, AMPKα1/α2; pharmacological inhibitors of CaMKII (CN21), AMPK (Compound C), and PKC isoforms (Gö6976/Gö6983); live-cell GLUT4 exocytosis and endocytosis kinetics American journal of physiology. Endocrinology and metabolism Medium 24895284

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
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2004 Strength training increases insulin-mediated glucose uptake, GLUT4 content, and insulin signaling in skeletal muscle in patients with type 2 diabetes. Diabetes 424 14747278
2008 Emerging role for AS160/TBC1D4 and TBC1D1 in the regulation of GLUT4 traffic. American journal of physiology. Endocrinology and metabolism 360 18477703
2008 AMP-activated protein kinase regulates GLUT4 transcription by phosphorylating histone deacetylase 5. Diabetes 337 18184930
1999 Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart. The Journal of clinical investigation 292 10606624
2015 Insulin resistance and impaired adipogenesis. Trends in endocrinology and metabolism: TEM 282 25703677
2010 MicroRNA-223 regulates Glut4 expression and cardiomyocyte glucose metabolism. Cardiovascular research 277 20080987
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2006 Effects of statins on the adipocyte maturation and expression of glucose transporter 4 (SLC2A4): implications in glycaemic control. Diabetologia 246 16685502
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2011 GLUT4 exocytosis. Journal of cell science 229 22247191
2006 Muscle GLUT4 regulation by estrogen receptors ERbeta and ERalpha. Proceedings of the National Academy of Sciences of the United States of America 213 16423895
2003 5-amino-imidazole carboxamide riboside increases glucose transport and cell-surface GLUT4 content in skeletal muscle from subjects with type 2 diabetes. Diabetes 191 12716734
2003 Enhanced basal activation of mitogen-activated protein kinases in adipocytes from type 2 diabetes: potential role of p38 in the downregulation of GLUT4 expression. Diabetes 186 12606502
2003 GLUT4 recycles via a trans-Golgi network (TGN) subdomain enriched in Syntaxins 6 and 16 but not TGN38: involvement of an acidic targeting motif. Molecular biology of the cell 182 12631717
2005 Sortilin is essential and sufficient for the formation of Glut4 storage vesicles in 3T3-L1 adipocytes. Developmental cell 175 15992544
2002 Placental glucose transfer and fetal growth. Endocrine 175 12583599
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2022 Metformin and Insulin Resistance: A Review of the Underlying Mechanisms behind Changes in GLUT4-Mediated Glucose Transport. International journal of molecular sciences 165 35163187
2009 Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip. American journal of human genetics 164 19913121
2003 GLUT4 is retained by an intracellular cycle of vesicle formation and fusion with endosomes. Molecular biology of the cell 164 14595108
2003 Functional cloning of TUG as a regulator of GLUT4 glucose transporter trafficking. Nature 163 14562105
2006 Bridging the GAP between insulin signaling and GLUT4 translocation. Trends in biochemical sciences 162 16540333
2015 Excessive caloric intake acutely causes oxidative stress, GLUT4 carbonylation, and insulin resistance in healthy men. Science translational medicine 158 26355033
2012 Multiple myeloma exhibits novel dependence on GLUT4, GLUT8, and GLUT11: implications for glucose transporter-directed therapy. Blood 157 22452979
2010 Rab8A and Rab13 are activated by insulin and regulate GLUT4 translocation in muscle cells. Proceedings of the National Academy of Sciences of the United States of America 146 21041651
2008 Regulation by exercise of skeletal muscle content of mitochondria and GLUT4. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society 138 19258654
2007 Nitric oxide increases GLUT4 expression and regulates AMPK signaling in skeletal muscle. American journal of physiology. Endocrinology and metabolism 138 17666490
2014 Signal transduction meets vesicle traffic: the software and hardware of GLUT4 translocation. American journal of physiology. Cell physiology 134 24598362
2011 Mapping insulin/GLUT4 circuitry. Traffic (Copenhagen, Denmark) 118 21401839
2007 Ins (endocytosis) and outs (exocytosis) of GLUT4 trafficking. Current opinion in cell biology 116 17644329
2023 Insulin signalling and GLUT4 trafficking in insulin resistance. Biochemical Society transactions 113 37248992
2004 Protein kinase B phosphorylation of PIKfyve regulates the trafficking of GLUT4 vesicles. Journal of cell science 113 15546921
2006 Insulin receptor signals regulating GLUT4 translocation and actin dynamics. Endocrine journal 112 16702775
2001 Troglitazone induces GLUT4 translocation in L6 myotubes. Diabetes 111 11334413
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1997 Sortilin is a major protein component of Glut4-containing vesicles. The Journal of biological chemistry 103 9305862
2002 Activation of the glucose transporter GLUT4 by insulin. Biochemistry and cell biology = Biochimie et biologie cellulaire 100 12440698
2010 Biogenesis and regulation of insulin-responsive vesicles containing GLUT4. Current opinion in cell biology 99 20417083
2000 Rab11 is associated with GLUT4-containing vesicles and redistributes in response to insulin. Diabetologia 96 11151761
2008 Rab10 in insulin-stimulated GLUT4 translocation. The Biochemical journal 92 18076383
2014 Molecular mechanisms of GLUT4 regulation in adipocytes. Diabetes & metabolism 90 24656589
2003 Syntaxin 6 regulates Glut4 trafficking in 3T3-L1 adipocytes. Molecular biology of the cell 90 12857877
2012 Critical illness myopathy and GLUT4: significance of insulin and muscle contraction. American journal of respiratory and critical care medicine 87 23239154
2001 Subcellular compartmentalization and trafficking of the insulin-responsive glucose transporter, GLUT4. Experimental cell research 86 11697884
2001 GLUT4--at the cross roads between membrane trafficking and signal transduction. Traffic (Copenhagen, Denmark) 79 11208163
1998 Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise. Acta physiologica Scandinavica 78 9578375
2011 The sugar is sIRVed: sorting Glut4 and its fellow travelers. Traffic (Copenhagen, Denmark) 76 21306486
2008 Molecular mechanisms controlling GLUT4 intracellular retention. Molecular biology of the cell 72 18550797
2007 The GLUT4 code. Molecular endocrinology (Baltimore, Md.) 71 17717074
2011 Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. Cellular and molecular life sciences : CMLS 70 21547502
2017 Sortilin and retromer mediate retrograde transport of Glut4 in 3T3-L1 adipocytes. Molecular biology of the cell 68 28450454
2003 The insulin-regulated aminopeptidase: a companion and regulator of GLUT4. Frontiers in bioscience : a journal and virtual library 67 12700100
2011 Regulation of mitochondrial biogenesis and GLUT4 expression by exercise. Comprehensive Physiology 66 23737207
2010 Pachymic acid stimulates glucose uptake through enhanced GLUT4 expression and translocation. European journal of pharmacology 66 20816811
2018 Action of Phytochemicals on Insulin Signaling Pathways Accelerating Glucose Transporter (GLUT4) Protein Translocation. Molecules (Basel, Switzerland) 65 29382104
2012 The role of CaMKII in regulating GLUT4 expression in skeletal muscle. American journal of physiology. Endocrinology and metabolism 64 22496345
2020 Exercise and GLUT4. Exercise and sport sciences reviews 63 32568924
2014 Insulin-regulated Glut4 translocation: membrane protein trafficking with six distinctive steps. The Journal of biological chemistry 63 24778187
2008 The Glut1 and Glut4 glucose transporters are differentially expressed during perinatal and postnatal erythropoiesis. Blood 63 18796630
2017 DHHC7 Palmitoylates Glucose Transporter 4 (Glut4) and Regulates Glut4 Membrane Translocation. The Journal of biological chemistry 61 28057756
2002 Roles of the N- and C-termini of GLUT4 in endocytosis. Journal of cell science 61 11801731
2014 Cellular regulation of glucose uptake by glucose transporter GLUT4. Advances in clinical chemistry 57 25344989
2012 Regulation of GLUT4 and Insulin-Dependent Glucose Flux. ISRN molecular biology 55 27335671
2003 Push/pull mechanisms of GLUT4 traffic in muscle cells. Acta physiologica Scandinavica 55 12864734
2007 Mechanisms of calcium-induced mitochondrial biogenesis and GLUT4 synthesis. Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme 54 18059607
1997 Regulatory elements in the insulin-responsive glucose transporter (GLUT4) gene. Biochemical and biophysical research communications 54 9405224
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2010 SPARC interacts with AMPK and regulates GLUT4 expression. Biochemical and biophysical research communications 52 20460104
2009 Kinetics of GLUT4 trafficking in rat and human skeletal muscle. Diabetes 51 19188436
2020 Insulin stimulated GLUT4 translocation - Size is not everything! Current opinion in cell biology 48 32182545
2016 Acute resistance exercise-induced IGF1 expression and subsequent GLUT4 translocation. Physiological reports 48 27550988
2013 Testosterone increases GLUT4-dependent glucose uptake in cardiomyocytes. Journal of cellular physiology 48 23757167
2021 Ginsenoside Rg3 inhibits angiogenesis in gastric precancerous lesions through downregulation of Glut1 and Glut4. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 47 34799220
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2021 AKT ISOFORMS-AS160-GLUT4: The defining axis of insulin resistance. Reviews in endocrine & metabolic disorders 44 33928491
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2011 SNARE proteins underpin insulin-regulated GLUT4 traffic. Traffic (Copenhagen, Denmark) 42 21226814
2003 Regulation of GLUT4 traffic and function by insulin and contraction in skeletal muscle. Frontiers in bioscience : a journal and virtual library 42 12957810
1993 Inverse relationship between GLUT-4 phosphorylation and its intrinsic activity. The Journal of biological chemistry 42 8429011
2015 Glut4 palmitoylation at Cys223 plays a critical role in Glut4 membrane trafficking. Biochemical and biophysical research communications 41 25824042
2009 Intracellular retention and insulin-stimulated mobilization of GLUT4 glucose transporters. Vitamins and hormones 41 19251038
2004 Muscle insulin resistance amended with exercise training: role of GLUT4 expression. Medicine and science in sports and exercise 41 15235327
2006 How many signals impinge on GLUT4 activation by insulin? Cellular signalling 39 16919913
2004 Glut4 storage vesicles without Glut4: transcriptional regulation of insulin-dependent vesicular traffic. Molecular and cellular biology 39 15282314
2020 CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis. The Journal of cell biology 38 31863584
2019 Estradiol stimulates adipogenesis and Slc2a4/GLUT4 expression via ESR1-mediated activation of CEBPA. Molecular and cellular endocrinology 38 31100494
2008 GLUT4 enhancer factor (GEF) interacts with MEF2A and HDAC5 to regulate the GLUT4 promoter in adipocytes. The Journal of biological chemistry 38 18216015
2017 Development of GLUT4-selective antagonists for multiple myeloma therapy. European journal of medicinal chemistry 37 28837922
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2014 Ca²⁺ signals promote GLUT4 exocytosis and reduce its endocytosis in muscle cells. American journal of physiology. Endocrinology and metabolism 36 24895284
2013 Identification of nuclear factor-κB sites in the Slc2a4 gene promoter. Molecular and cellular endocrinology 36 23462193
2015 Zinc finger protein 407 (ZFP407) regulates insulin-stimulated glucose uptake and glucose transporter 4 (Glut4) mRNA. The Journal of biological chemistry 35 25596527
2015 Impaired translocation of GLUT4 results in insulin resistance of atrophic soleus muscle. BioMed research international 32 25713812
2013 Posttranslational modifications of GLUT4 affect its subcellular localization and translocation. International journal of molecular sciences 32 23665900
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2009 Ready, set, internalize: mechanisms and regulation of GLUT4 endocytosis. Bioscience reports 31 19143591
2005 Protein kinase-zeta interacts with munc18c: role in GLUT4 trafficking. Diabetologia 31 15986239
2002 Functional consequence of targeting protein kinase B/Akt to GLUT4 vesicles. Journal of cell science 30 12082147
2015 Functional characterization of retromer in GLUT4 storage vesicle formation and adipocyte differentiation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 28 26581601
2015 Cardiac contraction-induced GLUT4 translocation requires dual signaling input. Trends in endocrinology and metabolism: TEM 27 26138758
2020 Insulin-promoted mobilization of GLUT4 from a perinuclear storage site requires RAB10. Molecular biology of the cell 25 33175605
2018 Cooperative actions of Tbc1d1 and AS160/Tbc1d4 in GLUT4-trafficking activities. The Journal of biological chemistry 25 30482843
2017 Peripheral insulin resistance in ILK-depleted mice by reduction of GLUT4 expression. The Journal of endocrinology 25 28490443
1997 Molecular cloning and mRNA expression of the bovine insulin-responsive glucose transporter (GLUT4). Journal of animal science 25 9027564
2008 Contractile activity per se induces transcriptional activation of SLC2A4 gene in soleus muscle: involvement of MEF2D, HIF-1a, and TRalpha transcriptional factors. American journal of physiology. Endocrinology and metabolism 24 18957617
2006 Participation of beta-adrenergic activity in modulation of GLUT4 expression during fasting and refeeding in rats. Metabolism: clinical and experimental 24 17046558
2022 GLUT4 On the move. The Biochemical journal 23 35147164
2019 Wogonin Alleviates Hyperglycemia Through Increased Glucose Entry into Cells Via AKT/GLUT4 Pathway. Current pharmaceutical design 23 31333118
2012 Adaptive evolution in the glucose transporter 4 gene Slc2a4 in Old World fruit bats (family: Pteropodidae). PloS one 23 22493665
2021 SLC2A12 of SLC2 Gene Family in Bird Provides Functional Compensation for the Loss of SLC2A4 Gene in Other Vertebrates. Molecular biology and evolution 22 33316072