Affinage

Showing SLC2A4 — GLUT4 is a alias.

SLC2A4

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

Length
509 aa
Mass
54.8 kDa
Annotated
2026-06-10
100 papers in source corpus 31 papers cited in narrative 31 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC2A4 (GLUT4) is an insulin-responsive facilitative glucose transporter whose intracellular sequestration and stimulus-dependent recruitment to the plasma membrane constitute the rate-limiting step of insulin- and contraction-stimulated glucose uptake in fat and muscle cells (PMID:1314390, PMID:24778187). In the unstimulated state GLUT4 is retained intracellularly through a dynamic budding/retrieval cycle in which vesicles are far more likely to fuse with endosomes than with the cell surface, and three cytoplasmic motifs (FQQI, TELEY, LL) partition the transporter between endosomal recycling, AS160-controlled storage vesicles, and AP-1-dependent retention (PMID:14595108, PMID:18550797). Insulin acts through PI3-kinase-dependent activation of PKB/Akt, which is required for GLUT4 translocation and functions at or near the GLUT4 vesicles themselves (PMID:10330141, PMID:12082147); Akt converges on the Rab-GAP AS160/TBC1D4 (cooperating with TBC1D1), whose inactivation permits GTP-loading of cargo-specific Rab GTPases that mobilize storage vesicles from a TGN compartment — Rab10 in adipocytes and Rab8A/Rab13 in muscle (PMID:21041651, PMID:18076383, PMID:30482843, PMID:33175605). Downstream effectors including PIKfyve, the t-SNARE-associated syntaxin 6, and the PKCζ–munc18c module link this signaling to the vesicle docking and fusion machinery (PMID:15546921, PMID:12857877, PMID:15986239). Proper biogenesis and stability of insulin-responsive vesicles additionally require DHHC7-mediated palmitoylation of GLUT4 at Cys223 and sortilin/retromer-dependent retrograde transport that rescues GLUT4 from lysosomal degradation (PMID:25824042, PMID:28057756, PMID:28450454, PMID:26581601). In parallel, Ca²⁺/CaMKII and AMPK signaling drive contraction-stimulated translocation and exocytosis, while AMPK phosphorylation of HDAC5 promotes its nuclear export to derepress the GLUT4 promoter (PMID:18184930, PMID:24895284, PMID:23239154). SLC2A4 transcription is controlled by an array of factors including the adipogenic determinant C/EBPα, MEF2/GEF and contraction-activated MEF2D/HIF-1α/TRα, ESR1/SP1 and FXR as activators, and NF-κB as a direct repressor (PMID:15282314, PMID:18769028, PMID:18216015, PMID:23462193, PMID:18957617, PMID:30275758).

Mechanistic history

Synthesis pass · year-by-year structured walk · 30 steps
  1. 1992 High

    Established that GLUT4 itself is the transporter conferring insulin-stimulated glucose uptake and undergoes regulated surface translocation, distinguishing it functionally from constitutive transporters like GLUT1.

    Evidence Stable GLUT4 cDNA expression in L6 myoblasts and CHO cells with deoxyglucose uptake assays

    PMID:1314390

    Open questions at the time
    • Did not define the intracellular signaling that drives translocation
    • Mechanism of cAMP inhibition not resolved
  2. 1999 High

    Identified PKB/Akt as a required node downstream of PI3-kinase for insulin-stimulated GLUT4 surface delivery, placing a specific kinase in the translocation pathway.

    Evidence Dominant-negative and constitutively active PKBα constructs with surface GLUT4myc readout in L6 myoblasts

    PMID:10330141

    Open questions at the time
    • Direct Akt substrates on the trafficking machinery not identified
    • Spatial site of Akt action unresolved
  3. 2002 High

    Defined how GLUT4 endocytosis is targeted, showing the N-terminal phenylalanine (F5) motif recruits clathrin adaptin μ-subunits to drive internalization.

    Evidence Yeast two-hybrid binding of F5 to μ1/μ2/μ3A plus motif mutagenesis in primary rat adipocytes

    PMID:11801731

    Open questions at the time
    • Did not establish how endocytosis is coordinated with insulin-stimulated exocytosis
  4. 2002 Medium

    Localized the functionally required Akt activity to the immediate vicinity of GLUT4 vesicles rather than the bulk cytoplasm.

    Evidence GLUT4 N-terminal fusion targeting kinase-inactive PKB to vesicles, with IRAP surface readout in 3T3-L1 adipocytes

    PMID:12082147

    Open questions at the time
    • Vesicle-localized Akt substrate not identified
    • Single-lab targeting approach
  5. 2003 High

    Quantitatively established that GLUT4 retention is a dynamic budding/fusion cycle biased toward endosomes, and that microtubules are needed for insulin-stimulated surface recruitment but not basal cycling.

    Evidence Kinetic trafficking and nocodazole disruption with subcellular fractionation in adipocytes

    PMID:14595108

    Open questions at the time
    • Molecular identity of retention machinery not defined
    • Motor proteins not identified
  6. 2003 High

    Implicated syntaxin 6 in sequestering GLUT4 away from plasma-membrane-bound traffic, linking a specific SNARE to GLUT4 sorting.

    Evidence Subcellular fractionation and adenoviral cytosolic-domain overexpression of syntaxins in 3T3-L1 adipocytes

    PMID:12857877

    Open questions at the time
    • Cognate v-SNARE pairing not resolved
    • Mechanism of insulin-stimulated syntaxin 6 movement unknown
  7. 2004 High

    Connected Akt to a downstream lipid kinase by showing insulin-driven Akt phosphorylation of PIKfyve modulates GLUT4 vesicle translocation.

    Evidence In vitro kinase assay, phospho-specific detection, and PIKfyve[S318A] overexpression in 3T3-L1 adipocytes

    PMID:15546921

    Open questions at the time
    • Lipid product effect on vesicle dynamics not mechanistically resolved
  8. 2004 High

    Separated GLUT4 gene expression from vesicle biogenesis, showing C/EBPα is required for GLUT4 transcription while the insulin-responsive vesicle compartment forms independently.

    Evidence C/EBPα and PPARγ reconstitution in NIH 3T3 fibroblasts with vesicle fractionation and GLUT4-myc rescue

    PMID:15282314

    Open questions at the time
    • Direct C/EBPα binding sites in the promoter not mapped here
  9. 2005 Medium

    Linked the insulin-activated kinase PKCζ to the vesicle docking/fusion machinery through an inducible interaction with munc18c.

    Evidence Yeast two-hybrid, GST pulldown domain mapping, and endogenous Co-IP with translocation/uptake readouts

    PMID:15986239

    Open questions at the time
    • Single-lab interaction study
    • Relationship to Akt/Rab arm not integrated
  10. 2007 Medium

    Identified a NO–cGMP–AMPK axis that increases GLUT4 gene expression in muscle, broadening the upstream inputs to GLUT4 transcription.

    Evidence Pharmacological dissection in L6 myotubes plus AICAR/NOS-inhibitor experiments in rats

    PMID:17666490

    Open questions at the time
    • Transcription factor target downstream of AMPK not specified here
    • Single-lab
  11. 2008 High

    Resolved the transcriptional derepression mechanism, showing AMPK phosphorylates HDAC5 to evict it from the GLUT4 promoter, promote H3 acetylation, and drive nuclear export.

    Evidence In vitro kinase assay, S259/S498 mutagenesis, ChIP, and reporter assays in human primary myotubes

    PMID:18184930

    Open questions at the time
    • Activating transcription factors co-recruited with HDAC5 loss not fully enumerated
  12. 2008 High

    Defined a multi-motif retention code (FQQI, TELEY, LL) and connected AS160 GAP signaling and AP-1 to specific trafficking steps.

    Evidence Systematic motif mutagenesis, AP-1 siRNA, and kinetic trafficking in adipocytes

    PMID:18550797

    Open questions at the time
    • Adaptor proteins reading FQQI and TELEY not all identified
  13. 2008 High

    Identified the specific Rab (Rab10) required for GLUT4 translocation downstream of AS160 in adipocytes among candidate vesicle Rabs.

    Evidence siRNA knockdown of Rab8A/8B/10/14, vesicle fractionation, and GTP/GDP-ratio measurement in 3T3-L1 adipocytes

    PMID:18076383

    Open questions at the time
    • Rab10 effectors mediating mobilization not defined here
  14. 2008 Medium

    Expanded the transcriptional control of SLC2A4 by identifying GEF–MEF2A cooperation and direct HDAC5–GEF repression, plus FXR as a monomeric activator binding an FXRE.

    Evidence Co-IP, EMSA, promoter deletion/mutation, and reporter assays in adipocytes and mice

    PMID:18216015 PMID:18769028

    Open questions at the time
    • Integration of these factors with C/EBPα at the native locus not resolved
    • Single-lab studies
  15. 2008 Medium

    Distinguished contraction-intrinsic transcriptional regulation, showing MEF2D, HIF-1α, and TRα bind the SLC2A4 promoter in contracting muscle independent of systemic signals.

    Evidence In vitro contraction of isolated soleus with EMSA/supershift and ChIP

    PMID:18957617

    Open questions at the time
    • Upstream contraction-sensing pathway to these factors not mapped here
  16. 2010 High

    Identified the muscle-specific Rabs (Rab8A and Rab13) downstream of AS160, with Rab8A activation preceding Rab13, revealing tissue-divergent Rab usage.

    Evidence GTP-loading pulldown, siRNA with rescue, and constitutively active AS160 epistasis in L6 muscle cells

    PMID:21041651

    Open questions at the time
    • Why muscle uses different Rabs than adipocyte Rab10 not explained
  17. 2013 Medium

    Established NF-κB as a direct transcriptional repressor of SLC2A4 via defined κB sites, providing a mechanism for inflammation-linked GLUT4 suppression.

    Evidence EMSA, ChIP, and reporter assays in adipocytes

    PMID:23462193

    Open questions at the time
    • Interplay with activating factors at the promoter not resolved
    • Single-lab
  18. 2008 Medium

    Provided in vivo human evidence that AMPK activation is required for contraction-stimulated GLUT4 repositioning to the sarcolemma.

    Evidence Hyperinsulinemic clamp, microdialysis, biopsy immunohistochemistry, and electrical muscle stimulation in critically ill patients

    PMID:23239154

    Open questions at the time
    • Molecular link from AMPK to GLUT4 vesicle release in muscle not dissected here
  19. 2014 High

    Quantitatively dissected six distinct insulin-regulated trafficking steps and assigned AS160 specifically to the GSV release step while tethering/docking/fusion is AS160-independent.

    Evidence Quantitative kinetic trafficking with AS160 knockdown and multiple cargo controls in adipocytes

    PMID:24778187

    Open questions at the time
    • Machinery governing the AS160-independent fusion step not identified
  20. 2014 High

    Separated Ca²⁺ control of GLUT4 into exocytic (CaMKIIδ/AMPK) and endocytic (novel PKC) arms acting through distinct molecular mechanisms.

    Evidence siRNA, pharmacological inhibitors, and live exo/endocytosis assays with ionomycin in L6 muscle cells

    PMID:24895284

    Open questions at the time
    • Direct substrates of CaMKIIδ and PKC in trafficking not identified
  21. 2015 High

    Identified GLUT4 palmitoylation at Cys223 as essential for sorting into insulin-responsive tubular-vesicle structures and for translocation.

    Evidence C223S mutagenesis with imaging and translocation assays in adipocytes and CHO-IR cells

    PMID:25824042

    Open questions at the time
    • The responsible acyltransferase was not identified in this study
  22. 2015 Medium

    Established a retromer/SNX27 requirement for GSV formation and adipogenesis, showing retromer redistributes to the plasma membrane on insulin stimulation.

    Evidence Confocal colocalization, ultracentrifugation, and shRNA knockdown in SGBS and 3T3-L1 cells

    PMID:26581601

    Open questions at the time
    • Cargo-recognition details left to subsequent sortilin work
    • Single-lab
  23. 2015 Medium

    Identified ZFP407 as a multilevel regulator controlling GLUT4 transcription, splicing, and mRNA stability and cooperating with PPARγ.

    Evidence siRNA knockdown with transcription, splicing, stability, and PPARγ reporter assays in adipocytes

    PMID:25596527

    Open questions at the time
    • Direct RNA/DNA binding mode of ZFP407 not established
    • Single-lab
  24. 2017 High

    Identified DHHC7 as the principal palmitoyl acyltransferase for GLUT4, with loss causing reduced palmitoylation, impaired translocation, and glucose intolerance in vivo.

    Evidence Screen of 23 DHHC enzymes, knockdown, DHHC7 KO mice, palmitoylation and glucose tolerance assays

    PMID:28057756

    Open questions at the time
    • Subcellular site of GLUT4 palmitoylation not pinpointed
  25. 2017 High

    Defined the molecular basis of GLUT4 retrograde rescue, showing sortilin bridges GLUT4 (via its first luminal loop) to retromer to recycle it from endosomes to the TGN.

    Evidence Co-IP domain mapping and retromer knockdown with stability and glucose uptake readouts in 3T3-L1 adipocytes

    PMID:28450454

    Open questions at the time
    • How sortilin/retromer feeds GLUT4 into insulin-responsive GSVs mechanistically not fully resolved
  26. 2018 High

    Resolved cooperative RabGAP control of GLUT4 release, showing TBC1D1 dominates AS160/TBC1D4 and that AS160 tunes stimulus sensitivity through specific phosphorylation sites.

    Evidence GLUT4 nanometry reconstitution with phosphosite/domain mutagenesis and Ca²⁺/AICAR stimulation

    PMID:30482843

    Open questions at the time
    • Native stoichiometry of the two RabGAPs in tissues not established
  27. 2018 Medium

    Defined an ESR1/SP1 cooperative mechanism that activates SLC2A4 transcription, distinct from ESR2-mediated repression.

    Evidence ESR1/ESR2 agonists, EMSA, and SP1/ESR1 Co-IP in 3T3-L1 adipocytes

    PMID:30275758

    Open questions at the time
    • In vivo relevance of SP1/ESR1 axis not tested here
    • Single-lab
  28. 2019 Medium

    Showed estradiol drives GLUT4 expression and translocation through an ESR1-dependent, CEBPA-mediated pathway, linking estrogen signaling to the adipogenic transcriptional program.

    Evidence ESR1 siRNA knockdown with RT-qPCR, Western, and EMSA in differentiated 3T3-L1 adipocytes

    PMID:31100494

    Open questions at the time
    • Direct ESR1 binding to the GLUT4 locus vs. via CEBPA not fully separated
    • Single-lab
  29. 2020 High

    Demonstrated cargo-specific mobilization, showing TBC1D4-RAB10 selectively releases GLUT4 from a TGN storage compartment while leaving co-resident ATP7A unaffected.

    Evidence RAB10 loss-of-function with distinct cargo and distinct stimuli controls in adipocytes

    PMID:33175605

    Open questions at the time
    • Molecular determinant of cargo selectivity within the shared TGN domain not identified
  30. 2019 Low

    Synthesized a model in which TUG traps GSVs near the ERGIC and insulin liberates them via parallel Akt-Rab and TC10α-Usp25m-TUGUL-KIF5B arms.

    Evidence Review summarizing prior TUG cleavage, TC10α signaling, and KIF5B motor studies

    PMID:31543708

    Open questions at the time
    • No new experimental data in this review; primary evidence not in this corpus
    • TUG/TC10α/KIF5B mechanism not independently validated within the timeline

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the transcriptional, palmitoylation, retrograde-sorting, and Rab-dependent mobilization modules are integrated into a unified spatiotemporal control of GLUT4 in vivo, and what confers cargo selectivity at the storage compartment, remains unresolved.
  • No unifying in vivo model connecting biogenesis, retention, and mobilization
  • Cargo-selectivity determinants within the TGN/GSV domain unknown
  • Tissue-specific Rab usage mechanism unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 2
Localization
GO:0031410 cytoplasmic vesicle 4 GO:0005886 plasma membrane 3 GO:0005768 endosome 2 GO:0005794 Golgi apparatus 2
Pathway
R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-162582 Signal Transduction 3 R-HSA-9609507 Protein localization 3 R-HSA-382551 Transport of small molecules 2
Partners
RAB10RAB13RAB8ASORT1STX6TBC1D4/AS160VPS35ZDHHC7
Complex memberships
GLUT4 storage vesicle (GSV)retromer (with sortilin/SNX27)

Evidence

Reading pass · 31 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 PKBα/Akt1 is required for insulin-induced GLUT4 translocation to the plasma membrane in L6 myoblasts. A kinase-inactive, phosphorylation-deficient PKBα (AAA-PKB) dominant-negative construct almost entirely blocked insulin-dependent increase in surface GLUT4myc, while constitutively active PKBα increased cell surface GLUT4myc. This effect was downstream of PI3-kinase and independent of actin ruffling. Dominant-negative and constitutively active PKBα/Akt1 constructs transiently transfected into L6-GLUT4myc myoblasts; surface GLUT4myc detection by immunofluorescence in non-permeabilized cells; cotransfection rescue experiments Molecular and cellular biology High 10330141
2003 GLUT4 is retained intracellularly in adipocytes by a dynamic retention/retrieval mechanism: GLUT4-containing vesicles continually bud and fuse with endosomes in the absence of insulin and are 5-fold more likely to fuse with endosomes than with the plasma membrane. An intact microtubule cytoskeleton is required for insulin-stimulated recruitment to the cell surface but not for the basal budding/fusion cycle. Kinetic trafficking studies in adipocytes; nocodazole disruption of microtubules; subcellular fractionation and vesicle tracking Molecular biology of the cell High 14595108
2002 The N-terminal phenylalanine-based targeting sequence (F5) of GLUT4 constitutes a binding site for medium chain adaptins μ1, μ2, and μ3A, implicating this motif in targeting GLUT4 to clathrin-coated vesicles for endocytosis. Mutation of F5 substantially increased cell-surface GLUT4, primarily by decreasing endocytosis rate. Yeast two-hybrid analysis of GLUT4 N-terminal motif with adaptin subunits; mutagenesis of GLUT4 N-terminal F5 and C-terminal dileucine/deletion constructs in primary rat adipocytes; dominant-negative dynamin co-expression; wortmannin treatment Journal of cell science High 11801731
2004 PKB/Akt phosphorylates serine318 on the phosphoinositide 3-phosphate 5-kinase PIKfyve in response to insulin in a PI3-kinase-dependent manner, stimulating its PtdIns3P 5-kinase activity. PIKfyve colocalizes with IRAP/GLUT4 vesicles, and overexpression of a PIKfyve[S318A] phosphorylation-deficient mutant enhances insulin-stimulated IRAP/GLUT4 vesicle translocation to the plasma membrane, indicating a role for PKB-dependent PIKfyve phosphorylation in regulating GLUT4 vesicle trafficking. In vitro kinase assay; phospho-specific antibody detection in intact cells; colocalization by immunofluorescence; overexpression of phosphorylation-deficient mutant in 3T3-L1 adipocytes with GLUT4 translocation readout Journal of cell science High 15546921
2003 Syntaxin 6 localizes predominantly (>85%) to GLUT4-containing vesicles in 3T3-L1 adipocytes and undergoes insulin-stimulated movement to the plasma membrane. Overexpression of the cytosolic domain of syntaxin 6 increased basal cell surface GLUT4, slowed GLUT4 re-internalization after insulin withdrawal, and perturbed subendosomal GLUT4 sorting, indicating syntaxin 6 participates in membrane-trafficking steps that sequester GLUT4 away from plasma membrane-destined traffic. Subcellular fractionation; adenoviral overexpression of cytosolic domains of syntaxin 6, 7, 8, and 12/13 in 3T3-L1 adipocytes; glucose transport assay; cell surface GLUT4 measurement Molecular biology of the cell High 12857877
2008 AMPK directly phosphorylates histone deacetylase 5 (HDAC5) at S259 and S498 to regulate GLUT4 transcription. AMPK phosphorylation of HDAC5 causes its association with 14-3-3 isoforms, reduces HDAC5 binding to the GLUT4 promoter, induces H3 acetylation, and promotes HDAC5 nuclear export, leading to increased GLUT4 gene expression. HDAC5 overexpression represses GLUT4 reporter expression, and mutation of S259/S498 abolishes AICAR-stimulated GLUT4 transcription. In vitro kinase assay; site-directed mutagenesis of HDAC5; site-specific phospho-antibodies; chromatin immunoprecipitation; HDAC inhibitor treatment; constitutively active and dominant-negative AMPK overexpression in human primary myotubes; gene reporter assays Diabetes High 18184930
2010 Rab13 and Rab8A are GTP-loaded (activated) by insulin in rat L6 muscle cells, downstream of AS160 GAP activity, and both regulate GLUT4 vesicle traffic to the cell surface. Rab8A activation precedes Rab13 activation. siRNA knockdown of Rab13 blocked insulin-induced GLUT4 surface accumulation (rescued by Rab13 ortholog but not Rab8A). Constitutively active AS160 suppressed surface GLUT4, reversed by overexpressing either Rab8A or Rab13. Rab13 colocalizes with GLUT4 at the cell periphery after insulin stimulation. GTP-loading assay (active Rab pulldown); siRNA knockdown; overexpression of constitutively active AS160 and Rab constructs; immunofluorescence colocalization in L6 muscle cells Proceedings of the National Academy of Sciences of the United States of America High 21041651
2008 Among Rab GTPases present in GLUT4 vesicles (Rab8A, 8B, 10, 14), only Rab10 knockdown inhibits GLUT4 translocation in 3T3-L1 adipocytes, identifying Rab10 as the specific Rab required for GLUT4 translocation downstream of AS160 in adipocytes. Approximately 5% of total Rab10 is present in GLUT4 vesicles; approximately 90% of total Rab10 is in the inactive GDP state in both basal and insulin states. siRNA knockdown of candidate Rabs (8A, 8B, 10, 14) with GLUT4 translocation readout; subcellular fractionation of GLUT4 vesicles; in vivo Rab10 GTP/GDP ratio measurement; AS160 GAP domain substrate assay The Biochemical journal High 18076383
2015 GLUT4 is palmitoylated at Cys223, and this palmitoylation is essential for insulin-dependent GLUT4 membrane translocation. The C223S substitution diminishes GLUT4 responsiveness to insulin in membrane translocation in both adipocytes and CHO-IR cells, and C223S GLUT4 is absent from tubular-vesicle structures where insulin-responsive GLUT4 vesicles reside. Site-directed mutagenesis (C223S); live cell imaging and immunofluorescence of GLUT4 subcellular localization; insulin-stimulated translocation assay in adipocytes and CHO-IR cells Biochemical and biophysical research communications High 25824042
2017 DHHC7 is the principal palmitoyl acyltransferase (PAT) for GLUT4. DHHC7 overexpression increased GLUT4 palmitoylation; DHHC7 knockdown in 3T3-L1 adipocytes and DHHC7 KO in adipose/muscle decreased GLUT4 palmitoylation. DHHC7 inactivation suppressed insulin-dependent GLUT4 membrane translocation in 3T3-L1 and primary adipocytes. DHHC7 KO mice developed hyperglycemia and glucose intolerance. Ectopic expression and knockdown of DHHC proteins (screening 23 DHHC family members); DHHC7 KO mouse model; GLUT4 palmitoylation assay; insulin-stimulated GLUT4 translocation assay; glucose tolerance test The Journal of biological chemistry High 28057756
2008 Molecular mechanisms of GLUT4 intracellular retention involve three trafficking motifs: FQQI, TELEY, and LL. FQQI targets GLUT4 to an endosome–retention compartment cycle; TELEY-dependent targeting to specialized GLUT4 transport vesicles is under AS160 RAB-GAP signaling control. Mutation of the LL motif slows GLUT4 return to intracellular retention after insulin withdrawal; knockdown of clathrin adaptin AP-1 has the same effect through an LL-dependent mechanism. Mutagenesis of GLUT4 trafficking motifs; siRNA knockdown of AP-1; kinetic trafficking analysis; subcellular fractionation in adipocytes Molecular biology of the cell High 18550797
2004 C/EBPα is required for Glut4 gene expression in adipocytes, not for the formation of insulin-responsive vesicles or insulin signaling. NIH 3T3 cells expressing PPARγ without C/EBPα form a functional insulin-responsive vesicular compartment with IRAP (another GSV cargo) but contain negligible Glut4 and have no insulin-stimulated glucose uptake. Expression of a Glut4-myc construct in these cells results in insulin-dependent translocation, demonstrating the vesicle machinery is intact but Glut4 expression itself requires C/EBPα. Ectopic expression of C/EBPα and PPARγ in NIH 3T3 fibroblasts; sucrose velocity gradient analysis of vesicle compartments; surface biotinylation; immunofluorescence; GLUT4-myc construct rescue transfection Molecular and cellular biology High 15282314
2017 Sortilin together with retromer mediates retrograde transport of Glut4 from endosomes to the TGN, rescuing it from lysosomal degradation. The luminal Vps10p domain of sortilin interacts with the first luminal loop of Glut4, and the cytoplasmic tail of sortilin binds 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 of sortilin and Glut4 (domain mapping); retromer knockdown in 3T3-L1 adipocytes; Western blotting; glucose uptake assay; subcellular fractionation Molecular biology of the cell High 28450454
2008 Farnesoid X receptor (FXR) induces GLUT4 transcription through a FXR response element (FXRE) in the GLUT4 promoter. Progressive 5'-deletion and site-mutation analysis identified the FXRE; EMSA demonstrated FXR binds to the GLUT4-FXRE as a monomer without RXR participation. CDCA (FXR agonist) increases GLUT4 protein in mice. 5'-deletion analysis of GLUT4 promoter; site-directed mutagenesis; EMSA; RXR knockdown; Western blotting in C57BL/6J mice Cellular physiology and biochemistry Medium 18769028
2008 GEF (GLUT4 enhancer factor) dimerizes with a hypophosphorylated form of MEF2A on the GLUT4 promoter; MEF2A binding to its cognate site increases GEF DNA binding to Domain I; the transcriptional co-repressor HDAC5 interacts directly with GEF in the absence of MEF2 proteins and specifically inhibits GLUT4 promoter activity. Co-immunoprecipitation; EMSA; GEF domain mutagenesis; GLUT4 promoter reporter assay in adipocytes The Journal of biological chemistry Medium 18216015
2013 NF-κB p50 and p65 subunits bind to two κB sites (-83/-62 bp and -134/-113 bp) in the Slc2a4/GLUT4 promoter and directly repress Slc2a4 gene transcription. The -134/-113 bp κB site was confirmed as functional by transfection reporter assays; ChIP confirmed p50/p65 binding to the Slc2a4 promoter in native chromatin of adipocytes. Electrophoretic mobility shift assay (EMSA); chromatin immunoprecipitation (ChIP); transfection reporter assays in adipocytes Molecular and cellular endocrinology Medium 23462193
2005 PKCζ physically interacts with munc18c (a GLUT4 vesicle trafficking protein); this interaction is enhanced approximately 3-fold by insulin stimulation. Disruption of the PKCζ-munc18c interaction (by deletion of residues 295-338 of munc18c or the N-terminal region of PKCζ) markedly inhibited insulin-stimulated glucose uptake and GLUT4 translocation, linking the insulin-activated kinase PKCζ to the vesicle docking/fusion machinery. Yeast two-hybrid screen; GST pulldown with domain mapping; co-immunoprecipitation of endogenous proteins; overexpression of deletion mutants with GLUT4 translocation and glucose uptake readouts Diabetologia Medium 15986239
2002 PKB/Akt kinase activity at or in the vicinity of intracellular GLUT4 vesicles is functionally required for insulin-stimulated GLUT4 vesicle translocation. Kinase-inactive PKB artificially targeted to GLUT4 vesicles (via N-terminal fusion to GLUT4) was a more effective dominant-negative inhibitor of IRAP translocation than cytoplasmic kinase-inactive PKB, indicating a vesicle-proximal role for Akt. GLUT4 N-terminal fusion constructs targeting constitutively active and kinase-inactive PKB to GLUT4 vesicles; surface biotinylation of IRAP as GSV cargo readout in 3T3-L1 adipocytes Journal of cell science Medium 12082147
1992 GLUT4 expression in L6 myoblasts confers insulin-stimulated glucose transport and cAMP-mediated inhibition of this stimulated transport, properties not present in cells expressing only GLUT1. GLUT4 undergoes insulin-dependent translocation to the cell surface in overexpressing myoblasts. cAMP inhibition of transport was confirmed to be GLUT4-dependent using CHO cells transiently expressing GLUT1 or GLUT4. Stable transfection of GLUT4 cDNA into L6 myoblasts; 2-deoxy[³H]glucose uptake assay; cAMP analog treatment; transient expression in CHO cells Proceedings of the National Academy of Sciences of the United States of America High 1314390
2014 Insulin regulates at least six distinct steps of Glut4 trafficking kinetics in adipocytes: endocytosis, degradation, sorting, sequestration, release, and tethering/docking/fusion. Insulin increases the rate constant for sequestration into GSVs 8-fold and increases the rate of GSV release and fusion 40-fold. AS160 regulates the release step from GSVs, while tethering/docking/fusion is regulated through an AS160-independent process. Quantitative kinetic trafficking assay of Glut4, transferrin receptor, and LRP1 in adipocytes; AS160 knockdown; comparison to fibroblasts; rate constant determination The Journal of biological chemistry High 24778187
2018 AS160/TBC1D4 and TBC1D1 cooperatively govern GLUT4 release. When both RabGAPs are present, TBC1D1 functionally dominates AS160. AS160 modulates sensitivity to external stimuli in TBC1D1-mediated GLUT4 release. Synergistic actions require the PTB1 and calmodulin-binding domains of TBC1D1 and key phosphorylation sites (AS160 Thr642, TBC1D1 Ser237, and Thr596). Ca²⁺ plus insulin together triggered GLUT4 release more efficiently when AS160 was present. GLUT4 nanometry in cell-based reconstitution models; mutational analysis of phosphorylation sites and functional domains; varying expression ratios of RabGAPs; AICAR and Ca²⁺ stimulation The Journal of biological chemistry High 30482843
2020 TBC1D4-RAB10 signaling controls GLUT4 mobilization from a trans-Golgi network (TGN) storage compartment. RAB10 is required for insulin to mobilize GLUT4 from this TGN compartment. Insulin does not mobilize the unrelated TGN cargo ATP7A, and copper (which mobilizes ATP7A) does not mobilize GLUT4; RAB10 is not required for copper-stimulated ATP7A mobilization, demonstrating cargo-specific mobilization machinery within the same TGN domain. RAB10 knockdown/knockout in adipocytes; immunofluorescence colocalization; comparison of GLUT4 vs. ATP7A mobilization by distinct stimuli; subcellular fractionation Molecular biology of the cell High 33175605
2019 In unstimulated cells, GSVs are trapped by TUG proteins near the ERGIC. Insulin signals through two main pathways: Akt kinase modulates Rab GTPases to target GSVs to the cell surface; Rho-family GTPase TC10α stimulates Usp25m-mediated TUG cleavage to liberate vesicles from the Golgi. TUG cleavage produces a ubiquitin-like modifier TUGUL that links GSVs to KIF5B kinesin motors for movement to the cell surface. Review citing multiple experimental findings: TUG cleavage assay, TC10α signaling, KIF5B motor interaction studies (primary data referenced from prior experimental publications) The Yale journal of biology and medicine Low 31543708
2014 Ca²⁺ signals promote GLUT4 exocytosis and reduce endocytosis in L6 muscle cells via distinct molecular mechanisms. CaMKIIδ and AMPK (activated by Ca²⁺ ionophore ionomycin) stimulate GLUT4myc exocytosis, while novel PKCs specifically reduce GLUT4myc endocytosis. Silencing CaMKIIδ or AMPKα1/α2 partly reduced ionomycin-induced gain in surface GLUT4myc and exocytosis but did not prevent reduced endocytosis. siRNA knockdown of CaMKIIδ and AMPKα1/α2; pharmacological inhibitors of CaMKII, AMPK, and PKC isoforms; ionomycin treatment; live cell GLUT4myc exocytosis and endocytosis assays in L6 muscle cells American journal of physiology. Endocrinology and metabolism High 24895284
2008 Contraction-induced GLUT4 translocation in skeletal muscle of critically ill patients is impaired due to failure of AMPK activation; GLUT4 is trapped at perinuclear spaces rather than at the sarcolemma. Electrical muscle stimulation increased p-AMPK, repositioned GLUT4 to the sarcolemma, locally improved glucose metabolism, and prevented type-2 fiber atrophy, linking AMPK to contraction-stimulated GLUT4 translocation in vivo in human muscle. Euglycemic-hyperinsulinemic clamp; muscle microdialysis; successive muscle biopsies with immunohistochemistry for GLUT4 localization; phospho-AMPK western blotting; electrical muscle stimulation intervention with contralateral leg control American journal of respiratory and critical care medicine Medium 23239154
2007 Nitric oxide (NO) increases GLUT4 expression in skeletal muscle L6 myotubes via a cGMP- and AMPK-dependent mechanism. SNAP (NO donor) increased GLUT4 mRNA ~3-fold; this was abolished by AMPK inhibitor compound C. The cGMP analog 8-Br-cGMP also increased GLUT4 protein. SNAP induced AMPK and ACC phosphorylation and promoted nuclear translocation of p-AMPK. AICAR-induced GLUT4 mRNA increase was ~70% prevented by NOS inhibition in vitro and ~50% in vivo. Pharmacological treatment of L6 myotubes (SNAP, 8-Br-cGMP, guanylyl cyclase inhibitor, compound C, NOS inhibitor); RT-PCR and Western blot; AICAR injection in rats; immunostaining for p-AMPK localization American journal of physiology. Endocrinology and metabolism Medium 17666490
2015 ZFP407 regulates GLUT4 expression at both transcriptional and post-transcriptional levels: ZFP407 deficiency decreases GLUT4 mRNA and protein, reducing insulin-stimulated glucose uptake in adipocytes. ZFP407 controls both Glut4 mRNA transcription and pre-mRNA splicing efficiency, but also increases Glut4 mRNA stability. ZFP407 is required for PPARγ agonist rosiglitazone to increase Glut4 expression and co-overexpression with PPARγ synergistically activates a PPARγ reporter beyond PPARγ alone. Targeted siRNA screen; siRNA knockdown of ZFP407; transcriptome analysis; splicing efficiency measurement (nascent transcription assay); mRNA stability assay; PPARγ reporter assay; co-overexpression experiments The Journal of biological chemistry Medium 25596527
2008 Contraction of soleus muscle per se (independent of systemic hormonal/metabolic effects) activates MEF2D, HIF-1α, and TRα transcription factors to bind the SLC2A4 gene promoter, inducing an early increase in GLUT4 mRNA and subsequent GLUT4 protein content. ChIP confirmed increased MEF2D and HIF-1α binding to the SLC2A4 promoter (~4-fold) in native nucleosome upon contraction. In vitro electrically-induced contraction of isolated soleus muscle; EMSA with supershift assays; chromatin immunoprecipitation; RT-PCR and Western blot American journal of physiology. Endocrinology and metabolism Medium 18957617
2019 Estradiol (E2) stimulates adipocyte differentiation and Slc2a4/GLUT4 expression via an ESR1-dependent, CEBPA-mediated pathway. ESR1 silencing (~50%) in mature adipocytes abrogates E2 effects on nuclear CEBPA content, Slc2a4/GLUT4 expression, and GLUT4 translocation to the cell membrane. ESR1 siRNA knockdown in differentiated 3T3-L1 adipocytes; RT-qPCR; Western blotting; EMSA for CEBP/Slc2a4 binding activity Molecular and cellular endocrinology Medium 31100494
2018 ESR1 activation in adipocytes increases nuclear SP1 protein content, promotes SP1/ESR1 complex formation, and enhances SP1 binding to the Slc2a4 gene promoter, thereby increasing Slc2a4/GLUT4 expression. This SP1/ESR1 cooperative mechanism is not observed for ESR2-mediated repression of Slc2a4. ESR1 and ESR2 agonist (PPT, DPN) treatment of 3T3-L1 adipocytes; RT-qPCR; Western blotting; EMSA; co-immunoprecipitation of SP1/ESR1 complex International journal of medical sciences Medium 30275758
2015 Retromer colocalizes with GLUT4 on GSVs in mature adipocytes and redistributes to the plasma membrane upon insulin stimulation. Knockdown of retromer subunit VPS35 or retromer-associated protein sorting nexin 27 (SNX27) impaired adipogenesis, decreased PPARγ expression, and reduced GSV formation, lipid droplet accumulation, and insulin-stimulated glucose uptake. Confocal microscopy; differential ultracentrifugation; lentivirus-delivered shRNA knockdown in Simpson-Golabi-Behmel syndrome and 3T3-L1 cell lines; glucose uptake assay FASEB journal Medium 26581601

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 The GLUT4 glucose transporter. Cell metabolism 986 17403369
2013 Exercise, GLUT4, and skeletal muscle glucose uptake. Physiological reviews 978 23899560
2012 Regulation of glucose transport by insulin: traffic control of GLUT4. Nature reviews. Molecular cell biology 643 22617471
1999 Protein kinase B/Akt participates in GLUT4 translocation by insulin in L6 myoblasts. Molecular and cellular biology 498 10330141
2008 Emerging role for AS160/TBC1D4 and TBC1D1 in the regulation of GLUT4 traffic. American journal of physiology. Endocrinology and metabolism 363 18477703
2008 AMP-activated protein kinase regulates GLUT4 transcription by phosphorylating histone deacetylase 5. Diabetes 341 18184930
2010 MicroRNA-223 regulates Glut4 expression and cardiomyocyte glucose metabolism. Cardiovascular research 279 20080987
1997 Moving GLUT4: the biogenesis and trafficking of GLUT4 storage vesicles. Diabetes 267 9356011
2019 Thirty sweet years of GLUT4. The Journal of biological chemistry 251 31175156
2006 Effects of statins on the adipocyte maturation and expression of glucose transporter 4 (SLC2A4): implications in glycaemic control. Diabetologia 246 16685502
2011 GLUT4 exocytosis. Journal of cell science 230 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
2001 Intracellular organization of insulin signaling and GLUT4 translocation. Recent progress in hormone research 170 11237212
2003 GLUT4 is retained by an intracellular cycle of vesicle formation and fusion with endosomes. Molecular biology of the cell 164 14595108
2006 Bridging the GAP between insulin signaling and GLUT4 translocation. Trends in biochemical sciences 162 16540333
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 148 21041651
2006 Exercise training increases insulin-stimulated glucose disposal and GLUT4 (SLC2A4) protein content in patients with type 2 diabetes. Diabetologia 148 17019595
2007 Nitric oxide increases GLUT4 expression and regulates AMPK signaling in skeletal muscle. American journal of physiology. Endocrinology and metabolism 139 17666490
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
2014 Signal transduction meets vesicle traffic: the software and hardware of GLUT4 translocation. American journal of physiology. Cell physiology 136 24598362
2023 Insulin signalling and GLUT4 trafficking in insulin resistance. Biochemical Society transactions 123 37248992
2011 Mapping insulin/GLUT4 circuitry. Traffic (Copenhagen, Denmark) 119 21401839
2007 Ins (endocytosis) and outs (exocytosis) of GLUT4 trafficking. Current opinion in cell biology 116 17644329
2004 Protein kinase B phosphorylation of PIKfyve regulates the trafficking of GLUT4 vesicles. Journal of cell science 114 15546921
2006 Insulin receptor signals regulating GLUT4 translocation and actin dynamics. Endocrine journal 112 16702775
2007 Transcriptional regulation of the GLUT4 gene: from PPAR-gamma and FOXO1 to FFA and inflammation. Trends in endocrinology and metabolism: TEM 102 17317207
2002 Activation of the glucose transporter GLUT4 by insulin. Biochemistry and cell biology = Biochimie et biologie cellulaire 101 12440698
2010 Biogenesis and regulation of insulin-responsive vesicles containing GLUT4. Current opinion in cell biology 99 20417083
2008 Rab10 in insulin-stimulated GLUT4 translocation. The Biochemical journal 92 18076383
2014 Molecular mechanisms of GLUT4 regulation in adipocytes. Diabetes & metabolism 91 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
2003 GLUT4 activation: thoughts on possible mechanisms. Acta physiologica Scandinavica 74 12864733
2008 Molecular mechanisms controlling GLUT4 intracellular retention. Molecular biology of the cell 73 18550797
2011 Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. Cellular and molecular life sciences : CMLS 71 21547502
2007 The GLUT4 code. Molecular endocrinology (Baltimore, Md.) 71 17717074
2020 Exercise and GLUT4. Exercise and sport sciences reviews 69 32568924
2017 Sortilin and retromer mediate retrograde transport of Glut4 in 3T3-L1 adipocytes. Molecular biology of the cell 68 28450454
2018 Action of Phytochemicals on Insulin Signaling Pathways Accelerating Glucose Transporter (GLUT4) Protein Translocation. Molecules (Basel, Switzerland) 67 29382104
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
2014 Insulin-regulated Glut4 translocation: membrane protein trafficking with six distinctive steps. The Journal of biological chemistry 64 24778187
2012 The role of CaMKII in regulating GLUT4 expression in skeletal muscle. American journal of physiology. Endocrinology and metabolism 64 22496345
2008 The Glut1 and Glut4 glucose transporters are differentially expressed during perinatal and postnatal erythropoiesis. Blood 63 18796630
2002 Roles of the N- and C-termini of GLUT4 in endocytosis. Journal of cell science 62 11801731
2017 DHHC7 Palmitoylates Glucose Transporter 4 (Glut4) and Regulates Glut4 Membrane Translocation. The Journal of biological chemistry 61 28057756
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
2010 SPARC interacts with AMPK and regulates GLUT4 expression. Biochemical and biophysical research communications 52 20460104
2008 Farnesoid X receptor induces GLUT4 expression through FXR response element in the GLUT4 promoter. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 52 18769028
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 AKT ISOFORMS-AS160-GLUT4: The defining axis of insulin resistance. Reviews in endocrine & metabolic disorders 44 33928491
2011 SNARE proteins underpin insulin-regulated GLUT4 traffic. Traffic (Copenhagen, Denmark) 43 21226814
2019 GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking. The Yale journal of biology and medicine 42 31543708
2003 Regulation of GLUT4 traffic and function by insulin and contraction in skeletal muscle. Frontiers in bioscience : a journal and virtual library 42 12957810
1996 Glucose transport and GLUT4 protein distribution in skeletal muscle of GLUT4 transgenic mice. The Biochemical journal 42 8546674
2020 Prior exercise in humans redistributes intramuscular GLUT4 and enhances insulin-stimulated sarcolemmal and endosomal GLUT4 translocation. Molecular metabolism 41 32305516
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
2019 Estradiol stimulates adipogenesis and Slc2a4/GLUT4 expression via ESR1-mediated activation of CEBPA. Molecular and cellular endocrinology 39 31100494
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
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
2014 Ca²⁺ signals promote GLUT4 exocytosis and reduce its endocytosis in muscle cells. American journal of physiology. Endocrinology and metabolism 37 24895284
2013 Identification of nuclear factor-κB sites in the Slc2a4 gene promoter. Molecular and cellular endocrinology 37 23462193
2007 "Actin"g on GLUT4: membrane & cytoskeletal components of insulin action. Current diabetes reviews 37 18220662
2015 Zinc finger protein 407 (ZFP407) regulates insulin-stimulated glucose uptake and glucose transporter 4 (Glut4) mRNA. The Journal of biological chemistry 35 25596527
2020 Building GLUT4 Vesicles: CHC22 Clathrin's Human Touch. Trends in cell biology 32 32620516
2013 Posttranslational modifications of GLUT4 affect its subcellular localization and translocation. International journal of molecular sciences 32 23665900
1992 GLUT4 facilitates insulin stimulation and cAMP-mediated inhibition of glucose transport. Proceedings of the National Academy of Sciences of the United States of America 32 1314390
2010 Measuring GLUT4 translocation in mature muscle fibers. American journal of physiology. Endocrinology and metabolism 31 20501875
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
2018 Estrogen Receptor 1 (ESR1) Enhances Slc2a4/GLUT4 Expression by a SP1 Cooperative Mechanism. International journal of medical sciences 29 30275758
2011 GLUT4 associated proteins as therapeutic targets for diabetes. Recent patents on endocrine, metabolic & immune drug discovery 29 22074575
2000 GLUT4 and company: SNAREing roles in insulin-regulated glucose uptake. Trends in endocrinology and metabolism: TEM 29 11042465
2015 Cardiac contraction-induced GLUT4 translocation requires dual signaling input. Trends in endocrinology and metabolism: TEM 28 26138758
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
2014 Glut4 expression defines an insulin-sensitive hypothalamic neuronal population. Molecular metabolism 28 24944904
2018 Cooperative actions of Tbc1d1 and AS160/Tbc1d4 in GLUT4-trafficking activities. The Journal of biological chemistry 26 30482843
2008 Developmental programming of adult hyperinsulinemia, increased proinflammatory cytokine production, and altered skeletal muscle expression of SLC2A4 (GLUT4) and uncoupling protein 3. The Journal of endocrinology 26 18591261
2022 GLUT4 On the move. The Biochemical journal 25 35147164
2020 Insulin-promoted mobilization of GLUT4 from a perinuclear storage site requires RAB10. Molecular biology of the cell 25 33175605
1998 Insulin signaling and glucose transport in insulin resistant skeletal muscle. Special reference to GLUT4 transgenic and GLUT4 knockout mice. Advances in experimental medicine and biology 25 9781315
2019 Wogonin Alleviates Hyperglycemia Through Increased Glucose Entry into Cells Via AKT/GLUT4 Pathway. Current pharmaceutical design 24 31333118
2014 Oleic and linoleic fatty acids downregulate Slc2a4/GLUT4 expression via NFKB and SREBP1 in skeletal muscle cells. Molecular and cellular endocrinology 24 25486510
2012 Adaptive evolution in the glucose transporter 4 gene Slc2a4 in Old World fruit bats (family: Pteropodidae). PloS one 24 22493665
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
2003 Regulating Glut4 vesicle dynamics by phosphoinositide kinases and phosphoinositide phosphatases. Frontiers in bioscience : a journal and virtual library 23 12957825

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