PaperBLAST
Full List of Papers Linked to P19357
GLUT4_RAT / P19357 Solute carrier family 2, facilitated glucose transporter member 4; Glucose transporter type 4, insulin-responsive; GLUT-4 from Rattus norvegicus (Rat) (see 6 papers)
XP_006246658 solute carrier family 2, facilitated glucose transporter member 4 isoform X2 from Rattus norvegicus
- function: Insulin-regulated facilitative glucose transporter, which plays a key role in removal of glucose from circulation (PubMed:2211693, PubMed:2645527, PubMed:2649253). Response to insulin is regulated by its intracellular localization: in the absence of insulin, it is efficiently retained intracellularly within storage compartments in muscle and fat cells (PubMed:2211693, PubMed:2645527, PubMed:2649253). Upon insulin stimulation, translocates from these compartments to the cell surface where it transports glucose from the extracellular milieu into the cell (PubMed:2211693, PubMed:2645527, PubMed:2649253).
catalytic activity: D-glucose(out) = D-glucose(in) (RHEA:60376)
subunit: Binds to DAXX. Interacts via its N-terminus with SRFBP1 (By similarity). Interacts with NDUFA9 (PubMed:16396496). Interacts with TRARG1; the interaction is required for proper SLC2A4 recycling after insulin stimulation (By similarity). - African walnut (Plukenetia conophora) oil promotes glucose uptake while improving energy metabolism and steroidogenesis and maintaining surface architecture in rat testes.
Erukainure, Frontiers in nutrition 2024 - “...2.15.1 Protein target selection and preparation The active site amino acid sequence of GLUT4 protein (P19357) was retrieved from https://www.uniprot.org/ , and the structure was modeled with https://swissmodel.expasy.org/ . The protein was prepared and refined using Discovery Studio 2021 ( https://discover.3ds.com/discovery-studio-visualizer-download ) for docking. This was...”
- Intestinal changes associated with fluoride exposure in rats: Integrative morphological, proteomic and microbiome analyses
Dionizio, Chemosphere 2021 - “...with changed expression interacted with Solute carrier family 2, facilitated glucose transporter member 4 (GLUT4, P19357), ( Fig. 1A ), Mitogen-activated protein kinase 3 (MAPK3, P21708), 5-AMP-activated protein kinase catalytic subunit alpha-1 (AMPK subunit alpha-1, P54645), 5-AMP-activated protein kinase subunit beta-1 (AMPK subunit beta-1, P80386), Polyubiquitin...”
- “...Dynein light chain 1 , cytoplasmic (P63170), Polyubiquitin-6 (Q63429) ( Fig. 2A ) or GLUT4 (P19357), MAPK3 (P21708), Dystrophin (P11530), Calcium/calmodulin-dependent protein kinase kinase 1 (CaM-kinase kinase 1, P97756) and Regulating synaptic membrane exocytosis protein 1 (Q9JIR4) ( Fig. 2B ). Subchronic fluoride exposure reduced Gastrotropin...”
- Identification of Aortic Proteins Involved in Arterial Stiffness in Spontaneously Hypertensive Rats Treated With Perindopril:A Proteomic Approach
Miotto, Frontiers in physiology 2021 - “...proteins Mitogen-activated protein kinase 3 (P21708), Solute carrier family 2, facilitated glucose transporter member 4 (P19357), UV excision repair protein RAD23 homolog B (Q4KMA2), Heterogeneous nuclear ribonucleoprotein K (P61980), Small ubiquitin-related modifier 3 (Q5XIF4), Desmin (P48675), Gap junction alpha-1 protein (P08050), and Tumor necrosis factor (P16599);...”
- “...three main interaction proteins, Mitogen-activated protein kinase 3 (P21708), solute carrier muscle family-2 glucose transporter (P19357), and UV excision Rad23 homolog (Q4KMA2), that interacted with several proteins up- or downregulated in the aorta sample, after SHRc Wistar comparisons, like long-chain specific acyl-CoA dehydrogenase- mitochondrial (P15650), heat...”
- Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats
Leão, International journal of molecular sciences 2020 - “...by its accession ID from Uniprot. Solute carrier family 2, facilitated glucose transporter member 4 (P19357); Sideroflexin-1 (Q63965); Ubiquitin-conjugating enzyme E2 N (Q9EQX9); Peroxiredoxin-6 (O35244); Dihydrolipoyl dehydrogenase, mitochondrial (Q6P6R2); Aspartate aminotransferase, mitochondrial (P00507); Isoaspartyl peptidase/L-asparaginase (Q8VI04); Runt-related transcription factor 2 (Q9Z2J9); Nicalin (Q5XIA1); Mammalian ependymin-related protein...”
- Inflammation and apoptosis accelerate progression to irreversible atrophy in denervated intrinsic muscles of the hand compared with biceps: proteomic analysis of a rat model of obstetric brachial plexus palsy.
Yu, Neural regeneration research 2020 - “...A0A0G2K5G8 * , Q3HSE5 * , P12369 * , G3V8R5 * , Q9Z2S9 * , P19357, M0RD75, D3ZM60, P13286, P27881, P62142, F1LLZ7, A2RRU1, P97531, G3V8V3, Q4G050, A0A0G2K9C8, Q6P727, Q9Z1N1 0.002 Pyruvate metabolism 17 A0A0G2K5G8 * , P52873 * , Q6P7Q4, P11980, P04636, A0A0G2K4C6, P35745, F7FKI5, P17764,...”
- “...AMPK signaling 16 P12785 * , A0A0G2K5G8 * , Q3HSE5 * , G3V8R5 * , P19357, A0A0G2JSQ0, Q52KS1, A2RRU1, Q5XIJ7, Q5PQN8, D4AC16, A0A0G2JYA4, Q9Z1N1, P62716, C9DRP4, Q63704 0.005 Fatty acid metabolism 12 P12785 * , A0A0G2K5G8 * , Q63151 * , P33124, P17764, Q9WVK7, Q9WVK3, P08503,...”
- Chronic treatment with fluoride affects the jejunum: insights from proteomics and enteric innervation analysis
Dionizio, Scientific reports 2018 - “...in expression interacted with Solute carrier family 2 , facilitated glucose transporter member 4 (GLUT4; P19357) and Small ubiquitin-related modifier 3 (Q5XIF4) (Fig. 5A ) or with Polyubiquitin-C (Q63429) and Elongation factor 2 (P05197) (Fig. 5B ). As for the group treated with 50 mgF/L, most...”
- “...dissociation inhibitor alpha (P50398) and Solute carrier family 2 , facilitated glucose transporter member 4 (P19357). The access numbers of the unique proteins of the control (dark red nodes) correspond to: Aconitate hydratase , mitochondrial (Q9ER34), Cytochrome c oxidase subunit 4 isoform 1 , mitochondrial (P10888)...”
- Hydrogen sulfide increases glutathione biosynthesis, and glucose uptake and utilisation in C2C12 mouse myotubes.
Parsanathan, Free radical research 2018 - “...(D4ADU2), and a similar comparison of sequences of Slc2a4/GLUT4 human (P14672), mouse (P14142), and rat (P19357) indicated that the localization of cysteine residues is conserved in all species. Amino acid sequences were aligned with default parameters and checked for transmembrane annotation to rule out the transmembrane...”
- Diabetic Retinopathy and Laser Therapy in Rats: A Protein-Protein Interaction Network Analysis.
Safaei, Journal of lasers in medical sciences 2017 - Proteomic analysis of gastrocnemius muscle in rats with streptozotocin-induced diabetes and chronically exposed to fluoride
Lima, PloS one 2014 - “...each comparison. The majority of the proteins presenting with a fold change interact with GLUT4 (P19357; 726 proteins) and 14-3-3 protein zeta/delta (P63102; 4-14 proteins) for all analyzed comparisons. Proteins presenting fold change also interacted with Erk1 (P21708; 818 proteins) in 4 comparisons. 10.1371/journal.pone.0106646.g003 Figure 3...”
- “...subnetworks revealed that many proteins ( Table 2 ) with fold changes interacted with GLUT4 (P19357) ( figure 3 ), a protein involved in glucose uptake and trafficking. In a study by Scherp et al. (2012), 18 proteins interacting with GLUT4 were identified in human skeletal...”
- Phosphoproteome mapping of cardiomyocyte mitochondria in a rat model of heart failure.
Giorgianni, Molecular and cellular biochemistry 2014 - “...st IEMPQQAR S16/T17 11 P23562 Band 3 anion transport protein VLEIPDRD s EEELEHVIEQIAYR S18 12 P19357 Solute carrier family 2, facilitated glucose transporter member 4 (GLUT-4) RTP s LLEQEVKPSTELEYLGPDEND S488 13 P08050 Gap junction alpha-1 protein (connexin-43) QA s EQNWANYSAEQNR S306 MGQAGSTI s NSHAQPFDFPDDNQNAK S328 MGQAGSTI...”
- Carbon source metabolism and its regulation in cancer cells.
Yin, Critical reviews in eukaryotic gene expression 2012 - “...Genes Regulated by MondoB:Mlx Complex Genes Swiss Prot References Carbon metabolism Slc2a4 Glucose transporter 4 P19357 100 Gckr Glucokinase regulatory protein Q07071 100 Pklr Liver-type pyruvate kinase P12928 98 Gpd1 Glycerol-3-phosphate dehydrogenase 1 O35077 100 Acaca Acetyl-CoA carboxylase 1 P11497 123 Fasn Fatty acid synthase P12785...”
- Targets of tyrosine nitration in diabetic rat retina.
Zhan, Molecular & cellular proteomics : MCP 2008 - Major facilitator superfamily
Pao, Microbiology and molecular biology reviews : MMBR 1998 - “...P47842 P28568 P11169 P32037 P47843 Q07647 P14672 P14142 P19357 P22732 P46408 P43427 Q00712 B30310 U39197 U29377 U43375 U52842 Z46381 L27651 X78855 D83045 A53153...”
- The SIRT3/GSK-3β/GLUT4 axis might be involved in maternal hypoxia-induced skeletal muscle insulin resistance in old male rat offspring.
Zhu, Toxicology and applied pharmacology 2024 (PubMed)- GeneRIF: The SIRT3/GSK-3beta/GLUT4 axis might be involved in maternal hypoxia-induced skeletal muscle insulin resistance in old male rat offspring.
- Immunoglobulin-Mediated Cardiac Protection From Ischemia/Reperfusion Injury in Diabetic Rats Is Associated With Endothelial Nitric Oxide Synthase/Glucose Transporter-4 Signaling Pathway.
Babiker, Journal of cardiovascular pharmacology 2024 (PubMed)- GeneRIF: Immunoglobulin-Mediated Cardiac Protection From Ischemia/Reperfusion Injury in Diabetic Rats Is Associated With Endothelial Nitric Oxide Synthase/Glucose Transporter-4 Signaling Pathway.
- Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.
Knudsen, eLife 2023 - GeneRIF: Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.
- Impact of Normal and Overweight Pregnancy in GLUT4 and Glucose-Dependent Vascular Contractility.
Juarez, Pharmacology 2023 (PubMed)- GeneRIF: Impact of Normal and Overweight Pregnancy in GLUT4 and Glucose-Dependent Vascular Contractility.
- Exercise preconditioning promotes myocardial GLUT4 translocation and induces autophagy to alleviate exhaustive exercise-induced myocardial injury in rats.
Guo, Journal of molecular histology 2023 (PubMed)- GeneRIF: Exercise preconditioning promotes myocardial GLUT4 translocation and induces autophagy to alleviate exhaustive exercise-induced myocardial injury in rats.
- Electrical stimulated GLUT4 signalling attenuates critical illness-associated muscle wasting.
Addinsall, Journal of cachexia, sarcopenia and muscle 2022 - GeneRIF: Electrical stimulated GLUT4 signalling attenuates critical illness-associated muscle wasting.
- Hydroxytyrosol modifies skeletal muscle GLUT4/AKT/Rac1 axis in trained rats.
Casuso, Journal of cellular physiology 2021 (PubMed)- GeneRIF: Hydroxytyrosol modifies skeletal muscle GLUT4/AKT/Rac1 axis in trained rats.
- Complexin-2 redistributes to the membrane of muscle cells in response to insulin and contributes to GLUT4 translocation.
Pavarotti, The Biochemical journal 2021 (PubMed)- GeneRIF: Complexin-2 redistributes to the membrane of muscle cells in response to insulin and contributes to GLUT4 translocation.
- Prolonged preoperative fasting induces postoperative insulin resistance by ER-stress mediated Glut4 down-regulation in skeletal muscles.
Lin, International journal of medical sciences 2021 - GeneRIF: Prolonged preoperative fasting induces postoperative insulin resistance by ER-stress mediated Glut4 down-regulation in skeletal muscles.
- Piperlongumine attenuates oxidative stress, inflammatory, and apoptosis through modulating the GLUT-2/4 and AKT signaling pathway in streptozotocin-induced diabetic rats.
Xu, Journal of biochemical and molecular toxicology 2021 (PubMed)- GeneRIF: Piperlongumine attenuates oxidative stress, inflammatory, and apoptosis through modulating the GLUT-2/4 and AKT signaling pathway in streptozotocin-induced diabetic rats.
- Gundelia tournefortii: Fractionation, Chemical Composition and GLUT4 Translocation Enhancement in Muscle Cell Line.
Kadan, Molecules (Basel, Switzerland) 2021 - GeneRIF: Gundelia tournefortii: Fractionation, Chemical Composition and GLUT4 Translocation Enhancement in Muscle Cell Line.
- Effect of resistance training on osteopenic rat bones in neonatal streptozotocin-induced diabetes: Analysis of GLUT4 content and biochemical, biomechanical, densitometric, and microstructural evaluation.
de, Life sciences 2021 (PubMed)- GeneRIF: Effect of resistance training on osteopenic rat bones in neonatal streptozotocin-induced diabetes: Analysis of GLUT4 content and biochemical, biomechanical, densitometric, and microstructural evaluation.
- MicroRNA-15a Inhibits Glucose Transporter 4 Translocation and Impairs Glucose Metabolism in L6 Skeletal Muscle Via Targeting of Vesicle-Associated Membrane Protein-Associated Protein A.
Guo, Canadian journal of diabetes 2020 (PubMed)- GeneRIF: MicroRNA-15a Inhibits Glucose Transporter 4 Translocation and Impairs Glucose Metabolism in L6 Skeletal Muscle Via Targeting of Vesicle-Associated Membrane Protein-Associated Protein A.
- Neuregulin-1 triggers GLUT4 translocation and enhances glucose uptake independently of insulin receptor substrate and ErbB3 in neonatal rat cardiomyocytes.
Heim, Biochimica et biophysica acta. Molecular cell research 2020 (PubMed)- GeneRIF: our results show that similar to insulin, rhNRG-1 can induce glucose uptake by activating the PI3Kalpha-Akt-AS160 pathway and GLUT4 translocation. Unlike insulin, the rhNRG-1-induced effect is not mediated by IRS proteins and is observed in neonatal, but not in adult rat cardiomyocytes.
- Glucose Transporter 2 and 4 Are Involved in Glucose Supply during Pulpal Wound Healing after Pulpotomy with Mineral Trioxide Aggregate in Rat Molars.
Tohma, Journal of endodontics 2020 (PubMed)- GeneRIF: Glut2 and Glut4 regulate glucose transport during wound healing beneath the injured dental pulp area. This may contribute to the development of new vital pulp therapy for patients with deep caries
- Stress adaptation disorders play a role in rat gestational diabetes with oxidative stress and glucose transporter-4 expression.
Feng, Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology 2020 (PubMed)- GeneRIF: Stress adaptation disorders play a role in rat gestational diabetes with oxidative stress and glucose transporter-4 expression.
- Nerve damage induced skeletal muscle atrophy is associated with increased accumulation of intramuscular glucose and polyol pathway intermediates.
Langer, Scientific reports 2020 - GeneRIF: Nerve damage induced skeletal muscle atrophy is associated with increased accumulation of intramuscular glucose and polyol pathway intermediates.
- Adaptations in GLUT4 Expression in Response to Exercise Detraining Linked to Downregulation of Insulin-Dependent Pathways in Cardiac but not in Skeletal Muscle Tissue.
Lehnen, International journal of sport nutrition and exercise metabolism 2020 (PubMed)- GeneRIF: Adaptations in GLUT4 Expression in Response to Exercise Detraining Linked to Downregulation of Insulin-Dependent Pathways in Cardiac but not in Skeletal Muscle Tissue.
- miR-150 regulates glucose utilization through targeting GLUT4 in insulin-resistant cardiomyocytes.
Ju, Acta biochimica et biophysica Sinica 2020 (PubMed)- GeneRIF: miR-150 regulates glucose utilization through targeting GLUT4 in insulin-resistant cardiomyocytes.
- Aging alters glucose uptake in the naïve and injured rodent spinal cord.
von, Neuroscience letters 2019 - GeneRIF: findings show that age alters glucose uptake and GLUT3/4 expression profiles before and after Spinal Cord Injury.
- Diabetes induces tri-methylation at lysine 9 of histone 3 at Slc2a4 gene in skeletal muscle: A new target to improve glycemic control.
Yonamine, Molecular and cellular endocrinology 2019 (PubMed)- GeneRIF: Study reveals for the first time that diabetes triggers epigenetic modifications in the Slc2a4 gene in skeletal muscle, which can participate in decreasing GLUT4 expression, thus contributing to impaired glycemic control.
- A glucose-insulin-potassium solution improves glucose intake in hypoxic cardiomyocytes by a differential expression of glucose transporters in a metabolic syndrome model.
Carbo, Journal of biosciences 2019 (PubMed)- GeneRIF: Oxygenated control myocytes consumed 1.7 +/- 0.2 mug of glucose per gram of fresh tissue per hour using the GLUT1, and during hypoxia, they incorporated 41.1% more glucose by GLUT1 and GLUT4. The GIK solution improved glucose uptake in oxygenation by 70.5% through GLUT1
- PKC and Rab13 mediate Ca2+ signal-regulated GLUT4 traffic.
Deng, Biochemical and biophysical research communications 2018 (PubMed)- GeneRIF: In summary, ionomycin-promoted exocytosis of GLUT4 is partly reversed by siPKCtheta;, whereas ionomycin-inhibited endocytosis of GLUT4 requires both siPKCalpha and siPKCtheta;. PKCalpha and PKCtheta; contribute to ionomycin-induced phosphorylation of AS160 and TBC1D1. Rab13 is required for ionomycin-regulated GLUT4 exocytosis.
- Sphingolipid changes do not underlie fatty acid-evoked GLUT4 insulin resistance nor inflammation signals in muscle cells.
Pillon, Journal of lipid research 2018 - GeneRIF: Sphingolipid changes do not underlie fatty acid-evoked GLUT4 insulin resistance nor inflammation signals in muscle cells
- Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression.
Pinto-Junior, Scientific reports 2018 - GeneRIF: Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression
- Impact of flaxseed and soy nuts as dietary supplements on lipid profile, insulin sensitivity, and GLUT4 expression in ovariectomized rats.
Dresseno, Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme 2018 (PubMed)- GeneRIF: Studied the effects of a diet with flaxseed or soy nuts versus estradiol on the lipid profile, blood pressure (BP), insulin sensitivity, and solute carrier family 2 member 4 (GLUT4) expression of ovariectomized female rats.
- MicroRNA-17 impairs glucose metabolism in insulin-resistant skeletal muscle via repressing glucose transporter 4 expression.
Xiao, European journal of pharmacology 2018 (PubMed)- GeneRIF: Study findings unraveled a novel mechanism for insulin resistance that involves repression of GLUT4 by miR-17 and suggested miR-17 as a potential molecular target for the development of new therapeutic approaches for the treatment of type 2 diabetes mellitus.
- Central injection of GALR1 agonist M617 attenuates diabetic rat skeletal muscle insulin resistance through the Akt/AS160/GLUT4 pathway.
Fang, Mechanisms of ageing and development 2017 (PubMed)- GeneRIF: central injection of M617 mitigated insulin resistance of skeletal muscle by enhancing GLUT4 translocation from intracellular pools to plasma membranes via the activation of the Akt/AS160/GLUT4 signaling pathway.
- Brain GLUT4 Knockout Mice Have Impaired Glucose Tolerance, Decreased Insulin Sensitivity, and Impaired Hypoglycemic Counterregulation.
Reno, Diabetes 2017 - GeneRIF: Pharmacological inhibition of central GLUT4 attenuates the counterregulatory response to hypoglycemia.
- GLUT4 Mobilization Supports Energetic Demands of Active Synapses.
Ashrafi, Neuron 2017 - GeneRIF: during action potential (AP) firing, nerve terminals rely on the glucose transporter GLUT4 as a glycolytic regulatory system to meet the activity-driven increase in energy demands. Activity at synapses triggers insertion of GLUT4 into the axonal plasma membrane driven by activation of the metabolic sensor AMP kinase.
- Aerobic training prior to myocardial infarction increases cardiac GLUT4 and partially preserves heart function in spontaneously hypertensive rats.
Schaun, Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme 2017 (PubMed)- GeneRIF: Increased GLUT4 in the microsomal and plasma membrane fractions in response to physical training can increase glucose uptake by cardiomyocytes, producing a cardioprotective effect in the post acute myocardial infarction energy environment.
- Short-Term Hypoxia Reverses Ox-LDL-Induced CD36 and GLUT4 Switching Metabolic Pathways in H9c2 Cardiomyoblast Cells.
Chen, Journal of cellular biochemistry 2017 (PubMed)- GeneRIF: Short-Term Hypoxia Reverses Ox-LDL-Induced CD36 and GLUT4 Switching Metabolic Pathways in H9c2 Cardiomyoblast Cells
- A systems biology analysis connects insulin receptor signaling with glucose transporter translocation in rat adipocytes.
Bergqvist, The Journal of biological chemistry 2017 - GeneRIF: The developed combined model could describe data not used for training the model and was used to generate predictions of the relative contributions of the pathways from IR to translocation of GLUT4.
- High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte.
Wen, Journal of cellular physiology 2017 (PubMed)- GeneRIF: High density lipoprotein reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte.
- Acute bout of exercise induced prolonged muscle glucose transporter-4 translocation and delayed counter-regulatory hormone response in type 1 diabetes.
Sato, PloS one 2017 - GeneRIF: prolonged enhancement of GLUT-4 translocation and delayed counter-regulatory hormone responses may have contributed to the induction of hypoglycemia
- Regulation of GLUT4 activity in myotubes by 3-O-methyl-d-glucose.
Shamni, Biochimica et biophysica acta. Biomembranes 2017 (PubMed)- GeneRIF: MeGlc induced changes in GLUT4 or GLUT4 complexes within the plasma membrane.
- Ablating the protein TBC1D1 impairs contraction-induced sarcolemmal glucose transporter 4 redistribution but not insulin-mediated responses in rats.
Whitfield, The Journal of biological chemistry 2017 - GeneRIF: results highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocation of GLUT4 to the plasma membrane in skeletal muscle.
- A complex of Rab13 with MICAL-L2 and α-actinin-4 is essential for insulin-dependent GLUT4 exocytosis.
Sun, Molecular biology of the cell 2016 - GeneRIF: Findings suggest that MICAL-L2 is an effector of insulin-activated Rab13, which links to GLUT4 through ACTN4, localizing GLUT4 vesicles at the muscle cell periphery to enable their fusion with the membrane.
- The Effects of AS160 Modulation on Fatty Acid Transporters Expression and Lipid Profile in L6 Myotubes.
Mikłosz, Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2016 (PubMed)- GeneRIF: Modulation of AS160 level and activity led to significant increase in the concentration of DAG and PL, which was associated with changes in FAs composition and expression of fatty acid transporters.
- Maternal periodontitis decreases plasma membrane GLUT4 content in skeletal muscle of adult offspring.
Mattera, Life sciences 2016 (PubMed)- GeneRIF: GLUT4 content is decreased in the skeletal muscle of offspring from maternal periodontitis rats.
- Palmitic acid interferes with energy metabolism balance by adversely switching the SIRT1-CD36-fatty acid pathway to the PKC zeta-GLUT4-glucose pathway in cardiomyoblasts.
Chen, The Journal of nutritional biochemistry 2016 (PubMed)- GeneRIF: Although PA reduced CD36 and increased GLUT4 metabolic pathway proteins, when we pretreated cells with resveratrol to activate SIRT1 or transfected si-PKCzeta, both were able to significantly increase CD36 metabolic pathway proteins and reduce GLUT4 pathway proteins
- Zinc stimulates glucose consumption by modulating the insulin signaling pathway in L6 myotubes: essential roles of Akt-GLUT4, GSK3β and mTOR-S6K1.
Wu, The Journal of nutritional biochemistry 2016 (PubMed)- GeneRIF: Data suggest that insulin resistance of myotubes can be modulated by dietary factors; here, zinc, a dietary component and common dietary supplement, up-regulates glucose transport, Glut4 translocation, Akt phosphorylation, and Gsk3b phosphorylation/activation, and down-regulates mTOR and S6k1 in L6 cells. (Glut4 = glucose transporter 4; Akt = AKT serine/threonine kinase 1; Gsk3b = glycogen synthase kinase 3 beta)
- Fermented Red Ginseng Potentiates Improvement of Metabolic Dysfunction in Metabolic Syndrome Rat Models.
Kho, Nutrients 2016 - GeneRIF: Fermented red ginseng induced markedly upregulation of Insulin receptor substrate 1 (IRS-1) and glucose transporter type 4 (Glut4) in the muscle.
- Decreased expression of GLUT4 in male CG-IUGR rats may play a vital role in their increased susceptibility to diabetes mellitus in adulthood.
Duan, Acta biochimica et biophysica Sinica 2016 (PubMed)- GeneRIF: Data show that glucose transporter type 4 (GLUT4) down-regulation displayed strong negative correlations with the decreased glucose tolerance capability.
- Perinatal Brain Injury is Accompanied by Disturbances in Expression of SLC Protein Superfamily in Endotheliocytes of Hippocampal Microvessels.
Morgun, Bulletin of experimental biology and medicine 2016 (PubMed)- GeneRIF: Perinatal brain injury is accompanied by disturbances in expression of Glut4, Gsk3, and Hif-1a proteins in endotheliocytes of hippocampal microvessels.
- Novel Roles for the Insulin-Regulated Glucose Transporter-4 in Hippocampally Dependent Memory.
Pearson-Leary, The Journal of neuroscience : the official journal of the Society for Neuroscience 2016 - GeneRIF: the current study, we demonstrate that GluT4 is a critical component of hippocampal memory processes.
- Heat-shock-induced glucose transporter 4 in the slow-twitch muscle of rats.
Wu, Physiological research 2015 (PubMed)- GeneRIF: Collectively, our results indicated that heat-shock is critical factor that modulates GLUT4 and HSP70 in the skeletal muscle of rats.
- Fiber type effects on contraction-stimulated glucose uptake and GLUT4 abundance in single fibers from rat skeletal muscle.
Castorena, American journal of physiology. Endocrinology and metabolism 2015 - GeneRIF: Differences in GLUT4 abundance among the fiber types were not accompanied by significant differences in contraction-stimulated glucose uptake.
- Renal effects of glucose transporter 4 in Nω-nitro-L-arginine/ /high salt-induced hypertensive rats.
Igbe, Bratislavske lekarske listy 2015 (PubMed)- GeneRIF: GLUT4 exerts a renoprotective role which may be related to increase NO production. The antinatriuretic effects of GLUT4 appear to be due to enhancement of ion transport activity of ENaC and NCC at the renal tubules
- Impaired translocation of GLUT4 results in insulin resistance of atrophic soleus muscle.
Xu, BioMed research international 2015 - GeneRIF: The impaired GLUT4 translocation to sarcolemma under insulin stimulation may mediate insulin resistance in unloaded soleus muscle and further affect the insulin sensitivity of whole body in tail-suspended rats.
- Proteomic Analysis of GLUT4 Storage Vesicles Reveals Tumor Suppressor Candidate 5 (TUSC5) as a Novel Regulator of Insulin Action in Adipocytes.
Fazakerley, The Journal of biological chemistry 2015 - GeneRIF: findings functionally link TUSC5 to GLUT4 trafficking, insulin action, insulin resistance, and PPARgamma action in the adipocyte
- Effect of Intermittent Hypoxia and Rimonabant on Glucose Metabolism in Rats: Involvement of Expression of GLUT4 in Skeletal Muscle.
Wang, Medical science monitor : international medical journal of experimental and clinical research 2015 - GeneRIF: Intermittent Hypoxia can cause insulin resistance and reduced expression of GLUT4 in both mRNA and protein levels in skeletal muscle of rats
- Di(2-ethylhexyl)phthalate exposure impairs insulin receptor and glucose transporter 4 gene expression in L6 myotubes.
Rajesh, Human & experimental toxicology 2014 (PubMed)- GeneRIF: Di(2-ethylhexyl)phthalate exposure causes a decline in myotube GLUT4 expression.
- Suppression of the GLUT4 adaptive response to exercise in fructose-fed rats.
Goyaram, American journal of physiology. Endocrinology and metabolism 2014 - GeneRIF: Both fructose and maltodextrin modulate the GLUT4 adaptive response to exercise by mechanisms involving chromatin remodeling at the Glut4 promoter.
- Recovery of insulin sensitivity and Slc2a4 mRNA expression depend on T3 hormone during refeeding.
Zanquetta, Metabolism: clinical and experimental 2014 (PubMed)- GeneRIF: Post-fasting infusions surprisingly induced a further Slc2a4 mRNA decrease.
- Chronic stress modulates regional cerebral glucose transporter expression in an age-specific and sexually-dimorphic manner.
Kelly, Physiology & behavior 2014 - GeneRIF: Hypothalamic GLUT4 mRNA abundance increases with age and is sexually dimorphic.but decression in hippocampus and amygalda.
- Myosin Va mediates Rab8A-regulated GLUT4 vesicle exocytosis in insulin-stimulated muscle cells.
Sun, Molecular biology of the cell 2014 - GeneRIF: Insulin signaling to the molecular switch Rab8A connects with the motor protein MyoVa to mobilize GLUT4 vesicles toward the muscle cell plasma membrane.
- CYP2E1 impairs GLUT4 gene expression and function: NRF2 as a possible mediator.
Armoni, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2014 (PubMed)- GeneRIF: CYP2E1 and NRF2 are introduced as negative regulators of GLUT4 expression and function in insulin-sensitive cells.
- 5'-AMP-activated protein kinase increases glucose uptake independent of GLUT4 translocation in cardiac myocytes.
Lee, Canadian journal of physiology and pharmacology 2014 (PubMed)- GeneRIF: AMPK activation did not redistribute GLUT4 to the sarcolemmal membrane, suggesting that AMPK may regulate glucose uptake via another glucose transporter. These studies suggest that AMPK is a major regulator of glucose uptake in cardiac myocytes.
- Insulin sensitivity is inversely related to cellular energy status, as revealed by biotin deprivation.
Salvador-Adriano, American journal of physiology. Endocrinology and metabolism 2014 (PubMed)- GeneRIF: Data suggest that enhanced insulin sensitivity in biotin deficiency is due, in part, to up-regulation of AMPK (protein kinase AMP) subunits (Prkaa1, Prkaa2) and of translocation of GLUT4 glucose transporter to cell membrane in skeletal muscle.
- Calcium signaling recruits substrate transporters GLUT4 and CD36 to the sarcolemma without increasing cardiac substrate uptake.
Angin, American journal of physiology. Endocrinology and metabolism 2014 (PubMed)- GeneRIF: Ca(2+)-induced glut4 transporter translocation might be crucial under excessive cardiac stress conditions that require supraphysiological energy demands.
- Role of the guanine nucleotide exchange factor in Akt2-mediated plasma membrane translocation of GLUT4 in insulin-stimulated skeletal muscle.
Takenaka, Cellular signalling 2014 (PubMed)- GeneRIF: Role of the guanine nucleotide exchange factor in Akt2-mediated plasma membrane translocation of GLUT4 in insulin-stimulated skeletal muscle.
- Postnatal exposure to a high-carbohydrate diet interferes epigenetically with thyroid hormone receptor induction of the adult male rat skeletal muscle glucose transporter isoform 4 expression.
Raychaudhuri, The Journal of nutritional biochemistry 2014 - GeneRIF: High carbohydrate diet exposure limited to the suckling phase of life is associated with a reduction in adult male skeletal muscle Glut4 expression.
- Role of AMPK α in skeletal muscle glycometabolism regulation and adaptation in relation to sepsis.
Zheng, BioMed research international 2014 - GeneRIF: sepsis, may be related to glycometabolism disorder in the skeletal muscle, coming down to enhancement of GLUT4 translocation expression promoted by activation of AMPKa.
- Effect of endogenous galanin on glucose transporter 4 expression in cardiac muscle of type 2 diabetic rats.
Fang, Peptides 2014 (PubMed)- GeneRIF: These results demonstrate that endogenous galanin, acting through its central receptor, has an important attribute to increase GLUT4 expression, leading to enhance insulin sensitivity and glucose uptake in cardiac muscle of type 2 diabetic rats.
- Adverse cardiac remodeling due to maternal low protein diet is associated with alterations in expression of genes regulating glucose metabolism.
Tappia, Nutrition, metabolism, and cardiovascular diseases : NMCD 2013 (PubMed)- GeneRIF: Significant increases in IR b-subunit, IRS-1 and PTP1B protein contents were seen in the hearts of low protein diet group, also GLUT4 and PI3-kinase protein levels were markedly increased.
- Microtubule network is required for insulin-induced signal transduction and actin remodeling.
Liu, Molecular and cellular endocrinology 2013 (PubMed)- GeneRIF: investigation of role of microtubules/actin cytoskeleton in insulin-stimulated glucose uptake in skeletal muscle: Data suggest sequence of reorganization of microtubules, actin remodeling, translocation of GLUT4, and glucose uptake.
- Protective role of lycopene against Aroclor 1254-induced changes on GLUT4 in the skeletal muscles of adult male rat.
Williams, Drug and chemical toxicology 2013 (PubMed)- GeneRIF: Lycopene has a protective role against Aroclor 1254-induced changes on GLUT4 in the skeletal muscles of adult male rat.
- Insulin sensitization via partial agonism of PPARγ and glucose uptake through translocation and activation of GLUT4 in PI3K/p-Akt signaling pathway by embelin in type 2 diabetic rats.
Gandhi, Biochimica et biophysica acta 2013 (PubMed)- GeneRIF: Embelin bound to PPARgamma; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.
- Aspalathin improves hyperglycemia and glucose intolerance in obese diabetic ob/ob mice.
Son, European journal of nutrition 2013 (PubMed)- GeneRIF: Hypoglycemic effect of aspalathin is related to increased GLUT4 translocation to plasma membrane via AMPK activation.
- SIRT1 interacts with metabolic transcriptional factors in the pancreas of insulin-resistant and calorie-restricted rats.
Chen, Molecular biology reports 2013 (PubMed)- GeneRIF: These data suggest that SIRT1 and its regulators - FOXO3a, GLUT4, PPARg and PGC-1alpha are involved in the development of insulin resistance.
- Doc2b promotes GLUT4 exocytosis by activating the SNARE-mediated fusion reaction in a calcium- and membrane bending-dependent manner.
Yu, Molecular biology of the cell 2013 - GeneRIF: Doc2b promotes GLUT4 exocytosis by accelerating the calcium-SNARE-dependent fusion reaction.
- Insulin regulates Glut4 confinement in plasma membrane clusters in adipose cells.
Lizunov, PloS one 2013 - GeneRIF: GLUT4 confinement in clusters represents a novel kinetic mechanism for insulin regulation of glucose homeostasis.
- Effect of iridoid glucoside on plasma lipid profile, tissue fatty acid changes, inflammatory cytokines, and GLUT4 expression in skeletal muscle of streptozotocin-induced diabetic rats.
Sundaram, Molecular and cellular biochemistry 2013 (PubMed)- GeneRIF: Data indicate that the levels of GLUT4 expression were significantly decreased in the skeletal muscle of diabetic rats when compared to control rats.
- Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.
Chiu, The Journal of biological chemistry 2013 - GeneRIF: Elevation of Rac-1 activation alone suffices to drive insulin-independent GLUT4 translocation in muscle cells.
- Overexpression of mitofusin 2 improves translocation of glucose transporter 4 in skeletal muscle of high‑fat diet‑fed rats through AMP‑activated protein kinase signaling.
Kong, Molecular medicine reports 2013 (PubMed)- GeneRIF: Overexpression of mitofusin 2 improves translocation of glucose transporter 4 in skeletal muscle of highfat dietfed rats through AMPactivated protein kinase signaling.
- Impact of divergent effects of astaxanthin on insulin signaling in L6 cells.
Ishiki, Endocrinology 2013 (PubMed)- GeneRIF: Data indicate that astaxanthin enhanced insulin-stimulated GLUT4 translocation involving insulin receptor substrate-1 (IRS-1) phosphorylation.
- Impact of GLO1 knock down on GLUT4 trafficking and glucose uptake in L6 myoblasts.
Engelbrecht, PloS one 2013 - GeneRIF: GLO1 knock down augmented GLUT4 level on the cell surface of L6 myoblasts at least in part through reduction of GLUT4 internalization.
- Synthesis and mechanism of hypoglycemic activity of benzothiazole derivatives.
Meltzer-Mats, Journal of medicinal chemistry 2013 (PubMed)- GeneRIF: Data indicate that benzothiazole derivatives elevated the abundance of GLUT4 in the plasma membrane of the myotubes and activated AMPK.
- Testosterone increases GLUT4-dependent glucose uptake in cardiomyocytes.
Wilson, Journal of cellular physiology 2013 (PubMed)- GeneRIF: Testosterone increases GLUT4-dependent glucose uptake.
- Differential translocation of the fatty acid transporter, FAT/CD36, and the glucose transporter, GLUT4, coordinates changes in cardiac substrate metabolism during ischemia and reperfusion.
Heather, Circulation. Heart failure 2013 (PubMed)- GeneRIF: Differential translocation of the fatty acid transporter, FAT/CD36, and the glucose transporter, GLUT4, coordinates changes in cardiac substrate metabolism during ischemia and reperfusion.
- Whey protein hydrolysate increases translocation of GLUT-4 to the plasma membrane independent of insulin in wistar rats.
Morato, PloS one 2013 - GeneRIF: The objective of this study was to verify if consuming WP and WPH could also increase the concentration of the glucose transporters GLUT-1 and GLUT-4 in the plasma membrane (PM) of the muscle cells of sedentary and exercised animals.
- Daily profile of glut1 and glut4 expression in tissues inside and outside the blood-brain barrier in control and streptozotocin-treated rats.
Soltésová, Physiological research 2013 (PubMed)- GeneRIF: The expression of glut1 and glut4 in brain areas was not down-regulated, however, we observed trend to phase advance in glut1 expression in the cerebellum.
- Protein restriction during gestation alters histone modifications at the glucose transporter 4 (GLUT4) promoter region and induces GLUT4 expression in skeletal muscle of female rat offspring.
Zheng, The Journal of nutritional biochemistry 2012 (PubMed)- GeneRIF: Data suggest that maternal protein restriction during pregnancy induces GLUT4 expression in skeletal muscle of female offspring but not in males; this may indicate sex-dependent adaptation of glucose metabolism to a maternal low-protein diet.
- Exercise-induced galanin release facilitated GLUT4 translocation in adipocytes of type 2 diabetic rats.
Liang, Pharmacology, biochemistry, and behavior 2012 (PubMed)- GeneRIF: Swimming training increases GLUT4 expression in white adipocytes. Data suggest endogenous galanin accelerates GLUT4 translocation to plasma membrane in adipocytes to reach new equilibrium between exocytosis and endocytosis in type 2 diabetes.
- The effect of age on glucose uptake and GLUT1 and GLUT4 expression in rat skeletal muscle.
dos, Cell biochemistry and function 2012 (PubMed)- GeneRIF: The expression of GLUT4 was lower in older animals, but no relation between age and GLUT1 expression was found.
- T3 rapidly increases SLC2A4 gene expression and GLUT4 trafficking to the plasma membrane in skeletal muscle of rat and improves glucose homeostasis.
Brunetto, Thyroid : official journal of the American Thyroid Association 2012 (PubMed)- GeneRIF: T3 rapidly increases SLC2A4 gene expression and GLUT4 trafficking to the plasma membrane in skeletal muscle of rat and improves glucose homeostasis
- Regulation of insulin signaling and glucose transporter 4 (GLUT4) exocytosis by phosphatidylinositol 3,4,5-trisphosphate (PIP3) phosphatase, skeletal muscle, and kidney enriched inositol polyphosphate phosphatase (SKIP).
Ijuin, The Journal of biological chemistry 2012 - GeneRIF: Regulation of insulin signaling and glucose transporter 4 (GLUT4) exocytosis by phosphatidylinositol 3,4,5-trisphosphate (PIP3) phosphatase, skeletal muscle, and kidney enriched inositol polyphosphate phosphatase (SKIP).
- GLUT4 in the endocrine pancreas--indicating an impact in pancreatic islet cell physiology?
Bähr, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2012 (PubMed)- GeneRIF: These data provide evidence for the existence of GLUT4 in the endocrine pancreas and indicate a physiological relevance of this glucose transporter as well as characteristic changes in diabetic disease.
- 4-Hydroxyisoleucine stimulates glucose uptake by increasing surface GLUT4 level in skeletal muscle cells via phosphatidylinositol-3-kinase-dependent pathway.
Jaiswal, European journal of nutrition 2012 (PubMed)- GeneRIF: 4-Hydroxyisoleucine enhances surface GLUT4myc level in L6-GLUT4myc myotubes and stimulates GLUT4myc translocation via PI-3-K/AKT-dependent mechanisms, thus stimulating glucose uptake.
- GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome.
Leguisamo, Cardiovascular diabetology 2012 - GeneRIF: GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome.
- Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles.
Boguslavsky, Molecular biology of the cell 2012 - GeneRIF: Interaction of vesicular Myo1c with cortical actin filaments is required for insulin-mediated tethering of GLUT4 vesicles and for efficient GLUT4 surface delivery in muscle cells.
- Antidiabetic effect of plumbagin isolated from Plumbago zeylanica L. root and its effect on GLUT4 translocation in streptozotocin-induced diabetic rats.
Sunil, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 2012 (PubMed)- GeneRIF: Enhanced GLUT4 mRNA and protein expression were observed in diabetic rats after treatment with plumbagin.
- GLUT4 traffic through an ESCRT-III-dependent sorting compartment in adipocytes.
Koumanov, PloS one 2012 - GeneRIF: GLUT4 trafficking in response to insulin signaling is accomplished through an ESCRT-III-dependent sorting compartment in adipocytes.
- Insulin stimulated-glucose transporter Glut 4 is expressed in the retina.
Sánchez-Chávez, PloS one 2012 - GeneRIF: First evidence of Glut4 expression in the retina, suggesting it as an insulin- responsive tissue.
- Neuromuscular electrical stimulation improves GLUT-4 and morphological characteristics of skeletal muscle in rats with heart failure.
de, Acta physiologica (Oxford, England) 2011 (PubMed)- GeneRIF: Electrical stimulation improves morphological changes and raises GLUT-4 content in skeletal muscle of rats with heart failure.
- Prenylated chalcones 4-hydroxyderricin and xanthoangelol stimulate glucose uptake in skeletal muscle cells by inducing GLUT4 translocation.
Kawabata, Molecular nutrition & food research 2011 (PubMed)- GeneRIF: 4-hydroxyderricin and xanthoangelol induced GLUT4 translocation in L6 myotubes.
- Exercise-stimulated GLUT4 expression is similar in normotensive and hypertensive rats.
Lehnen, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2011 (PubMed)- GeneRIF: There were no differences between spontaneously hypertensive and normotensive rats in post-training GLUT4 expression.
- Perturbations of the stress-induced GLUT4 localization pathway in slow-twitch muscles of obese Zucker rats.
Chen, Journal of physiology and biochemistry 2011 (PubMed)- GeneRIF: following acute exercise, levels of GLUT4 translocated to the plasma membrane were significantly elevated in lean rats but remained unchanged in obese rats relative to their resting conditions
- AS160 phosphotyrosine-binding domain constructs inhibit insulin-stimulated GLUT4 vesicle fusion with the plasma membrane.
Koumanov, The Journal of biological chemistry 2011 - GeneRIF: AS160 phosphotyrosine-binding domain constructs inhibit insulin-stimulated GLUT4 vesicle fusion with the plasma membrane
- Interaction between insulin and estradiol in regulation of cardiac glucose and free fatty acid transporters.
Tepavcevic, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2011 (PubMed)- GeneRIF: Insulin increased plasma membrane GLUT4 and GLUT1 content 30 and 40 min after treatment and CD36 content in plasma membrane fraction.
- Clustering of GLUT4, TUG, and RUVBL2 protein levels correlate with myosin heavy chain isoform pattern in skeletal muscles, but AS160 and TBC1D1 levels do not.
Castorena, Journal of applied physiology (Bethesda, Md. : 1985) 2011 - GeneRIF: Significant differences found among the muscles for GLUT4 (2.5-fold), TUG (1.7-fold), RUVBL2 (2.0-fold), and TBC1D1 (2.7-fold), but not AS160.
- [Effects of Chinese herbal medicine Yiqi Zengmin formula on expression of glucose transporter 4 in skeletal muscle in type 2 diabetic rats].
Xue, Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine 2011 (PubMed)- GeneRIF: Yiqi Zengmin formula enhanced GLUT4 translocation from the cytoplasm to the plasma membrane in skeletal muscle tissuesof type 2 diabetic rats.
- Observing GLUT4 translocation in live L6 cells using quantum dots.
Qu, Sensors (Basel, Switzerland) 2011 - GeneRIF: The translocation of GLUT4 targeted with photostable and bright quantum dots (QDs) in live L6 cells, is reported.
- Proteomic analysis of GLUT4 storage vesicles reveals LRP1 to be an important vesicle component and target of insulin signaling.
Jedrychowski, The Journal of biological chemistry 2010 - GeneRIF: LRP1 interacts with the lumenal domains of GLUT4 and other GLUT4 storage vesicle constituents.
- Adenosine monophosphate-activated protein kinase activation, substrate transporter translocation, and metabolism in the contracting hyperthyroid rat heart.
Heather, Endocrinology 2010 (PubMed)- GeneRIF: The combined effects of T(3)-induced AMPK activation and insulin stimulation were associated with increased sarcolemmal GLUT4 localization and glycolytic flux in the hyperthyroid heart.
- Effects of nonexhaustive bouts of high-intensity intermittent swimming training on GLUT-4 expression in rat skeletal muscle.
Fujimoto, The journal of physiological sciences : JPS 2010 - GeneRIF: These results suggest that GLUT-4 content in rat EPI muscle increases dramatically after very short (60 s) and nonexhaustive high-intensity intermittent exercise training.
- MicroRNA-223 regulates Glut4 expression and cardiomyocyte glucose metabolism.
Lu, Cardiovascular research 2010 (PubMed)- GeneRIF: Demonstrate a role for miR-223 in Glut4 regulation and glucose metabolism in the heart.
- Long-term ethanol exposure inhibits glucose transporter 4 expression via an AMPK-dependent pathway in adipocytes.
Feng, Acta pharmacologica Sinica 2010 - GeneRIF: Inhibition of AMP-activated protein kinase activity by ethanol leads to decreased myocyte enhancer factor 2 and GLUT4 expression in rat and human adipocytes
- Regulation of cardiomyocyte Glut4 expression by ZAC1.
Czubryt, The Journal of biological chemistry 2010 - GeneRIF: ZAC1 is a novel and previously unknown regulator of cardiomyocyte Glut4 expression and glucose uptake; MEF2 is a regulator of ZAC1 expression in response to induction of hypertrophy
- Alterations in adipocyte glucose transporter GLUT4 and circulating adiponectin and visfatin in rat adjuvant induced arthritis.
Jurcovicová, General physiology and biophysics 2010 (PubMed)- GeneRIF: AA induced cachexia results in reduction of adipocyte size, and paradoxically also in downregulation of GLUT4 in adipocyte membranes.
- Angiotensin II inhibits insulin-stimulated GLUT4 translocation and Akt activation through tyrosine nitration-dependent mechanisms.
Csibi, PloS one 2010 - GeneRIF: Ang II inhibits insulin-mediated GLUT4 translocation in this skeletal muscle model through at least two pathways: first through the transient activation of ERK1/2 which inhibit IRS-1/2 and second through a direct inhibitory nitration of Akt
- SPARC interacts with AMPK and regulates GLUT4 expression.
Song, Biochemical and biophysical research communications 2010 (PubMed)- GeneRIF: SPARC affects AMPK alpha 1-mediated glucose metabolism through regulation of Glut4 expression in L6 myocytes.
- [Effects of exercise on expression and phosphorylation of PI3K and PKB in insulin signaling in the skeletal muscles of type 2 diabetic rats].
Cao, Nan fang yi ke da xue xue bao = Journal of Southern Medical University 2010 (PubMed)- GeneRIF: Compared with the diabetic group, the diabetic rats in the exercise group showed significantly increased protein expression and phosphorylation of PKB and elevated GLUT4 protein and mRNA expressions in the skeletal muscles.
- Arp2/3- and cofilin-coordinated actin dynamics is required for insulin-mediated GLUT4 translocation to the surface of muscle cells.
Chiu, Molecular biology of the cell 2010 - GeneRIF: Arp2/3 and cofilin coordinate a dynamic cycle of actin branching and severing at the cell cortex, essential for insulin-mediated GLUT4 translocation in muscle cells.
- Insulin controls the spatial distribution of GLUT4 on the cell surface through regulation of its postfusion dispersal.
Stenkula, Cell metabolism 2010 - GeneRIF: Data demonstrate that insulin regulates not only the exocytosis of glucose transporter-4 (GLUT4) storage vesicles but also plasma membrane distribution of GLUT4 itself.
- Translocation of the Na+/H+ exchanger 1 (NHE1) in cardiomyocyte responses to insulin and energy-status signalling.
Lawrence, The Biochemical journal 2010 - GeneRIF: studies on protein translocation in cardiomyocytes in response to stimuli: translocation of GLUT4 & NHE1 appears linked, provide spatially/temporally co-ordinated responses to insulin or challenges in glucose metabolism & cell pH
- The beneficial effects of exercise in rodents are preserved after detraining: a phenomenon unrelated to GLUT4 expression.
Lehnen, Cardiovascular diabetology 2010 - GeneRIF: In detraining, despite reversion of the enhanced GLUT4 expression, cardiorespiratory and metabolic beneficial effects of exercise are preserved.
- Rab8A and Rab13 are activated by insulin and regulate GLUT4 translocation in muscle cells.
Sun, Proceedings of the National Academy of Sciences of the United States of America 2010 - GeneRIF: Rab13 and Rab8A are Rab-GTPases activated by insulin and downstream of AS160 they regulate traffic of GLUT4 vesicles.
- Effects of glucose deprivation or glucose instability on mesangial cells in culture.
de, American journal of nephrology 2009 (PubMed)- GeneRIF: GLUT-4 mRNA expression in mesangial cells was significantly decreased during the first 12 hours of low glucose incubation.
- Chronic-intermittent cold stress in rats induces selective ovarian insulin resistance.
Dorfman, Biology of reproduction 2009 (PubMed)- GeneRIF: The levels of mRNA and protein for IRS1 and SLC2A4 (also known as GLUT4), molecules involved in insulin signaling, decreased significantly in the ovaries but not in the muscle of stressed rats.
- Insulin regulates fusion of GLUT4 vesicles independent of Exo70-mediated tethering.
Lizunov, The Journal of biological chemistry 2009 - GeneRIF: fusion of GLUT4 vesicles is the rate-limiting step regulated by insulin downstream of Exo70-mediated tethering
- Insulin resistance and altered glucose transporter 4 expression in experimental uremia.
Aksentijević, Kidney international 2009 (PubMed)- GeneRIF: After six weeks of uremia, left ventricle tissue had a marked increase in the expression of GLUT4, consistent with hypertrophic remodeling, with no evidence of impaired GLUT4 translocation in the heart.
- Kinetics of GLUT4 trafficking in rat and human skeletal muscle.
Karlsson, Diabetes 2009 - GeneRIF: Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle.
- Up-regulating the hemeoxygenase system enhances insulin sensitivity and improves glucose metabolism in insulin-resistant diabetes in Goto-Kakizaki rats.
Ndisang, Endocrinology 2009 (PubMed)- GeneRIF: There is a synergistic interaction among the HO system, adiponectin, AMPK, and GLUT4 that could be explored to enhance insulin signaling and improve glucose metabolism in insulin-resistant diabetes.
- Permissive action of protein kinase C-zeta in insulin-induced CD36- and GLUT4 translocation in cardiac myocytes.
Luiken, The Journal of endocrinology 2009 (PubMed)- GeneRIF: Permissive action of protein kinase C-zeta in insulin-induced CD36- and GLUT4 translocation in cardiac myocytes.
- Cerebellar neurons possess a vesicular compartment structurally and functionally similar to Glut4-storage vesicles from peripheral insulin-sensitive tissues.
Bakirtzi, The Journal of neuroscience : the official journal of the Society for Neuroscience 2009 - GeneRIF: Glut4 in the cerebellum is localized in intracellular vesicles that have the sedimentation coefficient, buoyant density, and protein composition similar to insulin-responsive Glut4-storage vesicles from fat and skeletal muscle cells.
- The F-BAR protein CIP4 promotes GLUT4 endocytosis through bidirectional interactions with N-WASp and Dynamin-2.
Hartig, Journal of cell science 2009 - GeneRIF: Results support a previously unrecognized role for CIP4 in GLUT4 endocytosis, and show that interactions between CIP4 and Dynamin-2 and between CIP4 and NWASp are spatially coordinated to promote function.
- DHEA improves impaired activation of Akt and PKC zeta/lambda-GLUT4 pathway in skeletal muscle and improves hyperglycaemia in streptozotocin-induced diabetes rats.
Sato, Acta physiologica (Oxford, England) 2009 (PubMed)- GeneRIF: a single DHEA injection can improve hyperglycaemia and activate the glucose metabolism-related signalling pathway via Akt and PKC zeta/lambda-GLUT4 proteins of skeletal muscles in rats.
- Regulation of glucose uptake in mesangial cells stimulated by high glucose: role of angiotensin II and insulin.
Arnoni, Experimental biology and medicine (Maywood, N.J.) 2009 (PubMed)- GeneRIF: Losartan blunted the effects of high glucose on GLUT1, GLUT4, and fibronectin expression and on glucose uptake in mesangial cells.
- [Research of the relationship between insulin signal transduction and glucose transportation in rats after trauma].
Jiang, Zhonghua wai ke za zhi [Chinese journal of surgery] 2009 (PubMed)- GeneRIF: Uncoupling of signal transduction led to decrease in glucose uptake which associated with a defect in insulin-stimulated glucose transport and GLUT-4 translocation.
- Sex steroids deficiency impairs glucose transporter 4 expression and its translocation through defective Akt phosphorylation in target tissues of adult male rat.
Muthusamy, Metabolism: clinical and experimental 2009 (PubMed)- GeneRIF: sex steroids deficiency-induced defective glucose uptake in skeletal muscle and adipose tissue is mediated through defective Akt phosphorylation and GLUT4 expression in plasma membrane
- Effects of contraction on localization of GLUT4 and v-SNARE isoforms in rat skeletal muscle.
Rose, American journal of physiology. Regulatory, integrative and comparative physiology 2009 (PubMed)- GeneRIF: VAMP2, VAMP5, and VAMP7 may be involved in translocation of GLUT4 during muscle contractions.
- Insulin-stimulated translocation of GLUT4 to the plasma membrane in rat hippocampus is PI3-kinase dependent.
Grillo, Brain research 2009 - GeneRIF: These results suggest that insulin-mediated translocation of GLUT4 may provide a mechanism through which hippocampal neurons rapidly increase glucose utilization during increases in neuronal activity associated with hippocampal-dependent learning.
- Impairment of insulin-stimulated Akt/GLUT4 signaling is associated with cardiac contractile dysfunction and aggravates I/R injury in STZ-diabetic rats.
Huang, Journal of biomedical science 2009 - GeneRIF: The STZ-induced insulin deficient & hyperglycemic rat heart showed reduced GLUT4 translocation to plasma membrane associated with cardiac contractile dysfunction.
- MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes.
Horie, Biochemical and biophysical research communications 2009 (PubMed)- GeneRIF: The present results indicated that miR-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiomyocytes.
- Beta-adrenergic activity preserves GLUT4 protein in glycolytic fibers in fasting.
Alves-Wagner, Muscle & nerve 2009 (PubMed)- GeneRIF: GLUT4 gene expression during fasting is regulated by beta-adrenergic activity in skeletal muscle.
- Chemical hypoxia-induced glucose transporter-4 translocation in neonatal rat cardiomyocytes.
Guan, Archives of medical research 2008 (PubMed)- GeneRIF: Azide-induced chemical hypoxia increased glucose uptake and GLUT-4 translocation in neonatal rat cardiomyocytes through a mechanism that at least was partially mediated by AMPK activation.
- Effects of caudal fourth ventricular lactate infusion on hypoglycemia-associated MCT2, GLUT3, GLUT4, GCK, and sulfonylurea receptor-1 gene expression in the ovariectomized female rat LHA and VMH: impact of estradiol.
Vavaiya, Journal of molecular neuroscience : MN 2008 (PubMed)- GeneRIF: Results describe the impact of estradiol on caudal fourth ventricular lactate infusion and hypoglycemia-associated MCT2, GLUT3, GLUT4, GCK, and sulfonylurea receptor-1 gene expression in the ovariectomized female rat lateral and ventromedial hypothalamus.
- The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6.
Roher, Endocrinology 2008 (PubMed)- GeneRIF: TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6.
- Oxidative stress induces GLUT4 translocation by activation of PI3-K/Akt and dual AMPK kinase in cardiac myocytes.
Horie, Journal of cellular physiology 2008 (PubMed)- GeneRIF: These results demonstrate that AMPK and PI3-K/Akt have an additive effect on oxidative stress-mediated GLUT4 translocation.
- Identification of protein kinase D as a novel contraction-activated kinase linked to GLUT4-mediated glucose uptake, independent of AMPK.
Luiken, Cellular signalling 2008 (PubMed)- GeneRIF: Elude to a role of PKD in contraction-induced GLUT4 translocation which does not involve AMPK-alpha2.
- Histone code modifications repress glucose transporter 4 expression in the intrauterine growth-restricted offspring.
Raychaudhuri, The Journal of biological chemistry 2008 - GeneRIF: epigenetic mechanisms consisting of histone code modifications repress skeletal muscle glut4 transcription in the postnatal period and persist in the adult female IUGR offspring
- Effects of continuous low-carbohydrate diet after long-term exercise on GLUT-4 protein content in rat skeletal muscle.
Kubota, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2008 (PubMed)- GeneRIF: The maintenance of glycogen depletion after exercise by continuous low carbohydrate diet results in the increment of the GLUT-4 protein content in skeletal muscle.
- Clathrin-dependent and independent endocytosis of glucose transporter 4 (GLUT4) in myoblasts: regulation by mitochondrial uncoupling.
Antonescu, Traffic (Copenhagen, Denmark) 2008 (PubMed)- GeneRIF: in muscle cells, GLUT4 internalizes simultaneously through clathrin-mediated endocytosis and a caveolae-independent but cholesterol- and dynamin-dependent route
- Alpha-actinin-4 is selectively required for insulin-induced GLUT4 translocation.
Talior-Volodarsky, The Journal of biological chemistry 2008 (PubMed)- GeneRIF: ACTN4 contributes to GLUT4 traffic, likely by tethering GLUT4 vesicles to the cortical actin cytoskeleton
- Lipocalin-type prostaglandin D(2) synthase stimulates glucose transport via enhanced GLUT4 translocation.
Ragolia, Prostaglandins & other lipid mediators 2008 (PubMed)- GeneRIF: L-PGDS, via production of prostaglandin D(2), is an important mediator of muscle and adipose glucose transport which is modulated by glycemic conditions and plays a significant role in the glucose intolerance associated with type 2 diabetes
- CaMK activation during exercise is required for histone hyperacetylation and MEF2A binding at the MEF2 site on the Glut4 gene.
Smith, American journal of physiology. Endocrinology and metabolism 2008 (PubMed)- GeneRIF: exercise increases GLUT4 expression via increased accessibility of MEF2A to its cis-element on the gene
- Decreasing intramuscular phosphagen content simultaneously increases plasma membrane FAT/CD36 and GLUT4 transporter abundance.
Pandke, American journal of physiology. Regulatory, integrative and comparative physiology 2008 (PubMed)- GeneRIF: decline in energy charge was associated with simultaneous increases in both glucose (GLUT4; +33 to 45%, P < 0.01) and FA (FAT/CD36; +28 to 33%, P < 0.05) transporters in the sarcolemma of red and white muscle
- Insulin resistance of pregnancy involves estrogen-induced repression of muscle GLUT4.
Barros, Molecular and cellular endocrinology 2008 (PubMed)- GeneRIF: Insulin resistance of pregnancy involves estrogen-induced repression of muscle GLUT4.
- Muscle cells engage Rab8A and myosin Vb in insulin-dependent GLUT4 translocation.
Ishikura, American journal of physiology. Cell physiology 2008 (PubMed)- GeneRIF: These results support a model whereby AS160, Rab8A, and myosin Vb are required for insulin-induced GLUT4 translocation in muscle cells, potentially as part of a linear signaling cascade.
- Exercise and CaMK activation both increase the binding of MEF2A to the Glut4 promoter in skeletal muscle in vivo.
Smith, American journal of physiology. Endocrinology and metabolism 2007 (PubMed)- GeneRIF: Exercise increases the binding of MEF2A to the Glut4 promoter in vivo.
- Immunogold labeling study of the distribution of GLUT-1 and GLUT-4 in cardiac tissue following stimulation by insulin or ischemia.
Davey, American journal of physiology. Heart and circulatory physiology 2007 (PubMed)- GeneRIF: independent spatial translocation of GLUT-4 occurs under insulin or ischemic stimulation; there may be independent roles for T-tubular and sarcolemmal GLUT-4
- Melatonin protects against oxidative damage and restores expression of GLUT4 gene in the hyperthyroid rat heart.
Ghosh, Journal of pineal research 2007 (PubMed)- GeneRIF: expression reduced in response to T3, completely restored by melatonin and partially by vitamin E
- Redox regulation of ischemic preconditioning is mediated by the differential activation of caveolins and their association with eNOS and GLUT-4.
Koneru, American journal of physiology. Heart and circulatory physiology 2007 (PubMed)- GeneRIF: In conclusion, we demonstrated a novel redox mechanism in IP-induced eNOS and GLUT-4 translocation and the role of caveolar paradox in making the heart euglycemic during the process of ischemia.
- Testicular regulation of neuronal glucose and monocarboxylate transporter gene expression profiles in CNS metabolic sensing sites during acute and recurrent insulin-induced hypoglycemia.
Vavaiya, Journal of molecular neuroscience : MN 2007 (PubMed)- GeneRIF: Data demonstrate site-specific, testes-dependent effects of acute and recurrent hypoglycemia on neuronal Mct2, GLUT3, and GLUT4 gene expression in rat brain metabolic sensing loci.
- Corticosterone impairs insulin-stimulated translocation of GLUT4 in the rat hippocampus.
Piroli, Neuroendocrinology 2007 (PubMed)- GeneRIF: Total GLUT4 levels were reduced in corticosterone-treated rats when compared to controls.
- Bi-directional transport of GLUT4 vesicles near the plasma membrane of primary rat adipocytes.
Xu, Biochemical and biophysical research communications 2007 (PubMed)- GeneRIF: It is likely that there are interactions between insulin signaling and microtubules, to regulating GLUT4 translocation in rat adipocytes.
- Two phases of palmitate-induced insulin resistance in skeletal muscle: impaired GLUT4 translocation is followed by a reduced GLUT4 intrinsic activity.
Alkhateeb, American journal of physiology. Endocrinology and metabolism 2007 (PubMed)- GeneRIF: Our study indicates that palmitate-induced insulin resistance is provoked by two distinct mechanisms.
- Nitric oxide increases GLUT4 expression and regulates AMPK signaling in skeletal muscle.
Lira, American journal of physiology. Endocrinology and metabolism 2007 (PubMed)- GeneRIF: In skeletal muscle, nitric oxide increases GLUT4 expression via a cGMP- and AMPK-dependent mechanism.
- Age related obesity-induced shortening of GLUT4 mRNA poly(A) tail length in rat gastrocnemius skeletal muscle.
Seraphim, Molecular and cellular endocrinology 2007 (PubMed)- GeneRIF: Age related obesity of 12-mo rats involves suppression of GLUT4 expression in adipose tissue; however, in muscle, GLUT4 mRNA content increases, but with a shorter poly(A) tail, thus unchanging the protein content.
- Retinoic acids increase expression of GLUT4 in dedifferentiated and hypertrophied cardiac myocytes.
Montessuit, Basic research in cardiology 2006 (PubMed)- GeneRIF: All-trans and 9-cis retinoic acids restored GLUT4 expression in dedifferentiated adult rat cardiomyocytes, while only 9-cisRA could increase GLUT4 expression in hypertrophic adult rat cardiomyocytes.
- Insulin-dependent interactions of proteins with GLUT4 revealed through stable isotope labeling by amino acids in cell culture (SILAC).
Foster, Journal of proteome research 2006 (PubMed)- GeneRIF: Insulin elicits changes in interactions between diverse proteins and GLUT4.
- Muscle cell depolarization induces a gain in surface GLUT4 via reduced endocytosis independently of AMPK.
Wijesekara, American journal of physiology. Endocrinology and metabolism 2006 (PubMed)- GeneRIF: We propose that K+ depolarization reduces GLUT4 internalization through signals and mechanisms distinct from those engaged by insulin. Such a pathway(s) is largely independent of PI3K, Akt, AMPK, and CaMKII but may involve PKC.
- Low doses of vanadate and Trigonella synergistically regulate Na+/K + -ATPase activity and GLUT4 translocation in alloxan-diabetic rats.
Siddiqui, Molecular and cellular biochemistry 2006 (PubMed)- GeneRIF: Treatment of diabetic rats with insulin, TRIGONELLA FOENUM GRAECUM SEED POWDER (TSP), vanadate and in a combined therapy of lower dose of vanadate with TSP revived normoglycemia and also induced the redistribution of GLUT4 transporter.
- Identification and characterization of p49/STRAP as a novel GLUT4-binding protein.
Lisinski, Biochemical and biophysical research communications 2006 (PubMed)- GeneRIF: 49-kDa protein (p49/STRAP) specifically interacts with an acidic amino acid motif (Q7IGSEDG) in the N-terminus of GLUT4.
- FOXO1 represses peroxisome proliferator-activated receptor-gamma1 and -gamma2 gene promoters in primary adipocytes. A novel paradigm to increase insulin sensitivity.
Armoni, The Journal of biological chemistry 2006 (PubMed)- GeneRIF: Way to increase insulin sensitivity in adipocytes in which FOXO1 repression of PPARgamma leads to GLUT4 derepression/up-regulation.
- Loss of cortical actin filaments in insulin-resistant skeletal muscle cells impairs GLUT4 vesicle trafficking and glucose transport.
McCarthy, American journal of physiology. Cell physiology 2006 - GeneRIF: A component of insulin-induced insulin resistance in skeletal muscle involves defects in PIP(2)/F-actin structure essential for insulin-regulated glucose transport.
- Regulation of GLUT4 gene expression by SREBP-1c in adipocytes.
Im, The Biochemical journal 2006 - GeneRIF: The expression of GLUT4 in response to insulin and fasting/refeeding in adipose tissue and the role of sterol regulatory binding protein-1c (SREBP-1c) in GLUT4 regulation are reported.[SREBP-1c]
- Role of insulin-dependent cortical fodrin/spectrin remodeling in glucose transporter 4 translocation in rat adipocytes.
Liu, Molecular biology of the cell 2006 - GeneRIF: Together, our data suggest that insulin induces remodeling of the fodrin-actin network, which is required for the fusion of GLUT4 storage vesicles with the plasma membrane by permitting their access to the t-SNARE syntaxin 4.
- Metformin increases the PGC-1alpha protein and oxidative enzyme activities possibly via AMPK phosphorylation in skeletal muscle in vivo.
Suwa, Journal of applied physiology (Bethesda, Md. : 1985) 2006 (PubMed)- GeneRIF: These results suggest that metformin enhances the PGC-1alpha expression and mitochondrial biogenesis possibly at least in part via AMPK phosphorylation in the skeletal muscle.
- Creatine feeding increases GLUT4 expression in rat skeletal muscle.
Ju, American journal of physiology. Endocrinology and metabolism 2005 (PubMed)- GeneRIF: Our data suggest that creatine feeding enhances the nuclear content and DNA binding activity of MEF2 isoforms, which is concomitant with an increase in GLUT4 gene expression.
- Insulin and contraction stimulate exocytosis, but increased AMP-activated protein kinase activity resulting from oxidative metabolism stress slows endocytosis of GLUT4 in cardiomyocytes.
Yang, The Journal of biological chemistry 2005 (PubMed)- GeneRIF: endocytosis of GLUT4 in cardiomyocytes is slowed by AMP-activated protein kinase activity resulting from oxidative metabolism stress
- GLUT4 expression and subcellular localization in the intrauterine growth-restricted adult rat female offspring.
Thamotharan, American journal of physiology. Endocrinology and metabolism 2005 (PubMed)- GeneRIF: We speculate that, in utero, GLUT4 aberrations may predict type 2 diabetes mellitus, whereas postnatal nutrient intake may predict obesity, thereby explaining the heterogeneous phenotype of the IUGR adult offspring.
- Reduced insulin-stimulated GLUT4 bioavailability in stroke-prone spontaneously hypertensive rats.
Collison, Diabetologia 2005 (PubMed)- GeneRIF: reduction in bioavailable GLUT4 in the stroke-prone spontaneously hypertensive rat that is likely to account, at least in part, for the reduced insulin-stimulated glucose uptake.
- Calcineurin does not mediate exercise-induced increase in muscle GLUT4.
Garcia-Roves, Diabetes 2005 (PubMed)- GeneRIF: Calcineurin activation does not mediate the adaptive increase in GLUT4 expression induced in skeletal muscle by exercise.
- Depletion of mitochondrial DNA causes impaired glucose utilization and insulin resistance in L6 GLUT4myc myocytes.
Park, The Journal of biological chemistry 2005 (PubMed)- GeneRIF: plasma membrane GLUT4 content and insulin signal pathway intermediates are modulated by the alteration of cellular mtDNA content
- Calorie restriction improves whole-body glucose disposal and insulin resistance in association with the increased adipocyte-specific GLUT4 expression in Otsuka Long-Evans Tokushima fatty rats.
Park, Archives of biochemistry and biophysics 2005 (PubMed)- GeneRIF: Calorie restriction improves whole body glucose disposal and insulin resistance in OLETF rats, and that these effects may associate with increased adipocyte-specific GLUT4 expression
- Insulin stimulates the halting, tethering, and fusion of mobile GLUT4 vesicles in rat adipose cells.
Lizunov, The Journal of cell biology 2005 - GeneRIF: It is likely that the primary mechanism of insulin action in GLUT4 translocation is to stimulate tethering and fusion of trafficking vesicles to specific fusion sites in the PM.
- Maternal food restriction enhances insulin-induced GLUT-4 translocation and insulin signaling pathway in skeletal muscle from suckling rats.
Gavete, Endocrinology 2005 (PubMed)- GeneRIF: The content of the main glucose transporters in muscle, GLUT-4 and GLUT-1, was not affected by undernutrition, but fractionation studies showed an improved insulin-stimulated GLUT-4 translocation.
- Demonstration of differential quantitative requirements for NSF among multiple vesicle fusion pathways of GLUT4 using a dominant-negative ATPase-deficient NSF.
Chen, Biochemical and biophysical research communications 2005 (PubMed)- GeneRIF: Thus, our data demonstrate that the multiple fusion steps in GLUT4 trafficking have differential quantitative requirements for NSF activity.
- Insulin regulates the membrane arrival, fusion, and C-terminal unmasking of glucose transporter-4 via distinct phosphoinositides.
Ishiki, The Journal of biological chemistry 2005 (PubMed)- GeneRIF: Role of class IA phosphatidylinositol (PI) 3-kinase and specific phosphoinositides in the steps of GLUT4 arrival and fusion with the membrane.
- NF-kappaB, MEF2A, MEF2D and HIF1-a involvement on insulin- and contraction-induced regulation of GLUT4 gene expression in soleus muscle.
Silva, Molecular and cellular endocrinology 2005 (PubMed)- GeneRIF: Insulin- and muscle contraction-induced regulation of GLUT4 expression involves transcriptional factors NF-kappaB, MEF2A, MEF2D and HIF1.
- Free fatty acids repress the GLUT4 gene expression in cardiac muscle via novel response elements.
Armoni, The Journal of biological chemistry 2005 (PubMed)- GeneRIF: Hyperlipidemia, exhibited as a high free fatty acid level, modulates GLUT4 gene expression in cardiac muscle via a complex mechanism including GLUT4 and the PPARgamma genes
- Insulin signaling meets vesicle traffic of GLUT4 at a plasma-membrane-activated fusion step.
Koumanov, Cell metabolism 2005 (PubMed)- GeneRIF: Insulin signaling meets vesocle traffic of GLut4 at a plasma-membrane-activated fusion step.
- Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein.
Chou, Journal of biomedical science 2005 (PubMed)- GeneRIF: glycogen overload by postexercise insulin administration significantly abolished the exercise-induced increases in GLUT4 protein and glucose tolerance
- Insulin resistance and GLUT-4 glucose transporter in adipocytes from hypertensive rats.
Chiappe, Metabolism: clinical and experimental 2004 (PubMed)- GeneRIF: a deficient GLUT-4 translocation to plasma membranes in response to insulin shown in adipocytes from SHR, which was accompanied by a decrease in GLUT-4 phosphorylation at serine site, could be one of the causes of insulin resistance in hypertension
- Insulin resistance in adult cardiomyocytes undergoing dedifferentiation: role of GLUT4 expression and translocation.
Rosenblatt-Velin, FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2004 (PubMed)- GeneRIF: The results suggest that transient insulin resistance in ARC is related to impairment of GLUT4 translocation.
- EHD2 interacts with the insulin-responsive glucose transporter (GLUT4) in rat adipocytes and may participate in insulin-induced GLUT4 recruitment.
Park, Biochemistry 2004 (PubMed)- GeneRIF: cellular insulin treatment selectively enhanced interaction with EH-domain containing 3 in an endosomal fraction thought to contain GLUT4 exocytic vesicles
- Disruption of cortical actin in skeletal muscle demonstrates an essential role of the cytoskeleton in glucose transporter 4 translocation in insulin-sensitive tissues.
Brozinick, The Journal of biological chemistry 2004 - GeneRIF: GLUT4 translocation in insulin-sensitive tissues requires cortical actin in the cytoskeleton
- Insulin but not PDGF relies on actin remodeling and on VAMP2 for GLUT4 translocation in myoblasts.
Török, Journal of cell science 2004 (PubMed)- GeneRIF: insulin and PDGF rely differently on the actin cytoskeleton and on tetanus-toxin-sensitive VAMPs for mobilizing GLUT4
- Protein kinase B phosphorylation of PIKfyve regulates the trafficking of GLUT4 vesicles.
Berwick, Journal of cell science 2004 (PubMed)- GeneRIF: Protein kinase B phosphorylation of PIKfyve regulates the trafficking of GLUT4 vesicles
- Effects of AICAR and exercise on insulin-stimulated glucose uptake, signaling, and GLUT-4 content in rat muscles.
Jessen, Journal of applied physiology (Bethesda, Md. : 1985) 2003 (PubMed)- GeneRIF: Chronic AICAR administration and long-term exercise both improve insulin-stimulated glucose transport in skeletal muscle in a fiber-type-specific way. Associated with increase in GLUT-4 content.
- Insulin-induced translocation of facilitative glucose transporters in fetal/neonatal rat skeletal muscle.
He, American journal of physiology. Regulatory, integrative and comparative physiology 2003 (PubMed)- GeneRIF: Insulin-induced translocation of facilitative glucose transporters in fetal/neonatal rat skeletal muscle
- GLUT4 recycles via a trans-Golgi network (TGN) subdomain enriched in Syntaxins 6 and 16 but not TGN38: involvement of an acidic targeting motif.
Shewan, Molecular biology of the cell 2003 - GeneRIF: Data suggest that GLUT4 is transported from the cell surface to a subdomain of the trans-Golgi network that is enriched in syntaxins 6 and 16 and that an acidic targeting motif in the C-terminal tail of GLUT4 plays an important role in this process.
- Maturation of the regulation of GLUT4 activity by p38 MAPK during L6 cell myogenesis.
Niu, The Journal of biological chemistry 2003 (PubMed)- GeneRIF: Regulation of GLUT4 activity by insulin develops upon muscle cell differentiation and correlates with p38 MAPK activation by insulin
- Peroxisome proliferator-activated receptor-gamma represses GLUT4 promoter activity in primary adipocytes, and rosiglitazone alleviates this effect.
Armoni, The Journal of biological chemistry 2003 (PubMed)- GeneRIF: PPARgamma represses transcriptional activity of the GLUT4 promoter via direct and specific binding of PPARgamma/retinoid X receptor-alpha to the GLUT4 promoter.
- Insulin recruits GLUT4 from distinct compartments via distinct traffic pathways with differential microtubule dependence in rat adipocytes.
Liu, The Journal of biological chemistry 2003 (PubMed)- GeneRIF: insulin recruits GLUT4 to the plasma membrane from at least two distinct intracellular compartments
- Prevention of glycogen supercompensation prolongs the increase in muscle GLUT4 after exercise.
Garcia-Roves, American journal of physiology. Endocrinology and metabolism 2003 (PubMed)- GeneRIF: These findings provide evidence that prevention of glycogen supercompensation after exercise results in persistence of exercise-induced increases in GLUT4 protein and enhanced capacity for glycogen supercompensation.
- Sorbitol activates atypical protein kinase C and GLUT4 glucose transporter translocation/glucose transport through proline-rich tyrosine kinase-2, the extracellular signal-regulated kinase pathway and phospholipase D.
Sajan, The Biochemical journal 2002 - GeneRIF: extracellular signal-regulated kinase required for sorbitol-stimulated GLUT4 translocation/glucose transport
- Indinavir inhibits the glucose transporter isoform Glut4 at physiologic concentrations.
Murata, AIDS (London, England) 2002 (PubMed) - Regulation of GLUT4 biogenesis in muscle: evidence for involvement of AMPK and Ca(2+).
Ojuka, American journal of physiology. Endocrinology and metabolism 2002 (PubMed)- GeneRIF: increases in cytosolic Ca(2+) and activation of AMPK, both of which occur in exercising muscle, increase GLUT4 protein in myocytes and skeletal muscle
- Interaction of exercise and diet on GLUT-4 protein and gene expression in Type I and Type II rat skeletal muscle.
Lee, Acta physiologica Scandinavica 2002 (PubMed)- GeneRIF: Interaction of exercise and diet on GLUT-4 protein and gene expression in Type I and Type II rat skeletal muscle.
- Lactate-induced translocation of GLUT1 and GLUT4 is not mediated by the phosphatidyl-inositol-3-kinase pathway in the rat heart.
Medina, Basic research in cardiology 2002 (PubMed)- GeneRIF: Lactate-induced translocation of GLUT1 and GLUT4 is not mediated by the phosphatidyl-inositol-3-kinase pathway in the rat heart.
- Changes in FAT/CD36, UCP2, UCP3 and GLUT4 gene expression during lipid infusion in rat skeletal and heart muscle.
Vettor, International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 2002 (PubMed)- GeneRIF: increased availability of NEFA resulted in a decrease of GLUT4 mRNA in both skeletal and heart muscle
- Terguride treatment attenuated prolactin release and enhanced insulin receptor affinity and GLUT 4 content in obese spontaneously hypertensive female, but not male rats.
Zorad, Annals of the New York Academy of Sciences 2002 (PubMed)- GeneRIF: results document downregulation of insulin receptors and GLUT 4 in obesity and suggest a role for prolactin in obesity-induced insulin resistance, particularly in female rats
- Regulation of glucose transport and transporter 4 (GLUT-4) in muscle and adipocytes of sucrose-fed rats: effects of N-3 poly- and monounsaturated fatty acids.
Peyron-Caso, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2002 (PubMed)- GeneRIF: dietary regulation of Glut-4 proteins appears to be tissue specific and might depend on insulin stimulation and/or duration of dietary interventions
- Expression of insulin-responsive glucose transporter GLUT4 mRNA in the rat brain and spinal cord: an in situ hybridization study.
El, Journal of chemical neuroanatomy 2002 (PubMed)- GeneRIF: post-transcriptional regulation of GLUT4 expression which may depend on the physiological conditions of the animals
- Transient changes in four GLUT4 compartments in rat adipocytes during the transition, insulin-stimulated to basal: implications for the GLUT4 trafficking pathway.
Hah, Biochemistry 2002 (PubMed)- GeneRIF: Okadaic acid-induced GLUT4 recruitment is accompanied by modulation of the rate coefficients linking individual endosomal GLUT4 compartments, demonstrating a significant role of the endosomal pathways in GLUT4 exocytosis.
- PTEN does not modulate GLUT4 translocation in rat adipose cells under physiological conditions.
Mosser, Biochemical and biophysical research communications 2001 (PubMed)- GeneRIF: mouse PTEN does not modulate GLUT4 translocation in rat adipose cells using physiologic insulin stimulation
- A novel functional co-operation between MyoD, MEF2 and TRalpha1 is sufficient for the induction of GLUT4 gene transcription.
Santalucía, Journal of molecular biology 2001 (PubMed)- GeneRIF: functional cooperation between MyoD, MEF2 and TRalpha1 is sufficient for the induction of GLUT4 gene transcription
- Effect of GLP-1 treatment on GLUT2 and GLUT4 expression in type 1 and type 2 rat diabetic models.
Villanueva-Peñacarrillo, Endocrine 2001 (PubMed)- GeneRIF: effect of GLP-1 treatment on GLUT4 expression in type 1 and type 2 rat diabetic models was studied
- Exploring the whereabouts of GLUT4 in skeletal muscle (review).
Ploug, Molecular membrane biology (PubMed)- GeneRIF: Review. GLUT4 biology in skeletal muscle, which is the predominant tissue for glucose homeostasis is compared to results obtained with the fat cell system.
- Glucose transporter content and glucose uptake in skeletal muscle constructs engineered in vitro.
Baker, In vitro cellular & developmental biology. Animal (PubMed)- GeneRIF: GLUT-4 transporter protein content was measured in basal and insulin-stimulated skeletal muscle cells.
- Effect of prolonged intermittent hypoxia and exercise training on glucose tolerance and muscle GLUT4 protein expression in rats.
Chiu, Journal of biomedical science (PubMed)- GeneRIF: muscle GLUT4 protein expression in rats is regulated by hypoxia and exercise training
- Insulin-induced translocation of CD36 to the plasma membrane is reversible and shows similarity to that of GLUT4.
van, Biochimica et biophysica acta (PubMed)- GeneRIF: insulin-induced CD36 translocation was shown to be phosphatidylinositol-3 kinase-dependent, and reversible (as evidenced by insulin wash-out) in a similar time frame as that for GLUT4
- Propolis extract promotes translocation of glucose transporter 4 and glucose uptake through both PI3K- and AMPK-dependent pathways in skeletal muscle.
Ueda, BioFactors (Oxford, England) (PubMed)- GeneRIF: Brazilian propolis has the potential to prevent hyperglycemia through the promotion of GLUT4 translocation in skeletal muscle.
For advice on how to use these tools together, see
Interactive tools for functional annotation of bacterial genomes.
The PaperBLAST database links 793,807 different protein sequences to 1,259,118 scientific articles. Searches against EuropePMC were last performed on March 13 2025.
PaperBLAST builds a database of protein sequences that are linked
to scientific articles. These links come from automated text searches
against the articles in EuropePMC
and from manually-curated information from GeneRIF, UniProtKB/Swiss-Prot,
BRENDA,
CAZy (as made available by dbCAN),
BioLiP,
CharProtDB,
MetaCyc,
EcoCyc,
TCDB,
REBASE,
the Fitness Browser,
and a subset of the European Nucleotide Archive with the /experiment tag.
Given this database and a protein sequence query,
PaperBLAST uses protein-protein BLAST
to find similar sequences with E < 0.001.
To build the database, we query EuropePMC with locus tags, with RefSeq protein
identifiers, and with UniProt
accessions. We obtain the locus tags from RefSeq or from MicrobesOnline. We use
queries of the form "locus_tag AND genus_name" to try to ensure that
the paper is actually discussing that gene. Because EuropePMC indexes
most recent biomedical papers, even if they are not open access, some
of the links may be to papers that you cannot read or that our
computers cannot read. We query each of these identifiers that
appears in the open access part of EuropePMC, as well as every locus
tag that appears in the 500 most-referenced genomes, so that a gene
may appear in the PaperBLAST results even though none of the papers
that mention it are open access. We also incorporate text-mined links
from EuropePMC that link open access articles to UniProt or RefSeq
identifiers. (This yields some additional links because EuropePMC
uses different heuristics for their text mining than we do.)
For every article that mentions a locus tag, a RefSeq protein
identifier, or a UniProt accession, we try to select one or two
snippets of text that refer to the protein. If we cannot get access to
the full text, we try to select a snippet from the abstract, but
unfortunately, unique identifiers such as locus tags are rarely
provided in abstracts.
PaperBLAST also incorporates manually-curated protein functions:
- Proteins from NCBI's RefSeq are included if a
GeneRIF
entry links the gene to an article in
PubMed®.
GeneRIF also provides a short summary of the article's claim about the
protein, which is shown instead of a snippet.
- Proteins from Swiss-Prot (the curated part of UniProt)
are included if the curators
identified experimental evidence for the protein's function (evidence
code ECO:0000269). For these proteins, the fields of the Swiss-Prot entry that
describe the protein's function are shown (with bold headings).
- Proteins from BRENDA,
a curated database of enzymes, are included if they are linked to a paper in PubMed
and their full sequence is known.
- Every protein from the non-redundant subset of
BioLiP,
a database
of ligand-binding sites and catalytic residues in protein structures, is included. Since BioLiP itself
does not include descriptions of the proteins, those are taken from the
Protein Data Bank.
Descriptions from PDB rely on the original submitter of the
structure and cannot be updated by others, so they may be less reliable.
(For SitesBLAST and Sites on a Tree, we use a larger subset of BioLiP so that every
ligand is represented among a group of structures with similar sequences, but for
PaperBLAST, we use the non-redundant set provided by BioLiP.)
- Every protein from EcoCyc, a curated
database of the proteins in Escherichia coli K-12, is included, regardless
of whether they are characterized or not.
- Proteins from the MetaCyc metabolic pathway database
are included if they are linked to a paper in PubMed and their full sequence is known.
- Proteins from the Transport Classification Database (TCDB)
are included if they have known substrate(s), have reference(s),
and are not described as uncharacterized or putative.
(Some of the references are not visible on the PaperBLAST web site.)
- Every protein from CharProtDB,
a database of experimentally characterized protein annotations, is included.
- Proteins from the CAZy database of carbohydrate-active enzymes
are included if they are associated with an Enzyme Classification number.
Even though CAZy does not provide links from individual protein sequences to papers,
these should all be experimentally-characterized proteins.
- Proteins from the REBASE database
of restriction enzymes are included if they have known specificity.
- Every protein with an evidence-based reannotation (based on mutant phenotypes)
in the Fitness Browser is included.
- Sequence-specific transcription factors (including sigma factors and DNA-binding response regulators)
with experimentally-determined DNA binding sites from the
PRODORIC database of gene regulation in prokaryotes.
- Putative transcription factors from RegPrecise
that have manually-curated predictions for their binding sites. These predictions are based on
conserved putative regulatory sites across genomes that contain similar transcription factors,
so PaperBLAST clusters the TFs at 70% identity and retains just one member of each cluster.
- Coding sequence (CDS) features from the
European Nucleotide Archive (ENA)
are included if the /experiment tag is set (implying that there is experimental evidence for the annotation),
the nucleotide entry links to paper(s) in PubMed,
and the nucleotide entry is from the STD data class
(implying that these are targeted annotated sequences, not from shotgun sequencing).
Also, to filter out genes whose transcription or translation was detected, but whose function
was not studied, nucleotide entries or papers with more than 25 such proteins are excluded.
Descriptions from ENA rely on the original submitter of the
sequence and cannot be updated by others, so they may be less reliable.
Except for GeneRIF and ENA,
the curated entries include a short curated
description of the protein's function.
For entries from BioLiP, the protein's function may not be known beyond binding to the ligand.
Many of these entries also link to articles in PubMed.
For more information see the
PaperBLAST paper (mSystems 2017)
or the code.
You can download PaperBLAST's database here.
Changes to PaperBLAST since the paper was written:
- November 2023: incorporated PRODORIC and RegPrecise. Many PRODORIC entries were not linked to a protein sequence (no UniProt identifier), so we added this information.
- February 2023: BioLiP changed their download format. PaperBLAST now includes their non-redundant subset. SitesBLAST and Sites on a Tree use a larger non-redundant subset that ensures that every ligand is represented within each cluster. This should ensure that every binding site is represented.
- June 2022: incorporated some coding sequences from ENA with the /experiment tag.
- March 2022: incorporated BioLiP.
- April 2020: incorporated TCDB.
- April 2019: EuropePMC now returns table entries in their search results. This has expanded PaperBLAST's database, but most of the new entries are of low relevance, and the resulting snippets are often just lists of locus tags with annotations.
- February 2018: the alignment page reports the conservation of the hit's functional sites (if available from from Swiss-Prot or UniProt)
- January 2018: incorporated BRENDA.
- December 2017: incorporated MetaCyc, CharProtDB, CAZy, REBASE, and the reannotations from the Fitness Browser.
- September 2017: EuropePMC no longer returns some table entries in their search results. This has shrunk PaperBLAST's database, but has also reduced the number of low-relevance hits.
Many of these changes are described in Interactive tools for functional annotation of bacterial genomes.
PaperBLAST cannot provide snippets for many of the papers that are
published in non-open-access journals. This limitation applies even if
the paper is marked as "free" on the publisher's web site and is
available in PubmedCentral or EuropePMC. If a journal that you publish
in is marked as "secret," please consider publishing elsewhere.
Many important articles are missing from PaperBLAST, either because
the article's full text is not in EuropePMC (as for many older
articles), or because the paper does not mention a protein identifier such as a locus tag, or because of PaperBLAST's heuristics. If you notice an
article that characterizes a protein's function but is missing from
PaperBLAST, please notify the curators at UniProt
or add an entry to GeneRIF.
Entries in either of these databases will eventually be incorporated
into PaperBLAST. Note that to add an entry to UniProt, you will need
to find the UniProt identifier for the protein. If the protein is not
already in UniProt, you can ask them to create an entry. To add an
entry to GeneRIF, you will need an NCBI Gene identifier, but
unfortunately many prokaryotic proteins in RefSeq do not have
corresponding Gene identifers.
References
PaperBLAST: Text-mining papers for information about homologs.
M. N. Price and A. P. Arkin (2017). mSystems, 10.1128/mSystems.00039-17.
Europe PMC in 2017.
M. Levchenko et al (2017). Nucleic Acids Research, 10.1093/nar/gkx1005.
Gene indexing: characterization and analysis of NLM's GeneRIFs.
J. A. Mitchell et al (2003). AMIA Annu Symp Proc 2003:460-464.
UniProt: the universal protein knowledgebase.
The UniProt Consortium (2016). Nucleic Acids Research, 10.1093/nar/gkw1099.
BRENDA in 2017: new perspectives and new tools in BRENDA.
S. Placzek et al (2017). Nucleic Acids Research, 10.1093/nar/gkw952.
The EcoCyc database: reflecting new knowledge about Escherichia coli K-12.
I. M. Keeseler et al (2016). Nucleic Acids Research, 10.1093/nar/gkw1003.
The MetaCyc database of metabolic pathways and enzymes.
R. Caspi et al (2018). Nucleic Acids Research, 10.1093/nar/gkx935.
CharProtDB: a database of experimentally characterized protein annotations.
R. Madupu et al (2012). Nucleic Acids Research, 10.1093/nar/gkr1133.
The carbohydrate-active enzymes database (CAZy) in 2013.
V. Lombard et al (2014). Nucleic Acids Research, 10.1093/nar/gkt1178.
The Transporter Classification Database (TCDB): recent advances
M. H. Saier, Jr. et al (2016). Nucleic Acids Research, 10.1093/nar/gkv1103.
REBASE - a database for DNA restriction and modification: enzymes, genes and genomes.
R. J. Roberts et al (2015). Nucleic Acids Research, 10.1093/nar/gku1046.
Deep annotation of protein function across diverse bacteria from mutant phenotypes.
M. N. Price et al (2016). bioRxiv, 10.1101/072470.
by Morgan Price,
Arkin group
Lawrence Berkeley National Laboratory