ArticleMolecular biology of the cell2008
Molecular mechanisms controlling GLUT4 intracellular retention.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
- Canonical and Alternative Pathways (Insulin and Exercise) of GLUT4 Synthesis, Signaling, Intracellular Clustering, and Recruitment to the Plasma Membrane.International journal of molecular sciences · 2026Review
- Lysosomal down-regulation of the mu opioid receptor is opposed by the Retromer complex.Science advances · 2026Article
- Neuronal activity-induced GLUT3 plasma translocation supports energy demands for memory acquisition.Communications biology · 2025Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- Regulated dynamic subcellular GLUT4 localization revealed by proximal proteome mapping in human muscle cells.Journal of cell science · 2023Article
- Methods to Quantify the Dynamic Recycling of Plasma Membrane Channels.Bio-protocol · 2023Article
- A Glimpse into Milestones of Insulin Resistance and an Updated Review of Its Management.Nutrients · 2023Review
- SNARE-binding protein synaptosomal-associated protein of 29 kDa (SNAP29) regulates the intracellular sequestration of glucose transporter 4 (GLUT4) vesicles in adipocytes.Journal of diabetes investigation · 2023Article
- GLUT4 translocation and dispersal operate in multiple cell types and are negatively correlated with cell size in adipocytes.Scientific reports · 2022Article
- Cryo-EM structure of human glucose transporter GLUT4.Nature communications · 2022Article
- AAGAB is an assembly chaperone regulating AP1 and AP2 clathrin adaptors.Journal of cell science · 2021Article
- Sequencing refractory regions in bird genomes are hotspots for accelerated protein evolution.BMC ecology and evolution · 2021Article
- Insulin-promoted mobilization of GLUT4 from a perinuclear storage site requires RAB10.Molecular biology of the cell · 2021Article
- Structure, function and regulation of mammalian glucose transporters of the SLC2 family.Pflugers Archiv : European journal of physiology · 2020Review
- BAG6 contributes to glucose uptake by supporting the cell surface translocation of the glucose transporter GLUT4.Biology open · 2020Article
- CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis.The Journal of cell biology · 2020Article
- Functional Characterization of Facilitative Glucose Transporter 4 With a Delay Responding to Plasma Glucose Level in Blunt Snout Bream (Frontiers in physiology · 2020Article
- Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019Review
- Functional and structural analysis of rare SLC2A2 variants associated with Fanconi-Bickel syndrome and metabolic traits.Human mutation · 2019Article
- Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin.Cell reports · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In basal adipocytes, glucose transporter 4 (GLUT4) is sequestered intracellularly by an insulin-reversible retention mechanism. Here, we analyze the roles of three GLUT4 trafficking motifs (FQQI, TELEY, and LL), providing molecular links between insulin signaling, cellular trafficking machinery, and the motifs in the specialized trafficking of GLUT4. Our results support a GLUT4 retention model that involves two linked intracellular cycles: one between endosomes and a retention compartment, and the other between endosomes and specialized GLUT4 transport vesicles. Targeting of GLUT4 to the former is dependent on the FQQI motif and its targeting to the latter is dependent on the TELEY motif. These two motifs act independently in retention, with the TELEY-dependent step being under the control of signaling downstream of the AS160 rab GTPase activating protein. Segregation of GLUT4 from endosomes, although positively correlated with the degree of basal retention, does not completely account for GLUT4 retention or insulin-responsiveness. Mutation of the LL motif slows return to basal intracellular retention after insulin withdrawal. Knockdown of clathrin adaptin protein complex-1 (AP-1) causes a delay in the return to intracellular retention after insulin withdrawal. The effects of mutating the LL motif and knockdown of AP-1 were not additive, establishing that AP-1 regulation of GLUT4 trafficking requires the LL motif.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.