ArticleMolecular biology of the cell2010
Identification of three distinct functional sites of insulin-mediated GLUT4 trafficking in adipocytes using quantitative single molecule imaging.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 67 citations in OpenAlex.
- WNKs regulate mouse behavior and alter central nervous system glucose uptake and insulin signaling.bioRxiv : the preprint server for biology · 2025Article
- Advanced optical microscopy methods forBiophysical reviews · 2025Review
- Hypoglycemia and hyperinsulinemia induced by phenolic uremic toxins in CKD and DKD patients.Scientific reports · 2025Article
- LRRK2 negatively regulates glucose tolerance via regulation of membrane translocation of GLUT4 in adipocytes.FEBS open bio · 2023Article
- GLUT4 dispersal at the plasma membrane of adipocytes: a super-resolved journey.Bioscience reports · 2023Review
- Article
- p300 or CBP is required for insulin-stimulated glucose uptake in skeletal muscle and adipocytes.JCI insight · 2022Article
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- Super-Resolution Live Cell Microscopy of Membrane-Proximal Fluorophores.International journal of molecular sciences · 2020Article
- BAG6 contributes to glucose uptake by supporting the cell surface translocation of the glucose transporter GLUT4.Biology open · 2020Article
- Article
- Cooperative actions of Tbc1d1 and AS160/Tbc1d4 in GLUT4-trafficking activities.The Journal of biological chemistry · 2019Article
- Action of Phytochemicals on Insulin Signaling Pathways Accelerating Glucose Transporter (GLUT4) Protein Translocation.Molecules (Basel, Switzerland) · 2018Review
- Bright Dots and Smart Optical Microscopy to Probe Intracellular Events in Single Cells.Frontiers in bioengineering and biotechnology · 2018Review
- Heterotypic endosomal fusion as an initial trigger for insulin-induced glucose transporter 4 (GLUT4) translocation in skeletal muscle.The Journal of physiology · 2017Article
- Live-cell single-molecule labeling and analysis of myosin motors with quantum dots.Molecular biology of the cell · 2017Article
- Skeletal muscle tissue engineering: methods to form skeletal myotubes and their applications.Tissue engineering. Part B, Reviews · 2014Review
- Dynamic GLUT4 sorting through a syntaxin-6 compartment in muscle cells is derailed by insulin resistance-causing ceramide.Biology open · 2014Article
- Single quantum dot tracking reveals that an individual multivalent HIV-1 Tat protein transduction domain can activate machinery for lateral transport and endocytosis.Molecular and cellular biology · 2013Article
- Specialized sorting of GLUT4 and its recruitment to the cell surface are independently regulated by distinct Rabs.Molecular biology of the cell · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin stimulation of glucose uptake is achieved by redistribution of insulin-responsive glucose transporters, GLUT4, from intracellular storage compartment(s) to the plasma membrane in adipocytes and muscle cells. Although GLUT4 translocation has been investigated using various approaches, GLUT4 trafficking properties within the cell are largely unknown. Our novel method allows direct analysis of intracellular GLUT4 dynamics at the single molecule level by using Quantum dot technology, quantitatively establishing the behavioral nature of GLUT4. Our data demonstrate the predominant mechanism for intracellular GLUT4 sequestration in the basal state to be "static retention" in fully differentiated 3T3L1 adipocytes. We also directly defined three distinct insulin-stimulated GLUT4 trafficking processes: 1) release from the putative GLUT4 anchoring system in storage compartment(s), 2) the speed at which transport GLUT4-containing vesicles move, and 3) the tethering/docking steps at the plasma membrane. Intriguingly, insulin-induced GLUT4 liberation from its static state appeared to be abolished by either pretreatment with an inhibitor of phosphatidylinositol 3-kinase or overexpression of a dominant-interfering AS160 mutant (AS160/T642A). In addition, our novel approach revealed the possibility that, in certain insulin-resistant states, derangements in GLUT4 behavior can impair insulin-responsive GLUT4 translocation.
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Registered trials
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.