ArticleThe Journal of cell biology2011
Dual-mode of insulin action controls GLUT4 vesicle exocytosis.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 131 citations in OpenAlex.
- A primordial synaptotagmin-independent function of complexin in regulated exocytosis.Nature communications · 2026Article
- Altered Molecular Regulation of TUG Is a Central Feature of Insulin-Resistant Human Adipose Tissue.Diabetes · 2026Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- TUG protein acts through a disordered region to organize the early secretory pathway.Nature communications · 2025Article
- Fibroblasts secrete fibronectin under lamellipodia in a microtubule- and myosin II-dependent fashion.The Journal of cell biology · 2023Article
- Use of Ecto-Tagged Integrins to Monitor Integrin Exocytosis and Endocytosis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Inhibitors of RNA and protein synthesis cause Glut4 translocation and increase glucose uptake in adipocytes.Scientific reports · 2022Article
- Sulfated Fucogalactan FromFrontiers in endocrinology · 2022Article
- Development and Application of Automatized Routines for Optical Analysis of Synaptic Activity Evoked by Chemical and Electrical Stimulation.Frontiers in bioinformatics · 2022Article
- Ubiquitin-like processing of TUG proteins as a mechanism to regulate glucose uptake and energy metabolism in fat and muscle.Frontiers in endocrinology · 2022Review
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- An active tethering mechanism controls the fate of vesicles.Nature communications · 2021Article
- Insulin-stimulated endoproteolytic TUG cleavage links energy expenditure with glucose uptake.Nature metabolism · 2021Article
- Effects of Polyphenols on Insulin Resistance.Nutrients · 2020Review
- Mutations in the exocyst component EXOC2 cause severe defects in human brain development.The Journal of experimental medicine · 2020Article
- Genetic evidence for an inhibitory role of tomosyn in insulin-stimulated GLUT4 exocytosis.Traffic (Copenhagen, Denmark) · 2020Article
- Structure, function and regulation of mammalian glucose transporters of the SLC2 family.Pflugers Archiv : European journal of physiology · 2020Review
- Tumor protein D54 defines a new class of intracellular transport vesicles.The Journal of cell biology · 2020Article
- Article
- A Recent Achievement In the Discovery and Development of Novel Targets for the Treatment of Type-2 Diabetes Mellitus.Journal of experimental pharmacology · 2020Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Insulin stimulates translocation of GLUT4 storage vesicles (GSVs) to the surface of adipocytes, but precisely where insulin acts is controversial. Here we quantify the size, dynamics, and frequency of single vesicle exocytosis in 3T3-L1 adipocytes. We use a new GSV reporter, VAMP2-pHluorin, and bypass insulin signaling by disrupting the GLUT4-retention protein TUG. Remarkably, in unstimulated TUG-depleted cells, the exocytic rate is similar to that in insulin-stimulated control cells. In TUG-depleted cells, insulin triggers a transient, twofold burst of exocytosis. Surprisingly, insulin promotes fusion pore expansion, blocked by acute perturbation of phospholipase D, which reflects both properties intrinsic to the mobilized vesicles and a novel regulatory site at the fusion pore itself. Prolonged stimulation causes cargo to switch from approximately 60 nm GSVs to larger exocytic vesicles characteristic of endosomes. Our results support a model whereby insulin promotes exocytic flux primarily by releasing an intracellular brake, but also by accelerating plasma membrane fusion and switching vesicle traffic between two distinct circuits.
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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.