ReviewThe Yale journal of biology and medicine2019
GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking.
Review in The Yale journal of biology and medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Adipocyte-Derived KIF13B Aggravates Obesity-Associated Metabolic Dysfunction via LRP1/PPARγ Signaling.MedComm · 2026Article
- 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
- Proteomic Analysis of Regulated Dendritic Cell Endosomes Reveals Dynamic Adaptation to Antigen Uptake and Cross-Presentation.European journal of immunology · 2026Article
- Unconventional Protein Transport Across the Golgi Ribbon.Sub-cellular biochemistry · 2026Review
- Inhibition of Unc119b improves insulin sensitivity through potentiation of Rac1 activation in skeletal muscle and brown adipose tissue.Molecular metabolism · 2025Article
- 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
- Proteomic Characterization of Human Peripheral Blood Mononuclear Cells Exposed to a 50 Hz Magnetic Field.International journal of molecular sciences · 2025Article
- Exploration of Conserved Human Adipose Subpopulations Using Targeted Single-Nuclei RNA Sequencing Data Sets.Journal of the American Heart Association · 2025Article
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Nature immunology · 2024Article
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Research square · 2024Article
- Plasma catestatin levels are related to metabolic parameters in patients with essential hypertension and type 2 diabetes mellitus.Heart and vessels · 2024Article
- The role of STAT3/VAV3 in glucolipid metabolism during the development of HFD-induced MAFLD.International journal of biological sciences · 2024Article
- Roles of ubiquitin-specific proteases in inflammatory diseases.Frontiers in immunology · 2024Review
- Monoamine oxidase mediated oxidative stress: a potential molecular and biochemical crux in the pathogenesis of obesity.Molecular biology reports · 2023Review
- Insulin sensitization by small molecules enhancing GLUT4 translocation.Cell chemical biology · 2023Article
- Review
- Article
- Extracellular Vesicles and Their Emerging Roles as Cellular Messengers in Endocrinology: An Endocrine Society Scientific Statement.Endocrine reviews · 2022Article
- Medium-chain fatty acids enhance expression and histone acetylation of genes related to lipid metabolism in insulin-resistant adipocytes.Biochemistry and biophysics reports · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Fat and muscle cells contain a specialized, intracellular organelle known as the GLUT4 storage vesicle (GSV). Insulin stimulation mobilizes GSVs, so that these vesicles fuse at the cell surface and insert GLUT4 glucose transporters into the plasma membrane. This example is likely one instance of a broader paradigm for regulated, non-secretory exocytosis, in which intracellular vesicles are translocated in response to diverse extracellular stimuli. GSVs have been studied extensively, yet these vesicles remain enigmatic. Data support the view that in unstimulated cells, GSVs are present as a pool of preformed small vesicles, which are distinct from endosomes and other membrane-bound organelles. In adipocytes, GSVs contain specific cargoes including GLUT4, IRAP, LRP1, and sortilin. They are formed by membrane budding, involving sortilin and probably CHC22 clathrin in humans, but the donor compartment from which these vesicles form remains uncertain. In unstimulated cells, GSVs are trapped by TUG proteins near the endoplasmic reticulum - Golgi intermediate compartment (ERGIC). Insulin signals through two main pathways to mobilize these vesicles. Signaling by the Akt kinase modulates Rab GTPases to target the GSVs to the cell surface. Signaling by the Rho-family GTPase TC10α stimulates Usp25m-mediated TUG cleavage to liberate the vesicles from the Golgi. Cleavage produces a ubiquitin-like protein modifier, TUGUL, that links the GSVs to KIF5B kinesin motors to promote their movement to the cell surface. In obesity, attenuation of these processes results in insulin resistance and contributes to type 2 diabetes and may simultaneously contribute to hypertension and dyslipidemia in the metabolic syndrome.
Indexed as
Identifiers
31543708PMC6747935W2980356421What Socratic holds
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 Socratic graph.