ArticleThe EMBO journal2004
Entry of newly synthesized GLUT4 into the insulin-responsive storage compartment is GGA dependent.
Article in The EMBO journal, 2004. 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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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
50 citing papers in PubMed, 109 citations in OpenAlex.
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
- Integrated analysis of the adipocyte plasma membrane proteome reveals KCC1 and PIT2 as novel insulin-responsive transporters.The Journal of biological chemistry · 2026Article
- Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes.Bulletin of mathematical biology · 2025Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- Akt may associate with insulin-responsive vesicles via interaction with sortilin.FEBS letters · 2024Article
- Regulated dynamic subcellular GLUT4 localization revealed by proximal proteome mapping in human muscle cells.Journal of cell science · 2023Article
- Cryo-EM structure of human glucose transporter GLUT4.Nature communications · 2022Article
- GLUT4 On the move.The Biochemical journal · 2022Article
- The WD40-Repeat Protein WDR-20 and the Deubiquitinating Enzyme USP-46 Promote Cell Surface Levels of Glutamate Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- GRAF2, WDR44, and MICAL1 mediate Rab8/10/11-dependent export of E-cadherin, MMP14, and CFTR ΔF508.The Journal of cell biology · 2020Article
- CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis.The Journal of cell biology · 2020Article
- GLUT4 Storage Vesicles: Specialized Organelles for Regulated Trafficking.The Yale journal of biology and medicine · 2019Review
- Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019Review
- Ent3 and GGA adaptors facilitate diverse anterograde and retrograde trafficking events to and from the prevacuolar endosome.Scientific reports · 2019Article
- The deubiquitinating enzyme USP25 binds tankyrase and regulates trafficking of the facilitative glucose transporter GLUT4 in adipocytes.Scientific reports · 2019Article
- Chemical biology probes of mammalian GLUT structure and function.The Biochemical journal · 2018Review
- CHC22 and CHC17 clathrins have distinct biochemical properties and display differential regulation and function.The Journal of biological chemistry · 2017Article
- Sortilin 1 knockout alters basal adipose glucose metabolism but not diet-induced obesity in mice.FEBS letters · 2017Article
- Trans, trans-farnesol as a mevalonate-derived inducer of murine 3T3-F442A pre-adipocyte differentiation.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Tumor necrosis factor (TNF)-α-induced repression of GKAP42 protein levels through cGMP-dependent kinase (cGK)-Iα causes insulin resistance in 3T3-L1 adipocytes.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Following biosynthesis, both GLUT1 and VSV-G proteins appear rapidly (2-3 h) at the plasma membrane, whereas GLUT4 is retained in intracellular membrane compartments and does not display any significant insulin responsiveness until 6-9 h. Surprisingly, the acquisition of insulin responsiveness did not require plasma membrane endocytosis, as expression of a dominant-interfering dynamin mutant (Dyn/K44A) had no effect on the insulin-stimulated GLUT4 translocation. Furthermore, expression of endocytosis-defective GLUT4 mutants or continuous surface labeling with an exofacial specific antibody demonstrated that GLUT4 did not transit the cell surface prior to the acquisition of insulin responsiveness. The expression of a dominant-interfering GGA mutant (VHS-GAT) had no effect on the trafficking of newly synthesized GLUT1 or VSV-G protein to the plasma membrane, but completely blocked the insulin-stimulated translocation of newly synthesized GLUT4. Furthermore, in vitro budding of GLUT4 vesicles but not GLUT1 or the transferrin receptor was inhibited by VHS-GAT. Together, these data demonstrate that following biosynthesis, GLUT4 directly sorts and traffics to the insulin-responsive storage compartment through a specific GGA-sensitive process.
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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.