ArticleMolecular biology of the cell2012
Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- The unconventional regulation of non-muscle myosins.Biophysical reviews · 2026Article
- Mechanosensitive interactions between Jag1 and Myo1c control Jag1 trafficking in endothelial cells.iScience · 2025Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Myosin-1C augments endothelial secretion of von Willebrand factor by linking contractile actomyosin machinery to the plasma membrane.Blood advances · 2024Article
- A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling.Oncogene · 2024Article
- Flow cytometry protocol for GLUT4-myc detection on cell surfaces.Bioscience reports · 2024Article
- Membrane-bound myosin IC drives the chiral rotation of the gliding actin filament around its longitudinal axis.Scientific reports · 2023Article
- Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice.Nature communications · 2023Article
- SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C.Cell death & disease · 2022Article
- Distinct actin-tropomyosin cofilament populations drive the functional diversification of cytoskeletal myosin motor complexes.iScience · 2022Article
- Review
- MYH10 Governs Adipocyte Function and Adipogenesis through Its Interaction with GLUT4.International journal of molecular sciences · 2022Article
- GLUT4 On the move.The Biochemical journal · 2022Article
- Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function.Cells · 2021Article
- Current understanding of glucose transporter 4 expression and functional mechanisms.World journal of biological chemistry · 2020Review
- Putting the brakes on a myosin motor.The Journal of biological chemistry · 2020Article
- The regulatory protein 14-3-3β binds to the IQ motifs of myosin-IC independent of phosphorylation.The Journal of biological chemistry · 2020Article
- BAG6 contributes to glucose uptake by supporting the cell surface translocation of the glucose transporter GLUT4.Biology open · 2020Article
- Downregulation of MYO1C mediated by cepharanthine inhibits autophagosome-lysosome fusion through blockade of the F-actin network.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
GLUT4-containing vesicles cycle between the plasma membrane and intracellular compartments. Insulin promotes GLUT4 exocytosis by regulating GLUT4 vesicle arrival at the cell periphery and its subsequent tethering, docking, and fusion with the plasma membrane. The molecular machinery involved in GLUT4 vesicle tethering is unknown. We show here that Myo1c, an actin-based motor protein that associates with membranes and actin filaments, is required for insulin-induced vesicle tethering in muscle cells. Myo1c was found to associate with both mobile and tethered GLUT4 vesicles and to be required for vesicle capture in the total internal reflection fluorescence (TIRF) zone beneath the plasma membrane. Myo1c knockdown or overexpression of an actin binding-deficient Myo1c mutant abolished insulin-induced vesicle immobilization, increased GLUT4 vesicle velocity in the TIRF zone, and prevented their externalization. Conversely, Myo1c overexpression immobilized GLUT4 vesicles in the TIRF zone and promoted insulin-induced GLUT4 exposure to the extracellular milieu. Myo1c also contributed to insulin-dependent actin filament remodeling. Thus we propose that interaction of vesicular Myo1c with cortical actin filaments is required for insulin-mediated tethering of GLUT4 vesicles and for efficient GLUT4 surface delivery in muscle cells.
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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.