ArticleThe Journal of biological chemistry2004
Disruption of cortical actin in skeletal muscle demonstrates an essential role of the cytoskeleton in glucose transporter 4 translocation in insulin-sensitive tissues.
Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 121 citations in OpenAlex.
- Trial
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- The Rho guanine dissociation inhibitor α inhibits skeletal muscle Rac1 activity and insulin action.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Insulin signalling and GLUT4 trafficking in insulin resistance.Biochemical Society transactions · 2023Review
- Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.eLife · 2023Article
- Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake.The Journal of physiology · 2022Review
- Gene deletion of γ-actin impairs insulin-stimulated skeletal muscle glucose uptake in growing mice but not in mature adult mice.Physiological reports · 2022Article
- p300 or CBP is required for insulin-stimulated glucose uptake in skeletal muscle and adipocytes.JCI insight · 2022Article
- Changes in Skeletal Muscle PAK1 Levels Regulate Tissue Crosstalk to Impact Whole Body Glucose Homeostasis.Frontiers in endocrinology · 2022Article
- Tmod3 Phosphorylation Mediates AMPK-Dependent GLUT4 Plasma Membrane Insertion in Myoblasts.Frontiers in endocrinology · 2021Article
- Computational Assessment of Transport Distances in Living Skeletal Muscle Fibers Studied In Situ.Biophysical journal · 2020Article
- β-catenin regulates muscle glucose transport via actin remodelling and M-cadherin binding.Molecular metabolism · 2020Article
- Excess membrane cholesterol is an early contributing reversible aspect of skeletal muscle insulin resistance in C57BL/6NJ mice fed a Western-style high-fat diet.American journal of physiology. Endocrinology and metabolism · 2019Article
- β-Actin shows limited mobility and is required only for supraphysiological insulin-stimulated glucose transport in young adult soleus muscle.American journal of physiology. Endocrinology and metabolism · 2018Article
- Characterization of the CLASP2 Protein Interaction Network Identifies SOGA1 as a Microtubule-Associated Protein.Molecular & cellular proteomics : MCP · 2017Article
- Exercise training prevents skeletal muscle plasma membrane cholesterol accumulation, cortical actin filament loss, and insulin resistance in C57BL/6J mice fed a western-style high-fat diet.Physiological reports · 2017Article
- Exercise-stimulated glucose uptake - regulation and implications for glycaemic control.Nature reviews. Endocrinology · 2017Review
- Promoting Glucose Transporter-4 Vesicle Trafficking along Cytoskeletal Tracks: PAK-Ing Them Out.Frontiers in endocrinology · 2017Review
- An actin filament population defined by the tropomyosin Tpm3.1 regulates glucose uptake.Traffic (Copenhagen, Denmark) · 2015Article
- Lipid-overloaded enlarged adipocytes provoke insulin resistance independent of inflammation.Molecular and cellular biology · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cell culture work suggests that signaling to polymerize cortical filamentous actin (F-actin) represents a required pathway for the optimal redistribution of the insulin-responsive glucose transporter, GLUT4, to the plasma membrane. Recent in vitro study further suggests that the actin-regulatory neural Wiskott-Aldrich syndrome protein (N-WASP) mediates the effect of insulin on the actin filament network. Here we tested whether similar cytoskeletal mechanics are essential for insulin-regulated glucose transport in isolated rat epitrochlearis skeletal muscle. Microscopic analysis revealed that cortical F-actin is markedly diminished in muscle exposed to latrunculin B. Depolymerization of cortical F-actin with latrunculin B caused a time- and concentration-dependent decline in 2-deoxyglucose transport. The loss of cortical F-actin and glucose transport was paralleled by a decline in insulin-stimulated GLUT4 translocation, as assessed by photolabeling of cell surface GLUT4 with Bio-LC-ATB-BMPA. Although latrunculin B impaired insulin-stimulated GLUT4 translocation and glucose transport, activation of phosphatidylinositol 3-kinase and Akt by insulin was not rendered ineffective. In contrast, the ability of insulin to elicit the cortical F-actin localization of N-WASP was abrogated. These data provide the first evidence that actin cytoskeletal mechanics are an essential feature of the glucose transport process in intact skeletal muscle. Furthermore, these findings support a distal actin-based role for N-WASP in insulin action in vivo.
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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.