ArticleMolecular biology of the cell2006
Role of insulin-dependent cortical fodrin/spectrin remodeling in glucose transporter 4 translocation in rat adipocytes.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- The Mechanobiology of Adipocyte Hypertrophy: Cytoskeletal Remodelling as a Driver of Insulin Resistance in Obesity.Cell biochemistry and function · 2026Review
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- Assays of Platelet SNARE-actin Interactions.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The fat body cortical actin network regulateseLife · 2023Article
- An AMPK-dependent, non-canonical p53 pathway plays a key role in adipocyte metabolic reprogramming.eLife · 2020Article
- Cavin-1/PTRF mediates insulin-dependent focal adhesion remodeling and ameliorates high-fat diet-induced inflammatory responses in mice.The Journal of biological chemistry · 2019Article
- Exocytosis proteins as novel targets for diabetes prevention and/or remediation?American journal of physiology. Regulatory, integrative and comparative physiology · 2017Review
- Glucose transporter 4 promotes head and neck squamous cell carcinoma metastasis through the TRIM24-DDX58 axis.Journal of hematology & oncology · 2017Article
- Promoting Glucose Transporter-4 Vesicle Trafficking along Cytoskeletal Tracks: PAK-Ing Them Out.Frontiers in endocrinology · 2017Review
- PTRF/Cavin-1 promotes efficient ribosomal RNA transcription in response to metabolic challenges.eLife · 2016Article
- System model network for adipose tissue signatures related to weight changes in response to calorie restriction and subsequent weight maintenance.PLoS computational biology · 2015Article
- Article
- Signaling mechanisms of glucose-induced F-actin remodeling in pancreatic islet β cells.Experimental & molecular medicine · 2013Review
- Identification of P-Rex1 as a novel Rac1-guanine nucleotide exchange factor (GEF) that promotes actin remodeling and GLUT4 protein trafficking in adipocytes.The Journal of biological chemistry · 2011Article
- Real Time FRET Based Detection of Mechanical Stress in Cytoskeletal and Extracellular Matrix Proteins.Cellular and molecular bioengineering · 2011Article
- Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis.Trends in endocrinology and metabolism: TEM · 2011Review
- The platelet actin cytoskeleton associates with SNAREs and participates in alpha-granule secretion.Biochemistry · 2010Article
- Exocytosis mechanisms underlying insulin release and glucose uptake: conserved roles for Munc18c and syntaxin 4.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Review
- Insulin-regulated glucagon-like peptide-1 release from L cells: actin' out.Endocrinology · 2009Article
- Identification of a distal GLUT4 trafficking event controlled by actin polymerization.Molecular biology of the cell · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Fodrin or nonerythroid spectrin is an abundant component of the cortical cytoskeletal network in rat adipocytes. Fodrin has a highly punctate distribution in resting cells, and insulin causes a dramatic remodeling of fodrin to a more diffuse pattern. Insulin-mediated remodeling of actin occurs to a lesser extent than does that of fodrin. We show that fodrin interacts with the t-soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) syntaxin 4, and this interaction is increased by insulin stimulation and decreased by prior latrunculin A treatment. Latrunculin A disrupts all actin filaments, inhibits glucose transporter 4 (GLUT4) translocation, and causes fodrin to partially redistribute from the plasma membrane to the cytosol. In contrast, cytochalasin D disrupts only the short actin filament signal, and cytochalasin D neither inhibits GLUT4 translocation nor fodrin redistribution in adipocytes. Together, our data suggest that insulin induces remodeling of the fodrin-actin network, which is required for the fusion of GLUT4 storage vesicles with the plasma membrane by permitting their access to the t-SNARE syntaxin 4.
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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.