ArticleiScience2022
Three live-imaging techniques for comprehensively understanding the initial trigger for insulin-responsive intracellular GLUT4 trafficking.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- GULP1 enhances GLUT4 translocation by counteracting ACAP1-ARF6 inhibition.Nutrition & diabetes · 2026Article
- Advanced optical microscopy methods forBiophysical reviews · 2025Review
- Boron-containing compounds as labels, drugs, and theranostic agents for diabetes and its complications.World journal of diabetes · 2024Article
- GLUT4 dispersal at the plasma membrane of adipocytes: a super-resolved journey.Bioscience reports · 2023Review
- Single-molecule analysis of intracellular insulin granule behavior and its application to analyzing cytoskeletal dependence and pathophysiological implications.Frontiers in physiology · 2023Article
- Ubiquitin-like processing of TUG proteins as a mechanism to regulate glucose uptake and energy metabolism in fat and muscle.Frontiers in endocrinology · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Quantitative features of GLUT4 glucose transporter's behavior deep inside cells remain largely unknown. Our previous analyses with live-cell imaging of intracellular GLUT4 trafficking demonstrated two crucial early events responsible for triggering insulin-responsive translocation processes, namely, heterotypic fusion and liberation. To quantify the regulation, interrelationships, and dynamics of the initial events more accurately and comprehensively, we herein applied three analyses, each based on our distinct dual-color live-cell imaging approaches. With these approaches, heterotypic fusion was found to be the first trigger for insulin-responsive GLUT4 redistributions, preceding liberation, and to be critically regulated by Akt substrate of 160 kDa (AS160) and actin dynamics. In addition, demonstrating the subcellular regional dependence of GLUT4 dynamics revealed that liberated GLUT4 molecules are promptly incorporated into the trafficking itinerary of transferrin receptors. Our approaches highlight the physiological significance of endosomal "GLUT4 molecule trafficking" rather than "GLUT4 vesicle delivery" to the plasma membrane in response to insulin.
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