ArticleMolecular biology of the cell2001
Insulin-regulated release from the endosomal recycling compartment is regulated by budding of specialized vesicles.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Who cites it
56 citing papers in PubMed, 129 citations in OpenAlex.
- Article
- Regulated dynamic subcellular GLUT4 localization revealed by proximal proteome mapping in human muscle cells.Journal of cell science · 2023Article
- Influence of Protein Carbonylation on Human Adipose Tissue Dysfunction in Obesity and Insulin Resistance.Biomedicines · 2022Article
- Insulin-promoted mobilization of GLUT4 from a perinuclear storage site requires RAB10.Molecular biology of the cell · 2021Article
- Article
- Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019Review
- AMPA Receptor Trafficking for Postsynaptic Potentiation.Frontiers in cellular neuroscience · 2018Review
- Article
- Adenovirus Protein E4-ORF1 Activation of PI3 Kinase Reveals Differential Regulation of Downstream Effector Pathways in Adipocytes.Cell reports · 2016Article
- SEC16A is a RAB10 effector required for insulin-stimulated GLUT4 trafficking in adipocytes.The Journal of cell biology · 2016Article
- Disruption of Adipose Rab10-Dependent Insulin Signaling Causes Hepatic Insulin Resistance.Diabetes · 2016Article
- Charge-mediated influence of the antibody variable domain on FcRn-dependent pharmacokinetics.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Influenza Virus Induces Cholesterol-Enriched Endocytic Recycling Compartments for Budozone Formation via Cell Cycle-Independent Centrosome Maturation.PLoS pathogens · 2015Article
- Identification of novel insulin mimetic drugs by quantitative total internal reflection fluorescence (TIRF) microscopy.British journal of pharmacology · 2014Article
- A naturally occurring GIP receptor variant undergoes enhanced agonist-induced desensitization, which impairs GIP control of adipose insulin sensitivity.Molecular and cellular biology · 2014Article
- Rab5 activity regulates GLUT4 sorting into insulin-responsive and non-insulin-responsive endosomal compartments: a potential mechanism for development of insulin resistance.Endocrinology · 2014Article
- Insulin-regulated Glut4 translocation: membrane protein trafficking with six distinctive steps.The Journal of biological chemistry · 2014Article
- Αvβ3-integrin-mediated adhesion is regulated through an AAK1L- and EHD3-dependent rapid-recycling pathway.Journal of cell science · 2013Article
- Specialized sorting of GLUT4 and its recruitment to the cell surface are independently regulated by distinct Rabs.Molecular biology of the cell · 2013Article
- Notch signaling from the endosome requires a conserved dileucine motif.Molecular biology of the cell · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
In several cell types, specific membrane proteins are retained intracellularly and rapidly redistributed to the surface in response to stimulation. In fat and muscle, the GLUT4 glucose transporter is dynamically retained because it is rapidly internalized and slowly recycled to the plasma membrane. Insulin increases the recycling of GLUT4, resulting in a net translocation to the surface. We have shown that fibroblasts also have an insulin-regulated recycling mechanism. Here we show that GLUT4 is retained within the transferrin receptor-containing general endosomal recycling compartment in Chinese hamster ovary (CHO) cells rather than being segregated to a specialized, GLUT4-recycling compartment. With the use of total internal reflection microscopy, we demonstrate that the TR and GLUT4 are transported from the pericentriolar recycling compartment in separate vesicles. These data provide the first functional evidence for the formation of distinct classes of vesicles from the recycling compartment. We propose that GLUT4 is dynamically retained within the endosomal recycling compartment in CHO cells because it is concentrated in vesicles that form more slowly than those that transport TR. In 3T3-L1 adipocytes, cells that naturally express GLUT4, we find that GLUT4 is partially segregated to a separate compartment that is inaccessible to the TR. We present a model for the formation of this specialized compartment in fat cells, based on the general mechanism described in CHO cells, which may explain the increased retention of GLUT4 and its insulin-induced translocation in fat 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.