ArticleProceedings of the National Academy of Sciences of the United States of America2007
Dissociation of the insulin receptor and caveolin-1 complex by ganglioside GM3 in the state of insulin resistance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.
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Who cites it
173 citing papers in PubMed, 379 citations in OpenAlex.
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- Insulin receptor trafficking and interactions in muscle cells.Journal of the Endocrine Society · 2026Article
- Gangliosides in molecular interactions and cell regulation.The Journal of biological chemistry · 2026Review
- Lipids regulate epidermal growth factor receptor activation by its ligands.Biochemical Society transactions · 2026Review
- SPR interaction analysis of GM3 glycan with the integrin α5β1 head domain.Glycoconjugate journal · 2026Article
- Electrostatic Interaction Analysis Between GM3 and Insulin Receptor.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Gangliosides and Membrane Microdomains.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Fructose uptake by brown adipose tissue is independent of carbohydrate response element-binding protein and does not cause elevatedActa biochimica et biophysica Sinica · 2025Article
- Gangliosides modulate the secretion of extracellular vesicles and their misfolded protein cargo.Science advances · 2025Article
- Effects of GM1 ganglioside and its derivatives on ETI-rescued F508del-CFTR maturation and host-pathogen interactions in cystic fibrosis bronchial cells.Glycoconjugate journal · 2025Article
- The enzyme SMPDL3b in podocytes decouples proteinuria from chronic kidney disease progression in experimental Alport Syndrome.Kidney international · 2025Article
- When ganglioside pathways go awry: congenital disorders and experimental insights.Journal of human genetics · 2025Review
- Regulation and function of insulin and insulin-like growth factor receptor signalling.Nature reviews. Molecular cell biology · 2025Review
- HEXA-FC protein therapy increases skeletal muscle glucose uptake and improves glycaemic control in mice with insulin resistance and in a mouse model of type 2 diabetes.Diabetologia · 2025Article
- Regulation of the terminal complement cascade in adipose tissue for control of its volume, cellularity, and fibrosis.Obesity (Silver Spring, Md.) · 2025Review
- Review
- Thieno[2,3-International journal of molecular sciences · 2025Article
- Glycolipidomics of Liver Flukes and Host Tissues during Fascioliasis: Insights from Mass Spectrometry Imaging.ACS infectious diseases · 2024Article
113 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membrane microdomains (lipid rafts) are now recognized as critical for proper compartmentalization of insulin signaling. We previously demonstrated that, in adipocytes in a state of TNFalpha-induced insulin resistance, the inhibition of insulin metabolic signaling and the elimination of insulin receptors (IR) from the caveolae microdomains were associated with an accumulation of the ganglioside GM3. To gain insight into molecular mechanisms behind interactions of IR, caveolin-1 (Cav1), and GM3 in adipocytes, we have performed immunoprecipitations, cross-linking studies of IR and GM3, and live cell studies using total internal reflection fluorescence microscopy and fluorescence recovery after photobleaching techniques. We found that (i) IR form complexes with Cav1 and GM3 independently; (ii) in GM3-enriched membranes the mobility of IR is increased by dissociation of the IR-Cav1 interaction; and (iii) the lysine residue localized just above the transmembrane domain of the IR beta-subunit is essential for the interaction of IR with GM3. Because insulin metabolic signal transduction in adipocytes is known to be critically dependent on caveolae, we propose a pathological feature of insulin resistance in adipocytes caused by dissociation of the IR-Cav1 complex by the interactions of IR with GM3 in microdomains.
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