ArticleBiochemistry. Biokhimiia2011
Cortactin, an actin binding protein, regulates GLUT4 translocation via actin filament remodeling.
Article in Biochemistry. Biokhimiia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Alterations of actin in aging.Journal of cell science · 2026Review
- Review
- Cytochalasans and Their Impact on Actin Filament Remodeling.Biomolecules · 2023Review
- Review
- Cortactin Is Required for Efficient FAK, Src and Abl Tyrosine Kinase Activation and Phosphorylation ofInternational journal of molecular sciences · 2021Article
- β-catenin regulates muscle glucose transport via actin remodelling and M-cadherin binding.Molecular metabolism · 2020Article
- Comparative Transcriptome and Methylome Analysis in Human Skeletal Muscle Anabolism, Hypertrophy and Epigenetic Memory.Scientific reports · 2019Article
- Multisite Phosphorylation of S6K1 Directs a Kinase Phospho-code that Determines Substrate Selection.Molecular cell · 2019Article
- The actin-related p41ARC subunit contributes to p21-activated kinase-1 (PAK1)-mediated glucose uptake into skeletal muscle cells.The Journal of biological chemistry · 2017Article
- Dynamin-2 mutations linked to Centronuclear Myopathy impair actin-dependent trafficking in muscle cells.Scientific reports · 2017Article
- Promoting Glucose Transporter-4 Vesicle Trafficking along Cytoskeletal Tracks: PAK-Ing Them Out.Frontiers in endocrinology · 2017Review
- Cortactin Mediates Apoptosis of Gastric Epithelial Cells Induced by VacA Protein of Helicobacter pylori.Digestive diseases and sciences · 2016Article
- Signaling of the p21-activated kinase (PAK1) coordinates insulin-stimulated actin remodeling and glucose uptake in skeletal muscle cells.Biochemical pharmacology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Insulin regulates glucose uptake into fat and skeletal muscle cells by modulating the translocation of GLUT4 between the cell surface and interior. We investigated a role for cortactin, a cortical actin binding protein, in the actin filament organization and translocation of GLUT4 in Chinese hamster ovary (CHO-GLUT4myc) and L6-GLUT4myc myotube cells. Overexpression of wild-type cortactin enhanced insulin-stimulated GLUT4myc translocation but did not alter actin fiber formation. Conversely, cortactin mutants lacking the Src homology 3 (SH3) domain inhibited insulin-stimulated formation of actin stress fibers and GLUT4 translocation similar to the actin depolymerizing agent cytochalasin D. Wortmannin, genistein, and a PP1 analog completely blocked insulin-induced Akt phosphorylation, formation of actin stress fibers, and GLUT4 translocation indicating the involvement of both PI3-K/Akt and the Src family of kinases. The effect of these inhibitors was even more pronounced in the presence of overexpressed cortactin suggesting that the same pathways are involved. Knockdown of cortactin by siRNA did not inhibit insulin-induced Akt phosphorylation but completely inhibited actin stress fiber formation and glucose uptake. These results suggest that the actin binding protein cortactin is required for actin stress fiber formation in muscle cells and that this process is absolutely required for translocation of GLUT4-containing vesicles to the plasma membrane.
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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 Socratic graph.