ArticleJournal of cellular physiology2009
Dystrophin glycoprotein complex-associated Gbetagamma subunits activate phosphatidylinositol-3-kinase/Akt signaling in skeletal muscle in a laminin-dependent manner.
Article in Journal of cellular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
- Obestatin Treatment Counteracts Muscle Wasting by Reactivation of Autophagy in Duchenne Muscular Dystrophy.MedComm · 2026Article
- miR-190 is a Key Regulator in Establishing Cell Polarity and Specification in the Drosophila Nervous System.bioRxiv : the preprint server for biology · 2025Article
- Review
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Transcriptome-wide RNA m6A methylation profiles in an endemic osteoarthropathy, Kashin-Beck disease.Journal of cellular and molecular medicine · 2024Article
- Leucyl-tRNA Synthetase Contributes to Muscle Weakness through Mammalian Target of Rapamycin Complex 1 Activation and Autophagy Suppression in a Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2024Article
- The BALB/c.mdx62 mouse exhibits a dystrophic muscle pathology and is a model of Duchenne muscular dystrophy.Disease models & mechanisms · 2024Article
- Therapeutic Efficacy of Medicinal Plants with Allopathic Medicine in Musculoskeletal Diseases.International journal of plant, animal and environmental sciences · 2024Article
- Signaling through the dystrophin glycoprotein complex affects the stress-dependent transcriptome in Drosophila.Disease models & mechanisms · 2023Article
- Defective autophagy and increased apoptosis contribute toward the pathogenesis of FKRP-associated muscular dystrophies.Stem cell reports · 2021Article
- Bioactive potential of natural biomaterials: identification, retention and assessment of biological properties.Signal transduction and targeted therapy · 2021Review
- Duchenne muscular dystrophy.Nature reviews. Disease primers · 2021Review
- Spatiotemporal Mapping Reveals Regional Gastrointestinal Dysfunction in mdx Dystrophic Mice Ameliorated by Oral L-arginine Supplementation.Journal of neurogastroenterology and motility · 2020Article
- Gene expression profile of muscle adaptation to high-intensity intermittent exercise training in young men.Scientific reports · 2018Article
- Follicular Stimulating Hormone Accelerates Atherogenesis by Increasing Endothelial VCAM-1 Expression.Theranostics · 2017Article
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- Resistance exercise increases active MMP and β1-integrin protein expression in skeletal muscle.Physiological reports · 2014Article
- Immobilization and therapeutic passive stretching generate thickening and increase the expression of laminin and dystrophin in skeletal muscle.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Article
- Stress-induced ECM alteration modulates cellular microRNAs that feedback to readjust the extracellular environment and cell behavior.Frontiers in genetics · 2013Review
- Autophagy is Impaired in the Tibialis Anterior of Dystrophin Null Mice.PLoS currents · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Previously, we showed that laminin-binding to the dystrophin glycoprotein complex (DGC) of skeletal muscle causes a heterotrimeric G-protein (Galphabetagamma) to bind, changing the activation state of the Gsalpha subunit. Others have shown that laminin-binding to the DGC also leads to Akt activation. Gbetagamma, released when Gsalpha is activated, is known to bind phosphatidylinositol-3-kinase (PI3K), which activates Akt in other cells. Here, we investigate whether muscle Akt activation results from Gbetagamma, using immunoprecipitation and immunoblotting, and purified Gbetagamma. In the presence of laminin, PI3K-binding to the DGC increases and Akt becomes phosphorylated and activated (pAkt), and glycogen synthase kinase is phosphorylated. Antibodies, which specifically block laminin-binding to alpha-dystroglycan, prevent PI3K-binding to the DGC. Purified bovine brain Gbetagamma also caused PI3K and Akt activation. These results show that DGC-Gbetagamma is binding PI3K and activating pAkt in a laminin-dependent manner. Mdx mice, which have greatly diminished amounts of DGC proteins, display elevated pAkt signaling and increased expression of integrin beta1 compared to normal muscle. This integrin binds laminin, Gbetagamma, and PI3K. Collectively, these suggest that PI3K is an important target for the Gbetagamma, which normally binds to DGC syntrophin, and activates PI3K/Akt signaling. Disruption of the DGC in mdx mouse is causing dis-regulation of the laminin-DGC-Gbetagamma-PI3K-Akt signaling and is likely to be important to the pathogenesis of muscular dystrophy. Upregulating integrin beta1 expression and activating the PI3K/Akt pathway in muscular dystrophy may partially compensate for the loss of the DGC. The results suggest new therapeutic approaches to muscle disease.
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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.