ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Focal adhesion kinase is required for IGF-I-mediated growth of skeletal muscle cells via a TSC2/mTOR/S6K1-associated pathway.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Transcriptomic meta-analysis of disuse muscle atrophy vs. resistance exercise-induced hypertrophy in young and older humans.Journal of cachexia, sarcopenia and muscle · 2021Pooled it
- Synchronous deficits in cumulative muscle protein synthesis and ribosomal biogenesis underlie age-related anabolic resistance to exercise in humans.The Journal of physiology · 2016Trial
- Impaired mTOR/SREBP1-Mediated Lipogenesis as a Mechanism of Hepatic Glycogen Accumulation in a Carnivorous Fish Model, Largemouth Bass (Micropterus salmoides).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Integrin-β1/FAK signaling is involved in electrical stimulation to prevent disuse muscular atrophy induced by tail suspension in mice.BMC musculoskeletal disorders · 2026Article
- Gut microbiota and their metabolites contribute to the heterosis of breast muscle yield in broilers.Journal of animal science and biotechnology · 2026Article
- Load-induced human skeletal muscle hypertrophy: Mechanisms, myths, and misconceptions.Journal of sport and health science · 2025Review
- Identification of Key Candidate Genes for Muscle Growth in Liaoning Black Pigs and Duroc Pigs via Longissimus Dorsi Muscle Transcriptome Analysis.Current issues in molecular biology · 2025Article
- Vitamin K2 Alleviates Insulin Resistance Associated Skeletal Muscle Atrophy via the AKT/mTOR Signalling Pathway.Journal of cachexia, sarcopenia and muscle · 2025Article
- Detrimental Effects of β2-Microglobulin on Muscle Metabolism: Evidence From In Vitro, Animal and Human Research.Journal of cachexia, sarcopenia and muscle · 2025Article
- YAP1 is a key regulator of EWS::FLI1-dependent malignant transformation upon IGF-1-mediated reprogramming of bone mesenchymal stem cells.Cell reports · 2025Article
- Nutritional Interventions to Attenuate Quadriceps Muscle Deficits following Anterior Cruciate Ligament Injury and Reconstruction.Sports medicine (Auckland, N.Z.) · 2025Review
- Strength training and sarcopenia-a mandatory link: focus on MicroRNAs.Frontiers in aging · 2025Review
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- Unlocking the Therapeutic Potential of Irisin: Harnessing Its Function in Degenerative Disorders and Tissue Regeneration.International journal of molecular sciences · 2023Review
- Older postmenopausal women with lower lean mass have hypermethylated sites in the PI3K-Akt pathway.Frontiers in physiology · 2023Article
- Effect of Mechanical Loading of Senescent Myoblasts on Their Myogenic Lineage Progression and Survival.Cells · 2022Article
- Molecular mechanisms of exercise contributing to tissue regeneration.Signal transduction and targeted therapy · 2022Review
- Inter-set stretch: A potential time-efficient strategy for enhancing skeletal muscle adaptations.Frontiers in sports and active living · 2022Review
- Sarcopenia: Etiology, Nutritional Approaches, and miRNAs.International journal of molecular sciences · 2021Review
- JNK activation in TA and EDL muscle is load-dependent in rats receiving identical excitation patterns.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Focal adhesion kinase (FAK) is an attachment complex protein associated with the regulation of muscle mass through as-of-yet unclear mechanisms. We tested whether FAK is functionally important for muscle hypertrophy, with the hypothesis that FAK knockdown (FAK-KD) would impede cell growth associated with a trophic stimulus. C₂C₁₂ skeletal muscle cells harboring FAK-targeted (FAK-KD) or scrambled (SCR) shRNA were created using lentiviral transfection techniques. Both FAK-KD and SCR myotubes were incubated for 24 h with IGF-I (10 ng/ml), and additional SCR cells (±IGF-1) were incubated with a FAK kinase inhibitor before assay of cell growth. Muscle protein synthesis (MPS) and putative FAK signaling mechanisms (immunoblotting and coimmunoprecipitation) were assessed. IGF-I-induced increases in myotube width (+41 ± 7% vs. non-IGF-I-treated) and total protein (+44 ± 6%) were, after 24 h, attenuated in FAK-KD cells, whereas MPS was suppressed in FAK-KD vs. SCR after 4 h. These blunted responses were associated with attenuated IGF-I-induced FAK Tyr³⁹⁷ phosphorylation and markedly suppressed phosphorylation of tuberous sclerosis complex 2 (TSC2) and critical downstream mTOR signaling (ribosomal S6 kinase, eIF4F assembly) in FAK shRNA cells (all P < 0.05 vs. IGF-I-treated SCR cells). However, binding of FAK to TSC2 or its phosphatase Shp-2 was not affected by IGF-I or cell phenotype. Finally, FAK-KD-mediated suppression of cell growth was recapitulated by direct inhibition of FAK kinase activity in SCR cells. We conclude that FAK is required for IGF-I-induced muscle hypertrophy, signaling through a TSC2/mTOR/S6K1-dependent pathway via means requiring the kinase activity of FAK but not altered FAK-TSC2 or FAK-Shp-2 binding.
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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.