ArticleGenes & development2001
TGF-beta inhibits muscle differentiation through functional repression of myogenic transcription factors by Smad3.
Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
187 citing papers in PubMed, 395 citations in OpenAlex.
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- Smad2/3 Signaling Mediates the Atrophic Response in Vocal Fold Myoblasts In Vitro.The Laryngoscope · 2026Article
- Aberrant skeletal muscle morphogenesis and myofiber differentiation characterize equine myotonic dystrophy.PloS one · 2026Article
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- Decellularized Extracellular Matrix-Derived Hydrogels: a Powerful Class of Biomaterials for Skeletal Muscle Regenerative Engineering Applications.Regenerative engineering and translational medicine · 2025Article
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment.Frontiers in oncology · 2025Review
- Optimisation of cell fate determination for cultivated muscle differentiation.Communications biology · 2024Article
- Regulatory Role ofInternational journal of molecular sciences · 2024Article
- Exploring the Integrated Role of miRNAs and lncRNAs in Regulating the Transcriptional Response to Amino Acids and Insulin-like Growth Factor 1 in Gilthead Sea Bream (International journal of molecular sciences · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- LEDT and Idebenone treatment modulate autophagy and improve regenerative capacity in the dystrophic muscle through an AMPK-pathway.PloS one · 2024Article
- Skeletal muscle regeneration failure in ischemic-damaged limbs is associated with pro-inflammatory macrophages and premature differentiation of satellite cells.Genome medicine · 2023Article
- SPSB1-mediated inhibition of TGF-β receptor-II impairs myogenesis in inflammation.Journal of cachexia, sarcopenia and muscle · 2023Article
127 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) is a potent inhibitor of skeletal muscle differentiation, but the molecular mechanism and signaling events that lead to this inhibition are poorly characterized. Here we show that the TGF-beta intracellular effector Smad3, but not Smad2, mediates the inhibition of myogenic differentiation in MyoD-expressing C3H10T1/2 cells and C2C12 myoblasts by repressing the activity of the MyoD family of transcriptional factors. The Smad3-mediated repression was directed at the E-box sequence motif within muscle gene enhancers and the bHLH region of MyoD, the domain required for its association with E-protein partners such as E12 and E47. The repression could be overcome by supplying an excess of E12, and covalent tethering of E47 to MyoD rendered the E-box-dependent transcriptional activity refractory to the effects of Smad3 and TGF-beta. Smad3 physically interacted with the HLH domain of MyoD, and this interaction correlated with the ability of Smad3 to interfere with MyoD/E protein heterodimerization and binding of MyoD complexes to oligomerized E-box sites. Together, these results reveal a model for how TGF-beta, through Smad3-mediated transcriptional repression, inhibits myogenic differentiation.
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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.