ArticleThe Journal of cell biology1998
The FGF receptor-1 tyrosine kinase domain regulates myogenesis but is not sufficient to stimulate proliferation.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 37 citations in OpenAlex.
- State-Dependent FGF Signaling in Satellite Cell-Mediated Skeletal Muscle Regeneration and Pathological Remodeling.Biomolecules · 2026Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this mapReview
- Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration.Skeletal muscle · 2016Article
- p38 MAPK signaling underlies a cell-autonomous loss of stem cell self-renewal in skeletal muscle of aged mice.Nature medicine · 2014Article
- The aged niche disrupts muscle stem cell quiescence.Nature · 2012Article
- The myogenic kinome: protein kinases critical to mammalian skeletal myogenesis.Skeletal muscle · 2011Article
- Reciprocal inhibition between Pax7 and muscle regulatory factors modulates myogenic cell fate determination.The Journal of cell biology · 2007Article
- Fibroblast growth factor 2 induced proliferation in osteoblasts and bone marrow stromal cells: a whole cell model.Biophysical journal · 2006Article
- Sprouty-2 overexpression in C2C12 cells confers myogenic differentiation properties in the presence of FGF2.Molecular biology of the cell · 2005Article
- Article
- Role of SHP-2 in fibroblast growth factor receptor-mediated suppression of myogenesis in C2C12 myoblasts.Molecular and cellular biology · 2002Article
- Atypical protein kinase Cs are the Ras effectors that mediate repression of myogenic satellite cell differentiation.Molecular and cellular biology · 2002Article
- Oncogenic Ras-induced proliferation requires autocrine fibroblast growth factor 2 signaling in skeletal muscle cells.The Journal of cell biology · 2001Article
- Regulation of myogenesis by fibroblast growth factors requires beta-gamma subunits of pertussis toxin-sensitive G proteins.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ligand-stimulated activation of FGF receptors (FGFRs) in skeletal muscle cells represses terminal myogenic differentiation. Skeletal muscle cell lines and subsets of primary cells are dependent on FGFs to repress myogenesis and maintain growth. To understand the intracellular events that transduce these signals, MM14 skeletal muscle cells were transfected with expression vectors encoding chimeric receptors. The chimeras are comprised of the PDGF beta receptor (PDGFbetaR) extracellular domain, the FGFR-1 intracellular domain, and either the PDGFbetaR or FGFR-1 transmembrane domain. The chimeric receptors were autophosphorylated upon PDGF-BB stimulation and are capable of stimulating mitogen-activated protein kinase activity. Activation of the tyrosine kinase domain of either chimera repressed myogenesis, suggesting intracellular responses regulating skeletal muscle differentiation are transduced by activation of the FGFR-1 tyrosine kinase. Unexpectedly, we found that activation of either chimeric receptor failed to stimulate cellular proliferation. Thus, it appears that regulation of skeletal muscle differentiation by FGFs requires only activation of the FGFR tyrosine kinase. In contrast, stimulation of proliferation may require additional, as yet unidentified, signals involving the receptor ectodomain, the FGF ligand, and heparan sulfate either alone, or in combination.
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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.