ArticleProceedings of the National Academy of Sciences of the United States of America2007
Skeletal overgrowth is mediated by deficiency in a specific isoform of fibroblast growth factor receptor 3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 56 citations in OpenAlex.
- Review
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- Exercise improves subchondral bone microenvironment through regulating bone-cartilage crosstalk.Frontiers in endocrinology · 2023Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Article
- Evaluation of the Radial Procurvatum Using the Center of Rotation of Angulation Methodology in Chondrodystrophic Dogs.Frontiers in veterinary science · 2021Article
- The Regulation of Growth in Developing, Homeostatic, and Regenerating Tetrapod Limbs: A Minireview.Frontiers in cell and developmental biology · 2021Review
- Dog as a Model for Osteoarthritis: The FGF4 Retrogene Insertion May Matter.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019Article
- Mouse Models of Syndromic Craniosynostosis.Molecular syndromology · 2019Review
- Prioritization of Candidate Genes for Congenital Diaphragmatic Hernia in a Critical Region on Chromosome 4p16 using a Machine-Learning Algorithm.Journal of pediatric genetics · 2018Article
- Phosphoproteomics of Fibroblast Growth Factor 1 (FGF1) Signaling in Chondrocytes: Identifying the Signature of Inhibitory Response.Molecular & cellular proteomics : MCP · 2017Article
- Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Review
- FGFR3 deficient mice have accelerated fracture repair.International journal of biological sciences · 2017Article
- Chondrocyte FGFR3 Regulates Bone Mass by Inhibiting Osteogenesis.The Journal of biological chemistry · 2016Article
- Genetic insights into the mechanisms of Fgf signaling.Genes & development · 2016Review
- Role of Genetic Factors in the Pathogenesis of Radial Deficiencies in Humans.Current genomics · 2015Article
- Fibroblast growth factor signaling in skeletal development and disease.Genes & development · 2015Review
- Mutant activated FGFR3 impairs endochondral bone growth by preventing SOX9 downregulation in differentiating chondrocytes.Human molecular genetics · 2015Article
- Recent research on the growth plate: Recent insights into the regulation of the growth plate.Journal of molecular endocrinology · 2014Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor receptor 3 (FGFR3) plays an important role in the control of chondrocyte proliferation and differentiation, a process critical for normal development of the skeleton. To reveal the contributions of the epithelial Fgfr3b isoform and the mesenchymal Fgfr3c isoform to skeletal overgrowth seen in mice, in which both isoforms have been inactivated (Fgf3c(-/-) mice), we have generated mice in which each of the two Fgfr3 isoforms has been selectively inactivated. Whereas no apparent phenotype was detected in Fgfr3b(-/-) mice, strong stimulation of chondrocyte proliferation in the growth plates of Fgf3c(-/-) mice caused dramatic skeletal overgrowth and other skeletal abnormalities resembling the phenotype of mice deficient in both Fgfr3 isoforms. In addition, Fgfr3c(-/-) mice exhibited decreased bone mineral density in the cortical and trabecular bone, whereas the bone mineral density of Fgfr3b(-/-) mice resembled that of WT mice. These experiments demonstrated that the mesenchymal Fgfr3c isoform is responsible for controlling chondrocyte proliferation and differentiation that mediate normal skeletal development, whereas the epithelial Fgfr3b isoform does not contribute toward this process.
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