ArticleBiochimica et biophysica acta2014
FGFR3 induces degradation of BMP type I receptor to regulate skeletal development.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- GREM1 acts in leptin receptor-expressing skeletal cells to mediate peri-implant fibrosis.Nature communications · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Achondroplasia: aligning mouse model with human clinical studies shows crucial importance of immediate postnatal start of the therapy.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- The role of E3 ubiquitin ligases in bone homeostasis and related diseases.Acta pharmaceutica Sinica. B · 2023Review
- Wnt signaling: Essential roles in osteoblast differentiation, bone metabolism and therapeutic implications for bone and skeletal disorders.Genes & diseases · 2023Review
- Article
- A registry of achondroplasia: a 6-year experience from the Czechia and Slovak Republic.Orphanet journal of rare diseases · 2022Article
- Article
- Targeting local lymphatics to ameliorate heterotopic ossification via FGFR3-BMPR1a pathway.Nature communications · 2021Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Progress of orthopaedic research in China over the last decade.Journal of orthopaedic translation · 2020Article
- Patterns of Geographical and Potential Adaptive Divergence in the Genome of the Common Carp (Frontiers in genetics · 2019Article
- TGF-β Family Signaling in Mesenchymal Differentiation.Cold Spring Harbor perspectives in biology · 2018Review
- Reprogramming of Dermal Fibroblasts into Osteo-Chondrogenic Cells with Elevated Osteogenic Potency by Defined Transcription Factors.Stem cell reports · 2017Article
- Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Review
- Developmental Regulation of the Growth Plate and Cranial Synchondrosis.Journal of dental research · 2016Review
- Exome sequencing identified FGF12 as a novel candidate gene for Kashin-Beck disease.Functional & integrative genomics · 2016Article
- TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease.Bone research · 2016Review
- Article
- Fibroblast growth factor signaling in skeletal development and disease.Genes & development · 2015Review
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factors (FGFs) and their receptors (FGFRs) play significant roles in vertebrate organogenesis and morphogenesis. FGFR3 is a negative regulator of chondrogenesis and multiple mutations with constitutive activity of FGFR3 result in achondroplasia, one of the most common dwarfisms in humans, but the molecular mechanism remains elusive. In this study, we found that chondrocyte-specific deletion of BMP type I receptor a (Bmpr1a) rescued the bone overgrowth phenotype observed in Fgfr3 deficient mice by reducing chondrocyte differentiation. Consistently, using in vitro chondrogenic differentiation assay system, we demonstrated that FGFR3 inhibited BMPR1a-mediated chondrogenic differentiation. Furthermore, we showed that FGFR3 hyper-activation resulted in impaired BMP signaling in chondrocytes of mouse growth plates. We also found that FGFR3 inhibited BMP-2- or constitutively activated BMPR1-induced phosphorylation of Smads through a mechanism independent of its tyrosine kinase activity. We found that FGFR3 facilitates BMPR1a to degradation through Smurf1-mediated ubiquitination pathway. We demonstrated that down-regulation of BMP signaling by BMPR1 inhibitor dorsomorphin led to the retardation of chondrogenic differentiation, which mimics the effect of FGF-2 on chondrocytes and BMP-2 treatment partially rescued the retarded growth of cultured bone rudiments from thanatophoric dysplasia type II mice. Our findings reveal that FGFR3 promotes the degradation of BMPR1a, which plays an important role in the pathogenesis of FGFR3-related skeletal dysplasia.
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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.