ArticleProceedings of the National Academy of Sciences of the United States of America2004
Defective lysosomal targeting of activated fibroblast growth factor receptor 3 in achondroplasia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 111 citations in OpenAlex.
- Advances in the mechanism and therapies of achondroplasia.Genes & diseases · 2025Review
- Cell-based screen identifies porphyrins as FGFR3 activity inhibitors with therapeutic potential for achondroplasia and cancer.JCI insight · 2023Article
- Review
- Advantages and Disadvantages of Different Treatment Methods in Achondroplasia: A Review.International journal of molecular sciences · 2021Review
- Precise base editing for theeLife · 2021Article
- DNA and RNA sequencing identified a novel oncogene VPS35 in liver hepatocellular carcinoma.Oncogene · 2020Article
- Endocytosis and Transport of Growth Factor Receptors in Peripheral Axon Regeneration: Novel Lessons from Neurons Expressing Lysine-Deficient FGF Receptor Type 1 in vitro.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
- Crosstalk between p38 and Erk 1/2 in Downregulation of FGF1-Induced Signaling.International journal of molecular sciences · 2019Article
- Impairment of the transition from proliferative stage to prehypertrophic stage in chondrogenic differentiation of human induced pluripotent stem cells harboring the causative mutation of achondroplasia in fibroblast growth factor receptor 3.Regenerative therapy · 2017Article
- Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Review
- Synergistic interaction between the fibroblast growth factor and bone morphogenetic protein signaling pathways in lens cells.Molecular biology of the cell · 2015Article
- Article
- Fibroblast growth factor receptor 3 activation plays a causative role in urothelial cancer pathogenesis in cooperation with Pten loss in mice.The Journal of pathology · 2014Article
- Primary and secondary dimer interfaces of the fibroblast growth factor receptor 3 transmembrane domain: characterization via multiscale molecular dynamics simulations.Biochemistry · 2014Article
- Functional roles of fibroblast growth factor receptors (FGFRs) signaling in human cancers.Apoptosis : an international journal on programmed cell death · 2013Review
- Structure of FGFR3 transmembrane domain dimer: implications for signaling and human pathologies.Structure (London, England : 1993) · 2013Article
- Integrative modelling of the influence of MAPK network on cancer cell fate decision.PLoS computational biology · 2013Article
- Multiple consequences of a single amino acid pathogenic RTK mutation: the A391E mutation in FGFR3.PloS one · 2013Article
- Physical-chemical principles underlying RTK activation, and their implications for human disease.Biochimica et biophysica acta · 2012Review
- Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias.Human mutation · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of fibroblast growth factor receptor 3 (FGFR3) are responsible for achondroplasia (ACH) and related dwarfing conditions in humans. The pathogenesis involves constitutive activation of FGFR3, which inhibits proliferation and differentiation of growth plate chondrocytes. Here we report that activating mutations in FGFR3 increase the stability of the receptor. Our results suggest that the mutations disrupt c-Cbl-mediated ubiquitination that serves as a targeting signal for lysosomal degradation and termination of receptor signaling. The defect allows diversion of actively signaling receptors from lysosomes to a recycling pathway where their survival is prolonged, and, as a result, their signaling capacity is increased. The lysosomal targeting defect is additive to other mechanisms proposed to explain the pathogenesis of ACH.
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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 Socratic graph.