ArticleScientific reports2017
Knock-in human FGFR3 achondroplasia mutation as a mouse model for human skeletal dysplasia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- C-Type Natriuretic Peptide Derivatives: Orthopaedic Implications in Achondroplasia.Journal of the Pediatric Orthopaedic Society of North America · 2026Review
- Functional Independence Assessment in Children and Adolescents with Achondroplasia: A Multicenter Cross-Sectional Study Using the WeeFIM Scale.Diagnostics (Basel, Switzerland) · 2025Article
- Phosphorylation-Dependent Regulation of Guanylyl Cyclase (GC)-A and Other Membrane GC Receptors.Endocrine reviews · 2024Review
- The IFITM5 mutation in osteogenesis imperfecta type V is associated with an ERK/SOX9-dependent osteoprogenitor differentiation defect.The Journal of clinical investigation · 2024Article
- Cell-based screen identifies porphyrins as FGFR3 activity inhibitors with therapeutic potential for achondroplasia and cancer.JCI insight · 2023Article
- Why Animal Experiments Are Still Indispensable in Bone Research: A Statement by the European Calcified Tissue Society.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Review
- Hypochondroplasia gain-of-function mutation in FGFR3 causes defective bone mineralization in mice.JCI insight · 2023Article
- Guanylyl Cyclase-B Dependent Bone Formation in Mice is Associated with Youth, Increased Osteoblasts, and Decreased Osteoclasts.Calcified tissue international · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Epitope-tagged and phosphomimetic mouse models for investigating natriuretic peptide-stimulated receptor guanylyl cyclases.Frontiers in molecular neuroscience · 2022Article
- Uncovering pathways regulating chondrogenic differentiation of CHH fibroblasts.Non-coding RNA research · 2021Article
- Article
- The RNA helicase Ddx52 functions as a growth switch in juvenile zebrafish.Development (Cambridge, England) · 2021Article
- Computational prediction of small molecules with predicted binding to FGFR3 and testing biological effects in bone cells.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Article
- Prevention of guanylyl cyclase-B dephosphorylation rescues achondroplastic dwarfism.JCI insight · 2021Article
- The Regulation of Growth in Developing, Homeostatic, and Regenerating Tetrapod Limbs: A Minireview.Frontiers in cell and developmental biology · 2021Review
- Chronic testicular Chlamydia muridarum infection impairs mouse fertility and offspring development†.Biology of reproduction · 2020Article
- A review of genetics of nasal development and morphological variation.Journal of family medicine and primary care · 2020Review
- New developments in the management of achondroplasia.Wiener medizinische Wochenschrift (1946) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Achondroplasia (ACH), the most common genetic dwarfism in human, is caused by a gain-of function mutation in fibroblast growth factor receptor 3 (FGFR3). Currently, there is no effective treatment for ACH. The development of an appropriate human-relevant model is important for testing potential therapeutic interventions before human clinical trials. Here, we have generated an ACH mouse model in which the endogenous mouse Fgfr3 gene was replaced with human FGFR3
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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.