ArticleTheranostics2020
Article in Theranostics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
27 citing papers in PubMed, 37 citations in OpenAlex.
- Regeneration programs buffer genetic defects in animal development.PLoS biology · 2026Article
- Fgfr3-Wnt signaling crosstalk is involved in maintaining cranial suture integrity.Bone research · 2026Article
- Evidence-based classification of genes implicated in skeletal disorders using the ClinGen curation framework.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Skeletal Softening inAnimals : an open access journal from MDPI · 2026Article
- Dkk1 inhibition restores mandibular growth in an achondroplasia mouse model.Biology open · 2026Article
- Article
- Advances in the mechanism and therapies of achondroplasia.Genes & diseases · 2025Review
- FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.Cancer communications (London, England) · 2024Review
- IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport.Cellular and molecular life sciences : CMLS · 2024Article
- Review
- METTL3-dependent mCell death & disease · 2024Article
- Infigratinib, a selective FGFR1-3 tyrosine kinase inhibitor, alters dentoalveolar development at high doses.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- The applications of CRISPR/Cas-mediated genome editing in genetic hearing loss.Cell & bioscience · 2023Review
- Ectodermal Wnt signaling, cell fate determination, and polarity of the skate gill arch skeleton.eLife · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Expansion of FGFR3-positive nucleus pulposus cells plays important roles in postnatal nucleus pulposus growth and regeneration.Stem cell research & therapy · 2022Article
- Probiotics Enhance Bone Growth and Rescue BMP Inhibition: New Transgenic Zebrafish Lines to Study Bone Health.International journal of molecular sciences · 2022Article
- PRDM paralogs antagonistically balance Wnt/β-catenin activity during craniofacial chondrocyte differentiation.Development (Cambridge, England) · 2022Article
- Natterin-like depletion by CRISPR/Cas9 impairs zebrafish (Danio rerio) embryonic development.BMC genomics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CATSHL syndrome, characterized by camptodactyly, tall stature and hearing loss, is caused by loss-of-function mutations of fibroblast growth factor receptors 3 (FGFR3) gene. Most manifestations of patients with CATSHL syndrome start to develop in the embryonic stage, such as skeletal overgrowth, craniofacial abnormalities, however, the pathogenesis of these phenotypes especially the early maldevelopment remains incompletely understood. Furthermore, there are no effective therapeutic targets for this skeleton dysplasia.
Indexed as
Identifiers
What OpenQuestion holds
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.