ArticleDisease models & mechanisms2018
Increased FGF8 signaling promotes chondrogenic rather than osteogenic development in the embryonic skull.
Article in Disease models & mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- FGF8-mediated TRIM16 regulation promotes K48-linked ubiquitination and degradation of RIG-I to facilitate Influenza a virus immune evasion.Virulence · 2026Article
- Intermittent intra-articular delivery of FGF8b enhances cartilage homeostasis and attenuates osteoarthritis progression.Journal of orthopaedic translation · 2026Article
- A head start: The relationship of placental factors to craniofacial and brain development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- Cranium growth, patterning and homeostasis.Development (Cambridge, England) · 2022Article
- Disrupted tenogenesis in masseter as a potential cause of micrognathia.International journal of oral science · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- The role of fibroblast growth factor 8 in cartilage development and disease.Journal of cellular and molecular medicine · 2022Review
- Skeletal Deformities in Osterix-Cre;Tgfbr2Genes · 2021Article
- Control of mesenchymal cell fate via application of FGF-8b in vitro.Stem cell research · 2021Article
- Dlx5-augmentation in neural crest cells reveals early development and differentiation potential of mouse apical head mesenchyme.Scientific reports · 2021Article
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
- Cranial Neural Crest Cells and Their Role in the Pathogenesis of Craniofacial Anomalies and Coronal Craniosynostosis.Journal of developmental biology · 2020Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Catalytically inactive Dnmt3b rescues mouse embryonic development by accessory and repressive functions.Nature communications · 2019Article
- The molecular anatomy of mammalian upper lip and primary palate fusion at single cell resolution.Development (Cambridge, England) · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The bones of the cranial vault are formed directly from mesenchymal cells through intramembranous ossification rather than via a cartilage intermediate. Formation and growth of the skull bones involves the interaction of multiple cell-cell signaling pathways, with fibroblast growth factors (FGFs) and their receptors exerting a prominent influence. Mutations within the FGF signaling pathway are the most frequent cause of craniosynostosis, which is a common human craniofacial developmental abnormality characterized by the premature fusion of the cranial sutures. Here, we have developed new mouse models to investigate how different levels of increased FGF signaling can affect the formation of the calvarial bones and associated sutures. Whereas moderate
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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.