ArticleThe American journal of pathology2001
In vivo modulation of FGF biological activity alters cranial suture fate.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Insights and future directions of potential genetic therapy for Apert syndrome: A systematic review.Gene therapy · 2021Pooled it
- Divergent Mechanisms of Cranial Suture Ossification in Normal Development and Pathologic Fusion.Journal of cellular and molecular medicine · 2026Review
- Targeted allele-specificMolecular therapy. Nucleic acids · 2025Article
- Nuclear factor I-C regulates intramembranous bone formation via control of FGF signalling.Heliyon · 2025Article
- 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
- FGF signaling in cranial suture development and related diseases.Frontiers in cell and developmental biology · 2023Review
- The clinical manifestations, molecular mechanisms and treatment of craniosynostosis.Disease models & mechanisms · 2022Review
- The Intertwined Evolution and Development of Sutures and Cranial Morphology.Frontiers in cell and developmental biology · 2021Review
- Isolation and Characterization of Human Suture Mesenchymal Stem CellsInternational journal of stem cells · 2020Article
- The Evolving Landscape of Gene Therapy in Plastic Surgery.Seminars in plastic surgery · 2019Review
- Current Approaches in the Development of Molecular and Pharmacological Therapies in Craniosynostosis Utilizing Animal Models.Molecular syndromology · 2019Review
- Rapamycin rescues BMP mediated midline craniosynostosis phenotype through reduction of mTOR signaling in a mouse model.Genesis (New York, N.Y. : 2000) · 2018Article
- Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis.BBA clinical · 2016Review
- BCL11B regulates sutural patency in the mouse craniofacial skeleton.Developmental biology · 2016Article
- New therapeutic targets in rare genetic skeletal diseases.Expert opinion on orphan drugs · 2015Article
- Bone morphogenetic protein is required for fibroblast growth factor 2-dependent later-stage osteoblastic differentiation in cranial suture cells.International journal of clinical and experimental pathology · 2015Article
- Craniosynostosis, psychomotor retardation, and facial dysmorphic features in a Spanish patient with a 4q27q28.3 deletion.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2014Article
- Augmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
- Article
- Models of cranial suture biology.The Journal of craniofacial surgery · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Gain-of-function mutations in fibroblast growth factor receptors have been identified in numerous syndromes associated with premature cranial suture fusion. Murine models in which the posterior frontal suture undergoes programmed fusion after birth while all other sutures remain patent provide an ideal model to study the biomolecular mechanisms that govern cranial suture fusion. Using adenoviral vectors and targeted in utero injections in rats, we demonstrate that physiological posterior frontal suture fusion is inhibited using a dominant-negative fibroblast growth factor receptor-1 construct, whereas the normally patent coronal suture fuses when infected with a construct that increases basic fibroblast growth factor biological activity. Our data may facilitate the development of novel, less invasive treatment options for children with craniosynostosis.
Indexed as
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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.