ArticleInternational journal of biological sciences2017
Deformed Skull Morphology Is Caused by the Combined Effects of the Maldevelopment of Calvarias, Cranial Base and Brain in FGFR2-P253R Mice Mimicking Human Apert Syndrome.
Article in International journal of biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Materialogenetics: an emerging and promising framework for cell-specific genetic manipulation.Bioactive materials · 2026Article
- An Hsp70 promoter-based mouse for heat shock-induced gene modulation.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Impact of Sonic Hedgehog-dependent sphenoid bone defect on craniofacial growth.Clinical and experimental dental research · 2024Article
- Mouse embryo phenotyping using X-ray microCT.Frontiers in cell and developmental biology · 2022Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Article
- ADAMTS9 and ADAMTS20 are differentially affected by loss of B3GLCT in mouse model of Peters plus syndrome.Human molecular genetics · 2019Article
- Adeno-Associated Virus-Mediated RNAi against Mutant Alleles Attenuates Abnormal Calvarial Phenotypes in an Apert Syndrome Mouse Model.Molecular therapy. Nucleic acids · 2018Article
- Fibroblast Growth Factor Receptor 2 (International journal of biological sciences · 2017Review
- Fibroblast Growth Factor Receptor 2 Signaling in Breast Cancer.International journal of biological sciences · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apert syndrome (AS) is a common genetic syndrome in humans characterized with craniosynostosis. Apert patients and mouse models showed abnormalities in sutures, cranial base and brain, that may all be involved in the pathogenesis of skull malformation of Apert syndrome. To distinguish the differential roles of these components of head in the pathogenesis of the abnormal skull morphology of AS, we generated mouse strains specifically expressing mutant FGFR2 in chondrocytes, osteoblasts, and progenitor cells of central nervous system (CNS) by crossing Fgfr2
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