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Updated: Jun 3, 2026
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Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
FGF signaling in craniofacial biological control and pathological craniofacial development
1Department of Orthodontics and Pediatric Dentistry, University of Michigan, Ann Arbor, MI, USA. nhatch@umich.edu
Critical Reviews in Eukaryotic Gene Expression
|March 15, 2011
Summary
Fibroblast growth factor receptors (FGFRs) are crucial for craniofacial development. Mutations in FGFRs cause craniosynostosis syndromes, leading to premature skull fusion and skeletal abnormalities.
Area of Science:
- Developmental Biology
- Genetics
- Skeletal Biology
Background:
- Fibroblast growth factor receptors (FGFRs) are transmembrane proteins vital for organ development.
- FGFR signaling regulates craniofacial skeleton development through specific isoforms, growth factors, and proteoglycans.
- Signaling is modulated by endogenous inhibitors.
Purpose of the Study:
- To review the role of FGF/FGFR signaling in craniofacial skeleton development.
- To discuss mechanisms linking FGFR signaling to craniosynostosis syndromes.
- To highlight recent in vitro and in vivo studies on FGFRs in skeletal development.
Main Methods:
- Literature review of in vitro and in vivo studies.
- Analysis of signaling regulation by FGFR isoforms, FGFs, and proteoglycans.
- Examination of gain-of-function mutations in FGFRs associated with craniosynostosis.
Main Results:
- FGFR signaling is critical for normal craniofacial development.
- Gain-of-function mutations in FGFRs lead to craniosynostosis syndromes.
- These mutations cause premature cranial bone fusion and affect facial skeleton, vertebrae, and digits.
Conclusions:
- FGFR signaling pathways are essential for skeletal development.
- Dysregulation of FGFR signaling contributes to congenital craniosynostosis syndromes.
- Further research into FGFR mechanisms can inform treatments for skeletal abnormalities.
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