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Article

FGFR2 mutation confers a less drastic gain of function in mesenchymal stem cells than in fibroblasts.

Stem cell reviews and reports - 1 Sept 2012

Yeh Erika, Atique Rodrigo, Ishiy Felipe A A, Fanganiello Roberto Dalto, Alonso Nivaldo, Matushita Hamilton, da Rocha Katia Maria, Passos-Bueno Maria Rita

Abstract excerpt

Gain-of-function mutations in FGFR2 cause Apert syndrome (AS), a disease characterized by craniosynostosis and limb bone defects both due to abnormalities in bone differentiation and remodeling. Although the periosteum is an important cell source for bone remodeling, its role in craniosynostosis remains poorly characterized. We hypothesized that periosteal mesenchymal stem cells (MSCs) and fibroblasts from AS...

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Source

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Identifiers

PMID: 22048896
DOI: 10.1007/s12015-011-9327-6
PMCID: PMC3412083

Genes

FGFR2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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FGFR2 mutation confers a less drastic gain of function in mesenchymal stem cells than in fibroblasts.PMID 22048896Read ↗

Apert p.Ser252Trp mutation in FGFR2 alters osteogenic potential and gene expression of cranial periosteal cells.Semantic proximity Read ↗

Cell Type-Dependent Nonspecific Fibroblast Growth Factor Signaling in Apert Syndrome.Semantic proximity Read ↗

A Ser252Trp mutation in fibroblast growth factor receptor 2 (FGFR2) mimicking human Apert syndrome reveals an essential role for FGF signaling in the regulation of endochondral bone formation.Semantic proximity Read ↗

Soluble form of FGFR2 with S252W partially prevents craniosynostosis of the apert mouse modelSemantic proximity Read ↗

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Novel molecular pathways elicited by mutant FGFR2 may account for brain abnormalities in Apert syndrome.Semantic proximity Read ↗

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