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Article

P253R fibroblast growth factor receptor-2 mutation induces RUNX2 transcript variants and calvarial osteoblast differentiation.

Journal of cellular physiology - 1 Feb 2005

Baroni Tiziano, Carinci Paolo, Lilli Cinzia, Bellucci Catia, Aisa Maria Cristina, Scapoli Luca, Volinia Stefano, Carinci Francesco, Pezzetti Furio, Calvitti Mario, Farina Antonio, Conte Carmela, Bodo Maria

Abstract excerpt

Unregulated fibroblast growth factor 2 (FGF2) signaling caused by mutations in the fibroblast growth factor receptor (FGFR2) leads to human craniosynostosis such as the Apert syndrome. In an in vitro control model of calvarial osteoblasts from Apert patients carrying the FGFR2 P253R mutation, we studied the changes in cellular phenotype and evaluated the effects of FGF2. Compared with wild-type controls,...

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Source

Identifiers

PMID: 15389579
DOI: 10.1002/jcp.20148

Genes

FGF2
FGFR2
RUNX2

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.

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P253R fibroblast growth factor receptor-2 mutation induces RUNX2 transcript variants and calvarial osteoblast differentiation.PMID 15389579Read ↗

A soluble form of fibroblast growth factor receptor 2 (FGFR2) with S252W mutation acts as an efficient inhibitor for the enhanced osteoblastic differentiation caused by FGFR2 activation in Apert syndrome.Semantic proximity Read ↗

Apert syndrome mutant FGFR2 and its soluble form reciprocally alter osteogenesis of primary calvarial osteoblasts.Semantic proximity Read ↗

Increased EFG- and PDGFalpha-receptor signaling by mutant FGF-receptor 2 contributes to osteoblast dysfunction in Apert craniosynostosis.Semantic proximity Read ↗

FGF2 effects in periosteal fibroblasts bearing the FGFR2 receptor Pro253 Arg mutation.Semantic proximity Read ↗

The study of abnormal bone development in the Apert syndrome Fgfr2+/S252W mouse using a 3D hydrogel culture model.Semantic proximity Read ↗

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

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

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

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

Negative autoregulation of fibroblast growth factor receptor 2 expression characterizing cranial development in cases of Apert (P253R mutation) and Pfeiffer (C278F mutation) syndromes and suggesting a basis for differences in their cranial phenotypes.Semantic proximity Read ↗

Abnormalities in cartilage and bone development in the Apert syndrome FGFR2(+/S252W) mouse.Semantic proximity Read ↗

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