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Article

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

Journal of cellular physiology - 1 Sept 2012

Suzuki Hiroyuki, Suda Naoto, Shiga Momotoshi, Kobayashi Yukiho, Nakamura Masataka, Iseki Sachiko, Moriyama Keiji

Abstract excerpt

Apert syndrome is characterized by craniosynostosis and syndactyly, and is predominantly caused by mutation of either S252W or P253W in the fibroblast growth factor receptor (FGFR) 2 gene. In this study, we characterized the effects of one of the mutations (S252W) using primary calvarial osteoblasts derived from transgenic mice, Ap-Tg and sAp-Tg, that expressed an Apert-type mutant FGFR2 (FGFR2IIIc-S252W;...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Share to p38 Mitogen-Activated Protein Kinases

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Share to Receptor, Fibroblast Growth Factor, Type 2

Source

Identifiers

PMID: 22105374
DOI: 10.1002/jcp.24021

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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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Apert syndrome mutant FGFR2 and its soluble form reciprocally alter osteogenesis of primary calvarial osteoblasts.PMID 22105374Read ↗

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

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 ↗

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 ↗

Activation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2+P253R miceSemantic proximity Read ↗

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

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

Inducible Activation of FGFR2 in Adult Mice Promotes Bone Formation After Bone Marrow Ablation.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 ↗

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

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

Therapeutic effect of nanogel-based delivery of soluble FGFR2 with S252W mutation on craniosynostosis.Semantic proximity Read ↗

A Pro253Arg mutation in fibroblast growth factor receptor 2 (Fgfr2) causes skeleton malformation mimicking human Apert syndrome by affecting both chondrogenesis and osteogenesis.Semantic proximity Read ↗

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