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Article

Cell Type-Dependent Nonspecific Fibroblast Growth Factor Signaling in Apert Syndrome.

Stem cells and development - 15 Aug 2016

Yeh Erika, Atique Rodrigo, Fanganiello Roberto Dalto, Sunaga Daniele Yumi, Ishiy Felipe Augusto André, Passos-Bueno Maria Rita

Abstract excerpt

Apert Syndrome (AS) is one of the most severe forms of craniosynostosis. It is caused by gain-of-function mutations in the receptor fibroblast growth factor receptor 2 (FGFR2), which leads to ligand-receptor promiscuity. Here, we aimed to better understand the behavior of mesenchymal stem cells (MSCs) and of fibroblastoid cells, cellular populations that are part of the suture complex, when stimulated with...

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Source

Identifiers

PMID: 27339175
DOI: 10.1089/scd.2016.0018

Genes

FGF19
FGFR2
FGF10
BMP2
MSC

Variants

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→

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Cell Type-Dependent Nonspecific Fibroblast Growth Factor Signaling in Apert Syndrome.PMID 27339175Read ↗

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

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

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

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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 ↗

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