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Article

RNA interference and inhibition of MEK-ERK signaling prevent abnormal skeletal phenotypes in a mouse model of craniosynostosis.

Nature genetics - 1 Sept 2007

Shukla Vivek, Coumoul Xavier, Wang Rui-Hong, Kim Hyun-Seok, Deng Chu-Xia

Abstract excerpt

Premature fusion of one or more of the cranial sutures (craniosynostosis) in humans causes over 100 skeletal diseases, which occur in 1 of approximately 2,500 live births. Among them is Apert syndrome, one of the most severe forms of craniosynostosis, primarily caused by missense mutations leading to amino acid changes S252W or P253R in fibroblast growth factor receptor 2 (FGFR2). Here we show that a small...

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Source

Identifiers

PMID: 17694057
DOI: 10.1038/ng2096

Genes

FGFR2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

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RNA interference and inhibition of MEK-ERK signaling prevent abnormal skeletal phenotypes in a mouse model of craniosynostosis.PMID 17694057Read ↗

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 ↗

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 ↗

Mouse models of Apert syndrome.Semantic proximity Read ↗

Evidence that Fgf10 contributes to the skeletal and visceral defects of an Apert syndrome mouse model.Semantic proximity Read ↗

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 ↗

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

De novo mutations in inhibitors of Wnt, BMP, and Ras/ERK signaling pathways in non-syndromic midline craniosynostosis.Semantic proximity Read ↗

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

A Ser252Trp [corrected] substitution in mouse fibroblast growth factor receptor 2 (Fgfr2) results in craniosynostosis.Semantic proximity Read ↗

Fibroblast growth factor receptor signaling crosstalk in skeletogenesis.Semantic proximity Read ↗

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