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Article

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

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research - 1 Nov 2017

Xu Wei, Luo Fengtao, Wang Quan, Tan Qiaoyan, Huang Junlan, Zhou Siru, Wang Zuqiang, Sun Xianding, Kuang Liang, Jin Min, Su Nan, Jiang Wanling, Chen Liang, Qi Huabing, Zhu Ying, Chen Bo, Chen Hangang, Chen Shuai, Gao Yu, Xu Xiaoling, Deng Chuxia, Chen Lin, Xie Yangli, Du Xiaolan

Abstract excerpt

Apert syndrome is one of the most severe craniosynostoses, resulting from gain-of-function mutations in fibroblast growth factor receptor 2 (FGFR2). Previous studies have shown that gain-of-function mutations of FGFR2 (S252W or P253R) cause skull malformation of human Apert syndrome by affecting both chondrogenesis and osteogenesis, underscoring the key role of FGFR2 in bone development. However, the effects of...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 28650109
DOI: 10.1002/jbmr.3204

Genes

FGFR2
BMX

Variants

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Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inducible Activation of FGFR2 in Adult Mice Promotes Bone Formation After Bone Marrow Ablation.PMID 28650109Read ↗

The Fgfr2(S252W/+) mutation in mice retards mandible formation and reduces bone mass as in human 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 ↗

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

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

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

Mouse models of Apert syndrome.Semantic proximity Read ↗

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

Bone morphogenetic protein receptor signaling is necessary for normal murine postnatal bone formationSemantic proximity Read ↗

An activating Fgfr3 mutation affects trabecular bone formation via a paracrine mechanism during growth.Semantic proximity Read ↗

Gain-of-function mutation in FGFR3 in mice leads to decreased bone mass by affecting both osteoblastogenesis and osteoclastogenesis.Semantic 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 ↗

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