RNA interference and inhibition of MEK-ERK signaling prevent abnormal skeletal phenotypes in a mouse model of craniosynostosis (Q56333589)

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Rui-Hong Wang

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Hyun-Seok Kim

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Chu-Xia Deng

Syndromes involving craniosynostosis and midface hypoplasia

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language of work or name

English

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publication date

September 2007

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published in

Nature Genetics

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volume

39

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issue

9

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page(s)

1145-50

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cites work

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Management of craniosynostoses

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Exclusive paternal origin of new mutations in Apert syndrome

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A Ser250Trp substitution in mouse fibroblast growth factor receptor 2 (Fgfr2) results in craniosynostosis

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Inducible suppression of Fgfr2 and Survivin in ES cells using a combination of the RNA interference (RNAi) and the Cre-LoxP system.

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Silencing mutant SOD1 using RNAi protects against neurodegeneration and extends survival in an ALS model

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Erk pathway and activator protein 1 play crucial roles in FGF2-stimulated premature cranial suture closure

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Feedback interactions between MKP3 and ERK MAP kinase control scleraxis expression and the specification of rib progenitors in the developing chick somite

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A model for the pharmacological treatment of crouzon syndrome

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Attenuation of signaling pathways stimulated by pathologically activated FGF-receptor 2 mutants prevents craniosynostosis.

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A DNA vector-based RNAi technology to suppress gene expression in mammalian cells

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TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage

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Fibroblast growth factor (FGF)-2 directly stimulates mature osteoclast function through activation of FGF receptor 1 and p42/p44 MAP kinase

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inferred from DOI database lookup

7 January 2021

based on heuristic

Sprouty proteins: antagonists of endothelial cell signaling and more

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