Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia.

doi:10.1016/j.ajhg.2012.10.014

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Article

Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia.

American journal of human genetics - 7 Dec 2012

Lorget Florence, Kaci Nabil, Peng Jeff, Benoist-Lasselin Catherine, Mugniery Emilie, Oppeneer Todd, Wendt Dan J, Bell Sean M, Bullens Sherry, Bunting Stuart, Tsuruda Laurie S, O'Neill Charles A, Di Rocco Federico, Munnich Arnold, Legeai-Mallet Laurence

Abstract excerpt

Achondroplasia (ACH), the most common form of dwarfism, is an inherited autosomal-dominant chondrodysplasia caused by a gain-of-function mutation in fibroblast-growth-factor-receptor 3 (FGFR3). C-type natriuretic peptide (CNP) antagonizes FGFR3 downstream signaling by inhibiting the pathway of mitogen-activated protein kinase (MAPK). Here, we report the pharmacological activity of a 39 amino acid CNP analog (BMN...

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Identifiers

PMID: 23200862
DOI: 10.1016/j.ajhg.2012.10.014
PMCID: PMC3516592

Genes

CNP
FGFR3

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