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Nanao Horike on Muck Rack

Nanao Horike

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Excess FGFR3 signaling in achondroplasia disrupts turnover of resting zone chondrocytes via CREB signaling - Nature Communications

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By Seiya Oura, Noriko Tanaka, Yuki Iimori, Takahiro Nemoto, Masahito Ikawa, Noriyuki Tsumaki, Nanao Horike, Saeko Koyamatsu, Kaori Fujita
| Nature Verified
Abstract Achondroplasia, associated with gain-of-function mutations in FGFR3, causes growth plate cartilage dysfunction, resulting in short-limb dwarfism. However, its precise molecular and cellular mechanisms remain unclear. To address this, we aimed to generate knock-in mice (Fgfr3Ach) harboring the achondroplasia mutation (p.Gly380Arg). In addition to previously reported abnormalities, we observe an expansion of the resting zone.
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