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

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 (Fgfr3 Ach ) harboring...

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Principais autores:	Nanao Horike, Seiya Oura, Saeko Koyamatsu, Noriko Tanaka, Yuki Iimori, Kaori Fujita, Takahiro Nemoto, Masahito Ikawa, Noriyuki Tsumaki
פורמט:	Artigo
שפה:	Inglês
יצא לאור:	Nature Portfolio 2026-02-01
סדרה:	Nature Communications
גישה מקוונת:	https://doi.org/10.1038/s41467-026-69507-9
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