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Article

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

Nature communications - 26 Feb 2026

Horike Nanao, Oura Seiya, Koyamatsu Saeko, Tanaka Noriko, Iimori Yuki, Fujita Kaori, Nemoto Takahiro, Ikawa Masahito, Tsumaki Noriyuki

Abstract excerpt

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...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Receptor, Fibroblast Growth Factor, Type 3

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Identifiers

PMID: 41748604
DOI: 10.1038/s41467-026-69507-9
PMCID: PMC12946275

Genes

FGFR3

Variants

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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Excess FGFR3 signaling in achondroplasia disrupts turnover of resting zone chondrocytes via CREB signaling.PMID 41748604Read ↗

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