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Article

Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype.

Genes & development - 1 Feb 2004

Murakami Shunichi, Balmes Gener, McKinney Sandra, Zhang Zhaoping, Givol David, de Crombrugghe Benoit

Abstract excerpt

We generated transgenic mice that express a constitutively active mutant of MEK1 in chondrocytes. These mice showed a dwarf phenotype similar to achondroplasia, the most common human dwarfism, caused by activating mutations in FGFR3. These mice displayed incomplete hypertrophy of chondrocytes in the growth plates and a general delay in endochondral ossification, whereas chondrocyte proliferation was unaffected....

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Source

Open in PubMed Open full text

Identifiers

PMID: 14871928
DOI: 10.1101/gad.1179104
PMCID: PMC338282

Genes

FGFR3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype.PMID 14871928Read ↗

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