Evidence that Fgf10 contributes to the skeletal and visceral defects of an apert syndrome mouse model

@article{Hajihosseini2009EvidenceTF,
  title={Evidence that Fgf10 contributes to the skeletal and visceral defects of an apert syndrome mouse model},
  author={Mohammad K. Hajihosseini and Raquel Duarte and Jean Pegrum and Annemarie A. Donjacour and Eva Lana‐Elola and David Rice and James Sharpe and Clive Dickson},
  journal={Developmental Dynamics},
  year={2009},
  volume={238}
}
Apert syndrome (AS) is a severe congenital disease caused by mutations in fibroblast growth factor receptor‐2 (FGFR2), and characterised by craniofacial, limb, visceral, and neural abnormalities. AS‐type FGFR2 molecules exert a gain‐of‐function effect in a ligand‐dependent manner, but the causative FGFs and their relative contribution to each of the abnormalities observed in AS remains unknown. We have generated mice that harbour an AS mutation but are deficient in or heterozygous for Fgf10… 
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TLDR
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