Transchromosomic cell model of Down syndrome shows aberrant migration, adhesion and proteome response to extracellular matrix

@article{Delom2009TranschromosomicCM,
  title={Transchromosomic cell model of Down syndrome shows aberrant migration, adhesion and proteome response to extracellular matrix},
  author={Fr{\'e}d{\'e}ric Delom and Emma Burt and Alex Hoischen and Joris A. Veltman and Juergen Groet and Finbarr E. Cotter and D. Nizetic},
  journal={Proteome Science},
  year={2009},
  volume={7},
  pages={31 - 31}
}
Down syndrome (DS), caused by trisomy of human chromosome 21 (HSA21), is the most common genetic birth defect. Congenital heart defects (CHD) are seen in 40% of DS children, and >50% of all atrioventricular canal defects in infancy are caused by trisomy 21, but the causative genes remain unknown. Here we show that aberrant adhesion and proliferation of DS cells can be reproduced using a transchromosomic model of DS (mouse fibroblasts bearing supernumerary HSA21). We also demonstrate a deacrease… CONTINUE READING