Knockdown of Myo-Inositol Transporter SMIT1 Normalizes Cholinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome)

@article{Crdenas2017KnockdownOM,
  title={Knockdown of Myo-Inositol Transporter SMIT1 Normalizes Cholinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome)},
  author={Ana Mar{\'i}a C{\'a}rdenas and Paola Fern{\'a}ndez-Olivares and Ignacio D{\'i}az-Franulic and Arlek M. Gonz{\'a}lez-Jamett and Takeshi Shimahara and Juan Segura-Aguilar and Ra{\'u}l Caviedes and Pablo Caviedes},
  journal={Neurotoxicity Research},
  year={2017},
  volume={32},
  pages={614-623}
}
The Na+/myo-inositol cotransporter (SMIT1) is overexpressed in human Down syndrome (DS) and in trisomy 16 fetal mice (Ts16), an animal model of the human condition. SMIT1 overexpression determines increased levels of intracellular myo-inositol, a precursor of phophoinositide synthesis. SMIT1 is overexpressed in CTb cells, an immortalized cell line… CONTINUE READING