interaction and its effect on AKT signaling, is supported by histological evidence of over-activation of AKT signaling in newborn neurons with DISC1 suppression, and by in vivo findings that multiple approaches to over-activate AKT signaling all lead to phenotypes similar to DISC1 suppression and pharmacological inhibition of mTOR rescues developmental defects of newborn neurons with DISC1 suppression or KIAA1212 overexpression in the adult brain.
