Collectively, the biochemical results suggest that DISC1 directly interacts with KIAA1212 and prevents its activation of AKT signaling. This model is consistent with the immunohistological evidence of increased pAKT and pS6 levels in newborn neurons with DISC1 knockdown in the adult brain (Figure 1). The model further predicts that an increase of AKT signaling would mimic DISC1 knockdown in affecting development of new neurons in the adult brain, whereas inhibition of AKT downstream signaling may rescue neuronal developmental defects from DISC1 knockdown.
