diverse processes of neuronal development, including morphogenesis, dendritic development, synapse formation and synaptic plasticity (Atwal et al., 2000; Jaworski et al., 2005; Jiang et al., 2005; Kuruvilla et al., 2000; Markus et al., 2002; Sanna et al., 2002; Yoshimura et al., 2006). Interestingly, conditional deletion of PTEN in differentiated dentate granule cells leads to soma hypertrophy, ectopic dendrites and much elongated dendritic process in the adult mice (Kwon et al., 2006). The phenotypic similarities between suppression of PTEN and DISC1 in the adult brain suggest a potential connection between signaling regulated by these two molecules. Among a large number of proteins identified as potential DISC1-interacting partners in a recent yeast two-hybrid screen (Camargo et al., 2007), KIAA1212 directly binds AKT and enhances its kinase activity in vitro (Anai et al., 2005). Also known as APE (AKT-phosphorylation enhancer) (Anai et al., 2005), GIV (Gα-interacting vesicle-associated protein) (Le-Niculescu et al., 2005), Girdin (girders of actin filaments) (Enomoto et al., 2005) and HkRP1 (Hook-related protein1) (Simpson et al., 2005), KIAA1212 regulates cytoskeletal dynamics in response to extracellular cues in non-neuronal cells (Enomoto et al., 2006). KIAA1212 is expressed in the developing nervous system and its expression is retained in dentate granule cells of
