FIGURE 7:

A schematic diagram of a model of how PIKE-A suppresses UNC5B's proapoptotic action. In response to UNC5B ligand netrin-1 treatment, PI3K/Akt signaling is activated, which phosphorylates PIKE-A on Ser-472 residue. This phosphorylation enhances PIKE-A association with UNC5B, blocking UNC5B apoptotic fragmentation and inhibiting programmed cell death. Moreover, phosphorylated PIKE-A further enhances Akt kinase activity that triggers p53 degradation, leading to suppression of UNC5B transcription and apoptosis.