Figure 7.

Schematic model of RASAL2 regulation on autophagy. Under normal circumstances, the complex of RASAL2 andphosphorytase PP1MB (RASAL2/PP1MB) can bind to phosphorylated PRKAA (p-PRKAA), dephosphorylating PRKAA and thus keeping autophagy at a low level. Additionally, RASAL2 is a direct substrate of PRKAA. Glucose deprivation can activate AMPK and release PP1MB from RASAL2. Activated PRKAA then phosphorylates RASAL2 at S351, resulting in an increase in the binding of RASAL2 with PI3KC3 complex, as well as the interaction between PI3KC3 and its substrate PtdIns to increase PI3KC3 activity toward PtdIns3P production and autophagy