Autophagy is initiated by the ULK-1 kinase complex which is activated by AMPK and inhibition of mTORC1. The ULK-1 complex activates a PI3K class III complex, which includes Beclin-1 and VPS34, which results in the development of an isolation membrane, which elongates and recruits the ATG5-ATG12-ATG16-L1 complex, which converts LC3-I to LC3-II through the interaction with phosphatidylethanolamine (PE). LC3-II binds to autophagy receptors, such as p62, which are bound to cargo proteins and organelles designated for degradation. Autophagosomes then fuse with lysosomes via SNARE proteins and BICD1 to form autolysosomes. The cargo is then degraded by lysosomal acid hydrolases and the degradation products (such as amino acids) are recycled.