Autophagy is generally activated by conditions of nutrient deprivation but has also been associated with a number of physiological processes including development, differentiation, neurodegeneration, infection, and cancer. Formation of the autophagosome involves a ubiquitin-like conjugation system in which Atg12 is covalently bound to Atg5 and targeted to autophagosome vesicles. This conjugation reaction is mediated by the ubiquitin E1-like enzyme Atg7 and the E2-like enzyme Atg10.Apg5 and the human homolog, APG5 (also designated apoptosis-specific protein or APS), function as substrates
for the autophagy protein Apg12. These proteins are covalently bonded together to form Apg12/APG5 conjugates, which are required for the progression of autophagy.
