Figure 2.

Apoptosis is Regulated by Numerous Phosphorylation Events. In the intrinsic apoptosis pathway, cell stress and DNA damage promotes mitochondria release cytochrome C into the cytoplasm, binds with Apaf1 and pro-caspase-9 to form an apoptosome. Apoptotic stimuli lead to MST autophosphorylation and triggers Beclin1 phosphorylation, which activate caspases. After initial DNA damage, p53 is phosphorylated at Ser15 and Ser20, if DNA damage is severe, phosphorylation of p53 protein at Ser-46 forms TP53INP1 and induce cell apoptosis. In the extrinsic apoptosis pathway, Fas/FasL, death receptor 4 (DR4), death receptor 5 (DR5) and TNFR1 bind to their ligands to induce pro-caspase-8 activation, which then cleaves and activates effector caspases, such as caspase-3 and caspase-7, further activation of downstream effector molecules then leads to apoptosis.