Figure 4 | Cell Death & Differentiation

Figure 4

From: MOMP, cell suicide as a BCL-2 family business

Figure 4

The unified model of BCL-2 protein interactions. In the 'unprimed', healthy cell, BAX and BAK reside in an inactive state that does not require active suppression of apoptosis via prosurvival BCL-2 family members. Cells 'primed for death' undergo MOMP with different kinetics upon derepression. In Mode 1, prosurvival proteins sequester BH3-only direct activators (BH3-DA). This reversible interaction can be easily overcome by BH3-only sensitizer (BH3-S) proteins. More effective inhibition of MOMP onset takes place in Mode 2, when prosurvival proteins directly sequester BAX and BAK under high-stress levels. Ultimately, when both modes of survival are overcome, BAX/BAK oligomerization leads to MOMP. Taking mitochondrial dynamics into account, in healthy cells inactive effectors BAX/ BAK support mitochondrial dynamics by promoting mitochondrial fusion. Increased activation of BAX/BAK leads to an imbalance in mitochondrial dynamics towards fission, leading to mitochondrial fragmentation

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