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. 2015 Mar 5;112(6):957–962. doi: 10.1038/bjc.2015.85

Figure 2.

Figure 2

Mitochondrial priming model. In non-primed cells (top panel), mitochondria have a low BH3-only protein load leaving excess prosurvival BCL2 proteins to neutralise pro-apoptotic BH3-only proteins resulting from cytotoxic chemotherapy or BH3-mimetic treatment. In primed cancer cells (bottom panel), stresses such as oncogene activation lead to a high BH3-only protein load blocked by a compensatory increase in pro-survival BCL2 members. Additional pro-apoptotic stimuli result in excess activator BH3-only proteins that cause BAX/BAK activation, MOMP and death in these cells.