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. 2006 Jan;26(2):569–579. doi: 10.1128/MCB.26.2.569-579.2006

FIG. 8.

FIG. 8.

A model of THG-induced apoptosis. In Bax+/− cells, Smac is released from mitochondria to inhibit IAPs in order to achieve caspase 3 activation and apoptosis. The tTGase-mediated cross-linking of caspase 3 is suppressed by unknown mechanisms, which may be controlled by caspase 9 and/or caspase 3. In Bax−/− cells, the full processing and activation of caspase 3 are blocked by IAPs at the early stage of THG treatment. At the late stage, IAPs are decreased and subsequently induced, and activated tTGase takes the role in inhibition of apoptosis by cross-linking caspase 3. Cyt C, cytochrome c.