Fig. 12.

Redox-based mechanism for BCL-2’s anti-apoptotic function. BCL-2 localizes to different cellular membranes. In mitochondria, it interacts with pro-apoptotic BCL-2 family members to inhibit apoptosis. Under normal, basal conditions, BCL-2 also interacts with the COX Va subunit complex to increase electron flow, oxygen consumption and ROS levels. This results in a pro-oxidant state that promotes proliferation, while leading to adaptations that allow the cells to survive under increased oxidative stress. In contrast, under conditions of even greater oxidative stress, BCL2 inhibits the COX Vb subunit, to lower ROS production to safe levels that will not trigger apoptosis [137].

Reproduced with permission from Krishna S., Low I.C., and Pervaiz S. (2011) Biochem. J. 435, 545–551. © the Biochemical Society.