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. 2013 Mar 12;14(4):328–336. doi: 10.1038/embor.2013.20

Figure 2.

Figure 2

The Bcl2 family rheostat. There is substantial evidence for functional redundancy between pro-survival members, especially Bcl2, Mcl1 and Bcl-XL (upper rheostat). In this case, reduction of any one member could adjust the pro-survival rheostat below a crucial threshold, resulting in cell death in the face of cell stress signals. Alternatively, there might be situations in which unique pathways are regulated by the individual pro-survival members (lower rheostats). Although the Bcl2 family is most closely associated with apoptosis, there are or might be many other cellular responses or fates that are controlled by these proteins. Of particular relevance to Mcl1, changes to many cellular pathways can result in changes in the levels of Bcl2 family proteins, thereby regulating cell fate in the face of stress stimuli. Bak, Bcl2 antagonist killer; Bax, Bcl2-associated protein; Bcl2, B-cell lymphoma 2; Bcl-XL, Bcl2-like protein XL; Bim, Bcl2-like 11; Mcl1, myeloid cell leukaemia 1; Puma, p53 upregulated modulator of apoptosis; ROS, reactive oxygen species; tBid, truncated BH3-interacting domain death agonist.