BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis.

By E. Cheng, M. Wei, S. Weiler, R. Flavell, T. Mak, T. Lindsten, S. Korsmeyer. Molecules and Cells, 2001

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View Paper: https://www.semanticscholar.org/paper/37545734d1816115e79a8d8776db2c83a787ad4e

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Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins (2002, background): “Recent experiments with transfected cells have shown that over-expression of Bim or other BH3-only proteins (Bad, Bid, Noxa) can only kill cells that contain either Bax or Bak.29,30 Since Bim, Bad and Noxa only bind to Bcl-2 and its pro-survival relatives but not to Bax/Bak-like proteins,17 we propo”
Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. (2007, background): “Like BIM, BID has been identified as an activator BH3-only protein (8, 13, 23).”
Apoptosis A Link between Cancer Genetics and Chemotherapy (2002, background): “…of this effect is not certain those lacking Bax and Bak, or overexpressing Bcl-2 (Ryan et al., 2000), these data provide novel insight into (Cheng et al., 2001). the molecular mechanisms of drug resistance and have The ability of some tumor cells with postmitochondrial therapeutic…”
p53 has a direct apoptogenic role at the mitochondria. (2003, background): “While endogenous tBid and Bim induce trimeric and tetrameric Bak complexes, recombinant GST-tBid mainly generates Bak dimers (Wei et al., 2000; Cheng et al., 2001).”
Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members. (2006, background): “Proapoptotic function of BH3-only proteins requires BAX or BAK (Cheng et al., 2001; Wei et al., 2001; Zong et al., 2001) and an intact BH3 domain (Chittenden et al., 1995; O'Connor et al., 1998; Wang et al., 1996; Zha et al., 1997), the only BCL-2 homology (BH) region this class of protein…”
Growth factor regulation of autophagy and cell survival in the absence of apoptosis. (2005, background): “…is required to direct the utilization of sufRecently, Bax and Bak have been demonstrated toficient exogenous nutrients to maintain cell viability. be required for cells to initiate apoptosis through the intrinsic mitochondrial pathway (Cheng et al., 2001; WeiIntroduction et al., 2001).”
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis (2003, background): “The existence of a Bax/Bak-dependent apoptotic pathway initiated from the ER may explain the observations that cells lacking Apaf-1, caspase 9, or cytochrome c showed only attenuated, but not complete, resistance to certain death stimuli (Cecconi et al., 1998; Kuida et al., 1998; Li et al., 2000), w”
Life in the balance: how BH3-only proteins induce apoptosis. (2005, background): “Models for the activation of Bak and Bax Although BH3-only proteins require either Bax or Bak for cell killing [3,4], it remains unresolved whether they control the activation of Bax and Bak directly or indirectly [10].”