PMID:15776018

Citation	Ruiz-Vela, A, Opferman, JT, Cheng, EH and Korsmeyer, SJ (2005) Proapoptotic BAX and BAK control multiple initiator caspases. EMBO Rep. 6:379-85
Abstract	BAX and BAK operate at both the mitochondria and endoplasmic reticulum (ER) to regulate the intrinsic apoptotic pathway. An unresolved issue is whether any caspases can be activated in response to intrinsic apoptotic signals in the absence of BAX and BAK. Following organelle-specific intrinsic stress signals, including DNA damage and ER stress, we detected no activation of CARD-containing caspases (initiator CASP)-1, -2, -9, -11 and -12 in Bax(-/-)Bak(-/-) doubly deficient (DKO) cells. BCL-2 overexpression in these DKO cells provided no further protection to their already strong protection from DNA damage and ER stress. Moreover, there was no activation of effector CASP-3 and -7 in DKO cells, consistent with the lack of initiator caspase activity and disfavouring a BAX, BAK-independent intrinsic apoptotic pathway to activate initiator caspases. Thus, BAX and BAK confer an essential gateway for the activation of caspases in the intrinsic apoptotic pathway.
Links	PubMed PMC1299285 Online version:10.1038/sj.embor.7400375
Keywords	Animals; Apoptosis/physiology; Caspases/metabolism; Cell Fractionation; Cell Line; DNA Damage; Endoplasmic Reticulum/metabolism; Enzyme Activation/physiology; Gene Transfer Techniques; Immunoblotting; Membrane Proteins/metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondria/metabolism; Oligonucleotides; Proto-Oncogene Proteins c-bcl-2/metabolism; RNA Interference; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein
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Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
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