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BAX and BAK1 are dispensable for ABT-737-induced dissociation of the BCL2-BECN1 complex and autophagy Bravo San Pedro, José Manuel Wei, Yongjie Sica, Valentina Maiuri, Maria Chiara Zou, Zhongju Kroemer, Guido Levine, Beth ABT-737 Autophagy BAX BAK1 BCL2 BECN1 Apoptosis BH3 mimetics Ciencias Biomédicas 32 Ciencias Médicas Disruption of the complex of BECN1 with BCL2 or BCL2L1/BCL-XL is an essential switch that turns on cellular autophagy in response to environmental stress or treatment with BH3 peptidomimetics. Recently, it has been proposed that BCL2 and BCL2L1/BCL-XL may inhibit autophagy indirectly through a mechanism dependent on the proapoptotic BCL2 family members, BAX and BAK1. Here we report that the BH3 mimetic, ABT-737, induces autophagy in parallel with disruption of BCL2-BECN1 binding in 2 different apoptosis-deficient cell types lacking BAX and BAK1, namely in mouse embryonic fibroblasts cells and in human colon cancer HCT116 cells. We conclude that the BH3 mimetic ABT-737 induces autophagy through a BAX and BAK1-independent mechanism that likely involves disruption of BECN1 binding to antiapoptotic BCL2 family members. Depto. de Fisiología Fac. de Medicina TRUE pub 2025-12-15T12:34:35Z 2025-12-15T12:34:35Z 2015-04 journal article VoR https://hdl.handle.net/20.500.14352/128969 1554-8627 10.1080/15548627.2015.1017191 1554-8635 eng Bravo-San Pedro JM, Wei Y, Sica V, Maiuri MC, Zou Z, Kroemer G, Levine B. Bax and bak1 are dispensable for abt-737-induced dissociation of the bcl2-becn1 complex and autophagy. Autophagy. 2015 Mar;11(3):452–459. Attribution-NonCommercial 4.0 International http://creativecommons.org/licenses/by-nc/4.0/ open access application/pdf Taylor & Francis Group