Bravo San Pedro, José ManuelWei, YongjieSica, ValentinaMaiuri, Maria ChiaraZou, ZhongjuKroemer, GuidoLevine, Beth2025-12-152025-12-152015-04Bravo-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):452–459.1554-862710.1080/15548627.2015.1017191https://hdl.handle.net/20.500.14352/128969Disruption 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.engAttribution-NonCommercial 4.0 Internationalhttp://creativecommons.org/licenses/by-nc/4.0/journal article1554-8635https://doi.org/10.1080/15548627.2015.101719125715028https://www.tandfonline.com/doi/full/10.1080/15548627.2015.1017191https://pubmed.ncbi.nlm.nih.gov/25715028/open accessABT-737AutophagyBAXBAK1BCL2BECN1ApoptosisBH3 mimeticsCiencias Biomédicas32 Ciencias Médicas