RT Journal Article
T1 BAX and BAK1 are dispensable for ABT-737-induced dissociation of the BCL2-BECN1 complex and autophagy
A1 Bravo San Pedro, José Manuel
A1 Wei, Yongjie
A1 Sica, Valentina
A1 Maiuri, Maria Chiara
A1 Zou, Zhongju
A1 Kroemer, Guido
A1 Levine, Beth
AB 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.
PB Taylor & Francis Group
SN 1554-8627
YR 2015
FD 2015-04
LK https://hdl.handle.net/20.500.14352/128969
UL https://hdl.handle.net/20.500.14352/128969
LA eng
NO 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.
DS Docta Complutense
RD 31 dic 2025