Journal article

BAX requires VDAC2 to mediate apoptosis and to limit tumor development

Hui San Chin, Mark van Delft, Robert Ninnis, Mark Li, Iris Tan, Boris Reljic, Kristen Scicluna, Laura Dagley, Jarrod Sandow, Gemma Kelly, Stephane Chappaz, Seong Khaw, Catherine Chang, Andrew Webb, Colin Hockings, Cathrine Hall, Andrew Kueh, Michael Ryan, Ruth Kluck, Philippe Bouillet Show all

Published : 2018

Abstract

Intrinsic apoptosis is critical for normal physiology including the prevention of tumor formation. BAX and BAK are essential for mediating this process and for the cytotoxic action of many anticancer drugs. BAX and BAK are thought to act in a functionally redundant manner and are considered to be regulated similarly. From an unbiased genome-wide CRISPR/Cas9 screen, we identified VDAC2 (voltage-dependent anion channel 2) as essential for BAX, but not BAK, to function. The genetic deletion of VDAC2 abrogated the association of BAX and BAK with mitochondrial complexes that contain VDAC1, VDAC2 and VDAC3. By disrupting its localization to mitochondria, BAX is rendered completely ineffective. Mor..

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