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VDAC2 promotes BAX apoptotic activity

ABSTRACT: Intrinsic apoptosis is critical for normal physiology including the prevention of tumor formation. BAX and BAK, which are essential for mediating this process and for the cytotoxic action of many anti-cancer drugs, are thought to be regulated through similar mechanisms and act redundantly to drive apoptosis. Here we have established the various mitochondrial complexes that contain VDAC1, VDAC2, VDAC3 and BAX or BAK.

INSTRUMENT(S): Bruker Daltonics micrOTOF series, Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Embryonic Fibroblast, Embryonic Fibroblast Cell Line

SUBMITTER: Laura Dagley

LAB HEAD: Grant Dewson

PROVIDER: PXD011195 | Pride | 2018-10-29

REPOSITORIES: Pride

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VDAC2 enables BAX to mediate apoptosis and limit tumor development.

Chin Hui San HS Li Mark X MX Tan Iris K L IKL Ninnis Robert L RL Reljic Boris B Scicluna Kristen K Dagley Laura F LF Sandow Jarrod J JJ Kelly Gemma L GL Samson Andre L AL Chappaz Stephane S Khaw Seong L SL Chang Catherine C Morokoff Andrew A Brinkmann Kerstin K Webb Andrew A Hockings Colin C Hall Cathrine M CM Kueh Andrew J AJ Ryan Michael T MT Kluck Ruth M RM Bouillet Philippe P Herold Marco J MJ Gray Daniel H D DHD Huang David C S DCS van Delft Mark F MF Dewson Grant G

Nature communications 20181126 1

Intrinsic apoptosis is critical to prevent tumor formation and is engaged by many anti-cancer agents to eliminate tumor cells. BAX and BAK, the two essential mediators of apoptosis, are thought to be regulated through similar mechanisms and act redundantly to drive apoptotic cell death. From an unbiased genome-wide CRISPR/Cas9 screen, we identified VDAC2 (voltage-dependent anion channel 2) as important for BAX, but not BAK, to function. Genetic deletion of VDAC2 abrogated the association of BAX ...[more]

PMID: 30478310

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