Proteomics

Dataset Information

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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):

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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Dataset's files

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Action DRS
P3037_FlagBakLower_01_01_1_01_3074.d.zip Other
P3037_FlagBakLower_01_02_1_01_3083.d.zip Other
P3037_FlagBakLower_01_03_1_01_3084.d.zip Other
P3037_FlagBakUpper_01_01_1_01_3070.d.zip Other
P3037_FlagBakUpper_01_02_1_01_3071.d.zip Other
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Publications

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]

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