VDAC2 is required for truncated BID-induced mitochondrial apoptosis by recruiting BAK to the mitochondria

EMBO Reports

Volumn 10, Issue 12, 2009, Pages 1341-1347

  Roy, Soumya Sinha ^a   Ehrlich, Amy M ^a   Craigen, William J ^b   Hajnóczky, György ^a  

^a THOMAS JEFFERSON UNIVERSITY   (United States)

^b BAYLOR COLLEGE OF MEDICINE   (United States)

Author keywords

Apoptosis; BAK; Mitochondria; TBID; VDAC2

Indexed keywords

PROTEIN BAK; PROTEIN BID; RECOMBINANT PROTEIN; VOLTAGE DEPENDENT ANION CHANNEL 1; VOLTAGE DEPENDENT ANION CHANNEL 2; VOLTAGE DEPENDENT ANION CHANNEL 3;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL MEMBRANE PERMEABILITY; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; EMBRYO; EMBRYO CELL; FIBROBLAST; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN EXPRESSION; REGULATORY MECHANISM;

ANIMALS; APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; BH3 INTERACTING DOMAIN DEATH AGONIST PROTEIN; CELLS, CULTURED; DRUG RESISTANCE; EMBRYO, MAMMALIAN; FIBROBLASTS; GENE DELETION; GENE KNOCKDOWN TECHNIQUES; MICE; MITOCHONDRIA; MITOCHONDRIAL MEMBRANES; PERMEABILITY; PROTEIN TRANSPORT; RECOMBINANT PROTEINS; VOLTAGE-DEPENDENT ANION CHANNEL 2;

EID: 73849084212     PISSN: 1469221X     EISSN: 14693178     Source Type: Journal    
DOI: 10.1038/embor.2009.219     Document Type: Article

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