Disruption of the VDAC2Bak interaction by Bcl-xS mediates efficient induction of apoptosis in melanoma cells

Cell Death and Differentiation

Volumn 19, Issue 12, 2012, Pages 1928-1938

  Plotz M ^a   Gillissen, B ^a   Hossini, A M ^a   Daniel, P T ^a   Eberle, J ^a  

^a CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

Author keywords

apoptosis; Bak; Bcl xS; melanoma; VDAC2

Indexed keywords

ADENOVIRUS VECTOR; BCL XS PROTEIN; CASPASE; COMPLEMENTARY DNA; CYTOCHROME C; PROTEIN; PROTEIN BAK; UNCLASSIFIED DRUG; VOLTAGE DEPENDENT ANION CHANNEL 2; MYELOID CELL LEUKEMIA SEQUENCE 1 PROTEIN; PROTEIN BCL 2; PROTEIN BCL X; SMALL INTERFERING RNA; VDAC2 PROTEIN, HUMAN;

APOPTOSIS; ARTICLE; CELL DISRUPTION; ENZYME ACTIVATION; GENE OVEREXPRESSION; HUMAN; HUMAN CELL; IMMUNOPRECIPITATION; MELANOMA CELL; MITOCHONDRIAL MEMBRANE POTENTIAL; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN PROTEIN INTERACTION; CELL STRAIN HCT116; DRUG ANTAGONISM; GENETICS; MELANOMA; METABOLISM; PATHOLOGY; RNA INTERFERENCE; TUMOR CELL LINE;

APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-X PROTEIN; CELL LINE, TUMOR; HCT116 CELLS; HUMANS; MELANOMA; PROTEIN BINDING; PROTO-ONCOGENE PROTEINS C-BCL-2; RNA INTERFERENCE; RNA, SMALL INTERFERING; VOLTAGE-DEPENDENT ANION CHANNEL 2;

EID: 84869081493     PISSN: 13509047     EISSN: 14765403     Source Type: Journal    
DOI: 10.1038/cdd.2012.71     Document Type: Article

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