Bak and Bax are non-redundant during infection- and DNA damage-induced apoptosis

EMBO Journal

Volumn 26, Issue 3, 2007, Pages 825-834

  Kepp, Oliver ^a   Rajalingam, Krishnaraj ^a,b   Kimmig, Sonja ^a   Rudel, Thomas ^a  

^a MAX PLANCK INSTITUTE FOR INFECTION BIOLOGY   (Germany)

^b UNIVERSITY OF WÜRZBURG   (Germany)

Author keywords

Apoptosis; Bak; Bax; DNA damage; Mitochondria; Neisseria

Indexed keywords

CASPASE; CISPLATIN; CYTOCHROME C; MITOCHONDRIAL PROTEIN; PROTEIN BAK; PROTEIN BAX; TUMOR NECROSIS FACTOR ALPHA;

APOPTOSIS; ARTICLE; CONTROLLED STUDY; DNA DAMAGE; ENZYME ACTIVATION; HUMAN; HUMAN CELL; MITOCHONDRION; NEISSERIA GONORRHOEAE; NEISSERIACEAE INFECTION; PRIORITY JOURNAL; PROTEIN SECRETION;

APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; BLOTTING, WESTERN; CASPASES; CELL FRACTIONATION; DNA DAMAGE; DNA PRIMERS; FLOW CYTOMETRY; HELA CELLS; HUMANS; IMMUNOPRECIPITATION; INTRACELLULAR MEMBRANES; MICROSCOPY, FLUORESCENCE; MITOCHONDRIA; NEISSERIA GONORRHOEAE; PERMEABILITY; RNA INTERFERENCE;

NEISSERIA; NEISSERIA GONORRHOEAE;

EID: 33846955741     PISSN: 02614189     EISSN: 14602075     Source Type: Journal    
DOI: 10.1038/sj.emboj.7601533     Document Type: Article

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