Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c

Cell Death and Differentiation

Volumn 7, Issue 12, 2000, Pages 1166-1173

  Korsmeyer, S J ^a   Wei, M C ^a,b   Saito, M ^b   Weiler, S ^a   Oh, K J ^a   Schlesinger, P H ^b  

^a DANA FARBER CANCER INSTITUTE   (United States)

^b WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

BAK; BAX; Mitochondria; TBID oligomerization

Indexed keywords

CELL SURFACE RECEPTOR; CYTOCHROME C; FLUORESCEIN ISOTHIOCYANATE; LIGAND; LIPOSOME; PROTEIN BAK; PROTEIN BAX; PROTEIN BCL 2;

ALLOSTERISM; APOPTOSIS; CELL DEATH; CELL MEMBRANE; CELL SURFACE; CELL VACUOLE; CHANNEL GATING; CONTROLLED STUDY; KNOCKOUT MOUSE; MITOCHONDRION; MODEL; MOLECULE; MOUSE; NONHUMAN; OLIGOMERIZATION; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN SECRETION; PROTEIN TARGETING; PROTEIN TRANSPORT; REVIEW; SEQUENCE HOMOLOGY;

ANIMALS; APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; BH3 INTERACTING DOMAIN DEATH AGONIST PROTEIN; CARRIER PROTEINS; CYTOCHROME C GROUP; HUMANS; MEMBRANE PROTEINS; MITOCHONDRIA; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; SIGNAL TRANSDUCTION;

EID: 0034523818     PISSN: 13509047     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.cdd.4400783     Document Type: Review

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