Bak can accelerate chemotherapy-induced cell death independently of its heterodimerization with Bcl-X(L) and Bcl-2

Oncogene

Volumn 15, Issue 15, 1997, Pages 1871-1875

  Simonian, Philip L ^a   Grillot, Didier A M ^a   Nuñez, Gabriel ^a  

^a UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

Author keywords

Apoptosis; Bak; Bcl 2; Bcl X(L); Cell death; Chemotherapy

Indexed keywords

ETOPOSIDE; FLUOROURACIL; MUTANT PROTEIN; PACLITAXEL; PROTEIN BCL 2;

APOPTOSIS; ARTICLE; CANCER CHEMOTHERAPY; CELL CLONE; CELL DEATH; CONTROLLED STUDY; DIMERIZATION; IMMUNOPRECIPITATION; PRIORITY JOURNAL; PROTEIN FAMILY; PROTEIN PROTEIN INTERACTION;

EID: 0030669561     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1201350     Document Type: Article

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