Bax Homodimerization Is Not Required for Bax to Accelerate Chemotherapy-induced Cell Death

Bax, a member of the Bcl-2 family of proteins, has been shown to accelerate apoptosis induced by growth factor withdrawal, γ-irradiation, and the chemotherapeutic agent, etoposide. The mechanism by which Bax promotes apoptosis is poorly understood. Bax forms homodimers which have been suggested to a...

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Veröffentlicht in:	The Journal of biological chemistry 1996-12, Vol.271 (50), p.32073-32077
Hauptverfasser:	Simonian, Philip L., Grillot, DidierA. M., Andrews, David W., Leber, Brian, Nuñez, Gabriel
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis bcl-2-Associated X Protein Cell Line Cell Survival Cisplatin - pharmacology Electrophoresis, Polyacrylamide Gel Etoposide - pharmacology Fluorouracil - pharmacology Mutagenesis, Site-Directed Protein Conformation Proto-Oncogene Proteins - chemistry Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2
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