Bid-induced Cytochrome c Release Is Mediated by a Pathway Independent of Mitochondrial Permeability Transition Pore and Bax

Bid, a pro-apoptosis “BH3-only” member of the Bcl-2 family, can be cleaved by caspase-8 after Fas/TNF-R1 engagement. The p15 form of truncated Bid (tBid) translocates to mitochondria and induces cytochrome c release, leading to the activation of downstream caspases and apoptosis. In the current stud...

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Veröffentlicht in:	The Journal of biological chemistry 2000-12, Vol.275 (50), p.39474-39481
Hauptverfasser:	Kim, Tae-Hyoung, Zhao, Yongge, Barber, Michael J., Kuharsky, Diane K., Yin, Xiao-Ming
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis bcl-2-Associated X Protein bcl-X Protein BH3 Interacting Domain Death Agonist Protein Bid protein Carrier Proteins - genetics Carrier Proteins - metabolism Caspase Inhibitors cytochrome c Cytochrome c Group - metabolism Dose-Response Relationship, Drug Escherichia coli - metabolism fas Receptor - metabolism Hepatocytes - metabolism Ion Channels Magnesium - metabolism Magnesium Chloride - pharmacology Membrane Potentials Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mitochondria - metabolism Mitochondria, Liver - metabolism Mitochondrial Membrane Transport Proteins Mitochondrial Permeability Transition Pore Oxidoreductases Acting on Sulfur Group Donors - metabolism Protein Binding Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Recombinant Proteins - metabolism Time Factors
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