Lack of Oxidative Phosphorylation and Low Mitochondrial Membrane Potential Decrease Susceptibility to Apoptosis and Do Not Modulate the Protective Effect of Bcl-xL in Osteosarcoma Cells
Open Access
- 1 March 2000
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 275 (10) , 7087-7094
- https://doi.org/10.1074/jbc.275.10.7087
Abstract
No abstract availableKeywords
This publication has 65 references indexed in Scilit:
- Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of ApoptosisScience, 1998
- Apoptosis induced by microinjection of cytochrome c is caspase-dependent and is inhibited by Bcl-2Cell Death & Differentiation, 1998
- The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of ApoptosisScience, 1997
- Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome cPublished by Elsevier ,1996
- Inhibitors of permeability transition interfere with the disruption of the mitochondrial transmembrane potential during apoptosisFEBS Letters, 1996
- Bax-independent inhibition of apoptosis by Bcl-XLNature, 1996
- The mitochondrial permeability transitionBiochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, 1995
- Mitochondrial respiratory chain inhibitors induce apoptosisFEBS Letters, 1994
- A New Method for the Cytofluorometric Analysis of Mitochondrial Membrane Potential Using the J-Aggregate Forming Lipophilic Cation 5,5′,6,6′-Tetrachloro-1,1′,3,3′-tetraethylbenzimidazolcarbocyanine Iodide (JC-1)Biochemical and Biophysical Research Communications, 1993
- bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell deathCell, 1993