ArticleBiochimica et biophysica acta2010
Dissimilar mechanisms of cytochrome c release induced by octyl glucoside-activated BAX and by BAX activated with truncated BID.
Article in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Inducible fold-switching as a mechanism to fibrillate pro-apoptotic BCL-2 proteins.Biopolymers · 2021Article
- Humanin selectively prevents the activation of pro-apoptotic protein BID by sequestering it into fibers.The Journal of biological chemistry · 2020Article
- Minor structural modifications of bisphenol A strongly affect physiological responses of HepG2 cells.Archives of toxicology · 2019Article
- Deletion of mitochondrial calcium uniporter incompletely inhibits calcium uptake and induction of the permeability transition pore in brain mitochondria.The Journal of biological chemistry · 2018Article
- Ca(2+) handling in isolated brain mitochondria and cultured neurons derived from the YAC128 mouse model of Huntington's disease.Journal of neurochemistry · 2015Article
- The dynamics of Bax channel formation: influence of ionic strength.Biophysical journal · 2012Article
- BAX insertion, oligomerization, and outer membrane permeabilization in brain mitochondria: role of permeability transition and SH-redox regulation.Biochimica et biophysica acta · 2010Article
- Bioenergetics and cell death.Annals of the New York Academy of Sciences · 2010Review
- The effect of mitochondrial calcium uniporter and cyclophilin D knockout on resistance of brain mitochondria to CaThe Journal of biological chemistryArticle
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
In the present study, we compared alkali-resistant BAX insertion into the outer mitochondrial membrane, mitochondrial remodeling, mitochondrial membrane potential changes, and cytochrome c (Cyt c) release from isolated brain mitochondria triggered by recombinant BAX oligomerized with 1% octyl glucoside (BAX(oligo)) and by a combination of monomeric BAX (BAX(mono)) and caspase 8-cleaved C-terminal fragment of recombinant BID (truncated BID, t(c)BID). We also examined whether the effects induced by BAX(oligo) or by BAX(mono) activated with t(c)BID depended on induction of the mitochondrial permeability transition. The results obtained in this study revealed that t(c)BID plus BAX(mono) produced BAX insertion and Cyt c release without overt changes in mitochondrial morphology. On the contrary, treatment of mitochondria with BAX(oligo) resulted in BAX insertion and Cyt c release, which were accompanied by gross distortion of mitochondrial morphology. The effects of BAX(oligo) could be at least partially suppressed by mitochondrial depolarization. The effects of t(c)BID plus BAX(mono) were insensitive to depolarization. BAX(oligo) produced similar BAX insertion, mitochondrial remodeling, and Cyt c release in KCl- and in N-methyl-D-glucamine-based incubation media indicating a non-essential role for K+ influx into mitochondria in these processes. A combination of cyclosporin A and ADP, inhibitors of the mitochondrial permeability transition, attenuated Cyt c release, mitochondrial remodeling, and depolarization induced by BAX(oligo), but failed to influence the effects produced by t(c)BID plus BAX(mono). Thus, our results suggest a significant difference in the mechanisms of the outer mitochondrial membrane permeabilization and Cyt c release induced by detergent-oligomerized BAX(oligo) and by BAX activated with t(c)BID.
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