ArticleThe Journal of biological chemistry2020
Mitochondrial residence of the apoptosis inducer BAX is more important than BAX oligomerization in promoting membrane permeabilization.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- Mitochondrial targeting strategies for mitigating oxidative damage and enhancing neuroprotection in ischemic stroke: A Review.IBRO neuroscience reports · 2026Review
- BCL2 inhibition in acute and chronic pancreatitis - is there a therapeutic perspective?Cell death discovery · 2026Review
- Modulation of Wnt/β-Catenin Pathway by Aesculus hippocastanum Extract Enhances Temozolomide Sensitivity in Glioblastoma Cells.Journal of cellular and molecular medicine · 2026Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Dose-dependent apoptotic effect of3 Biotech · 2025Article
- Article
- CREB1 Is Involved in miR-134-5p-Mediated Endometrial Stromal Cell Proliferation, Apoptosis, and Autophagy.Cells · 2023Article
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- BCL-2-family protein tBID can act as a BAX-like effector of apoptosis.The EMBO journal · 2022Article
- SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.eLife · 2022Article
- Tetrahydroquinolinone derivatives exert antiproliferative effect on lung cancer cells through apoptosis induction.Scientific reports · 2022Article
- Mitochondrial dynamics regulate genome stability via control of caspase-dependent DNA damage.Developmental cell · 2022Article
- The interplay between BAX and BAK tunes apoptotic pore growth to control mitochondrial-DNA-mediated inflammation.Molecular cell · 2022Article
- Bcl-2 Family Members and the Mitochondrial Import Machineries: The Roads to Death.Biomolecules · 2022Review
- Non-phosphorylatable mutants of Ser184 lead to incomplete activation of Bax.Frontiers in oncology · 2022Article
- High-resolution analysis of the conformational transition of pro-apoptotic Bak at the lipid membrane.The EMBO journal · 2021Article
- Incomptine A Induces Apoptosis, ROS Production and a Differential Protein Expression on Non-Hodgkin's Lymphoma Cells.International journal of molecular sciences · 2021Article
- Lipids modulate the BH3-independent membrane targeting and activation of BAX and Bcl-xL.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Contribution of Yeast Studies to the Understanding of BCL-2 Family Intracellular Trafficking.International journal of molecular sciences · 2021Review
- Mitochondrial outer membrane permeabilization at the single molecule level.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Permeabilization of the mitochondrial outer membrane is a key step in the intrinsic apoptosis pathway, triggered by the release of mitochondrial intermembrane space proteins into the cytoplasm. The BCL-2-associated X apoptosis regulator (BAX) protein critically contributes to this process by forming pores in the mitochondrial outer membrane. However, the relative roles of the mitochondrial residence of BAX and its oligomerization in promoting membrane permeabilization are unclear. To this end, using both cell-free and cellular experimental systems, including membrane permeabilization, size-exclusion chromatography-based oligomer, and retrotranslocation assays, along with confocal microscopy analysis, here we studied two BAX C-terminal variants, T182I and G179P. Neither variant formed large oligomers when activated in liposomes. Nevertheless, the G179P variant could permeabilize liposome membranes, suggesting that large BAX oligomers are not essential for the permeabilization. However, when G179P was transduced into BAX/BCL2 agonist killer (BAK) double-knockout mouse embryonic fibroblasts, its location was solely cytoplasmic, and it then failed to mediate cell death. In contrast, T182I was inefficient in both liposome insertion and permeabilization. Yet, when transduced into cells, BAXT182I resided predominantly on mitochondria, because of its slow retrotranslocation and mediated apoptosis as efficiently as WT BAX. We conclude that BAX's mitochondrial residence
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