ArticleBiophysical journal2013
Mechanistic differences in the membrane activity of Bax and Bcl-xL correlate with their opposing roles in apoptosis.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 81 citations in OpenAlex.
- Ferroptosis spreads to neighboring cells via plasma membrane contacts.Nature communications · 2025Article
- The minimal membrane requirements for BAX-induced pore opening upon exposure to oxidative stress.Biophysical journal · 2024Article
- Advances in the anti-tumor mechanisms of saikosaponin D.Pharmacological reports : PR · 2024Review
- Lipid unsaturation promotes BAX and BAK pore activity during apoptosis.Nature communications · 2024Article
- Article
- Lobetyolin inhibits cell proliferation and induces cell apoptosis by downregulating ASCT2 in gastric cancer.Cytotechnology · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Visualization of BOK pores independent of BAX and BAK reveals a similar mechanism with differing regulation.Cell death and differentiation · 2023Article
- The Important Role of Membrane Fluidity on the Lytic Mechanism of the α-Pore-Forming Toxin Sticholysin I.Toxins · 2023Article
- DRP1 interacts directly with BAX to induce its activation and apoptosis.The EMBO journal · 2022Article
- The interplay between BAX and BAK tunes apoptotic pore growth to control mitochondrial-DNA-mediated inflammation.Molecular cell · 2022Article
- LncRNA-GAS5 promotes spinal cord repair and the inhibition of neuronal apoptosis via the transplantation of 3D printed scaffold loaded with induced pluripotent stem cell-derived neural stem cells.Annals of translational medicine · 2021Article
- Neutron reflectometry and NMR spectroscopy of full-length Bcl-2 protein reveal its membrane localization and conformation.Communications biology · 2021Article
- Mitochondrial outer membrane permeabilization at the single molecule level.Cellular and molecular life sciences : CMLS · 2021Review
- Insight into Functional Membrane Proteins by Solution NMR: The Human Bcl-2 Protein-A Promising Cancer Drug Target.Molecules (Basel, Switzerland) · 2021Article
- Location of Peptide-Induced Submicron Discontinuities in the Membranes of Vesicles Using ImageJ.Journal of fluorescence · 2020Article
- The knockdown of the sepiapterin reductase gene suppresses the proliferation of breast cancer by inducing ROS-mediated apoptosis.International journal of clinical and experimental pathology · 2020Article
- A new perspective on membrane-embedded Bax oligomers using DEER and bioresistant orthogonal spin labels.Scientific reports · 2019Article
- Topology of active, membrane-embedded Bax in the context of a toroidal pore.Cell death and differentiation · 2018Article
- Lipid-dependence of target membrane stability during influenza viral fusion.Journal of cell science · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Based on their membrane-permeabilizing activity in vitro, it has been proposed that Bax-like proteins induce cytochrome c release during apoptosis via pore formation. However, antiapoptotic Bcl-2 proteins, which inhibit cytochrome c release, also display pore activity in model membranes. As a consequence, a unified description that aligns the pore activity of the Bcl-2 proteins with their apoptotic function is missing. Here, we studied the mechanism of membrane binding, oligomerization, and permeabilization by pro- and antiapoptotic Bcl-2 members at the single-vesicle level. We found that proapoptotic Bax forms large, stable pores via an all-or-none mechanism that can release cytochrome c. In contrast, antiapoptotic Bcl-xL induces transient permeability alterations in pure lipid membranes that have no consequences for the mitochondrial outer membrane but inhibit Bax membrane insertion. These differences in pore activity correlate with a distinct oligomeric state of Bax and Bcl-xL in membranes and can be reproduced in isolated mitochondria. Based on our findings, we propose new models for the mechanisms of action of Bax and Bcl-xL that relate their membrane activity to their opposing roles in apoptosis and beyond.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.