ArticleeLife2013
Bax and Bak function as the outer membrane component of the mitochondrial permeability pore in regulating necrotic cell death in mice.
Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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
181 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Pooled it
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Dying for Clarity: Common Pitfalls in Cardiac Cell Death Research.Cardiovascular drugs and therapy · 2026Article
- Reverse engineering of BNIP3 identifies a mitochondrial protective peptide.Nature communications · 2026Article
- Ice-Cold Temperature Enhances NADPH Oxidase-Dependent Release of Tissue Factor-Bearing Extracellular Vesicles from Human Monocytic Cells.Life (Basel, Switzerland) · 2026Article
- Research Progress on NINJ1-Mediated Plasma Membrane Rupture Regulation of Pathogen Infection Process.International journal of molecular sciences · 2026Review
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- Mitochondrial DNA release via mPTP and BAX/BAK drives inflammatory injury in intestinal ischemia reperfusion.Cell communication and signaling : CCS · 2025Article
- Yeast NatB Regulates Cell Death of Bax-Expressing Cells.Biomolecules · 2025Article
- Porcine Epidemic Diarrhea-Virus-Induced Cell Death: Mechanistic Insights and Therapeutic Strategies.Veterinary sciences · 2025Review
- Differential Chromatin Accessibility, Gene Expression, and mRNA Splicing Between Developing Cochlear Inner and Outer Hair Cells.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- Computational design of potent and selective binders of BAK and BAX.Science advances · 2025Article
- Regulated Cell Death in Myocardial Infarction.Circulation research · 2025Article
- BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral.Communications biology · 2025Article
- Bacterial programmed cell death and toxin-antitoxin system in bacteria.Archives of microbiology · 2025Review
- Synergistic effects of abietic acid combined with doxorubicin on apoptosis induction in a human colorectal cancer cell line.Scientific reports · 2025Article
- Regulation of lncRNA-ENST on Myc-mediated mitochondrial apoptosis in mesenchymal stem cells:World journal of stem cells · 2025Article
- Senolysis by GLS1 Inhibition Ameliorates Kidney Aging by Inducing Excessive mPTP Opening Through MFN1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
121 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
A critical event in ischemia-based cell death is the opening of the mitochondrial permeability transition pore (MPTP). However, the molecular identity of the components of the MPTP remains unknown. Here, we determined that the Bcl-2 family members Bax and Bak, which are central regulators of apoptotic cell death, are also required for mitochondrial pore-dependent necrotic cell death by facilitating outer membrane permeability of the MPTP. Loss of Bax/Bak reduced outer mitochondrial membrane permeability and conductance without altering inner membrane MPTP function, resulting in resistance to mitochondrial calcium overload and necrotic cell death. Reconstitution with mutants of Bax that cannot oligomerize and form apoptotic pores, but still enhance outer membrane permeability, permitted MPTP-dependent mitochondrial swelling and restored necrotic cell death. Our data predict that the MPTP is an inner membrane regulated process, although in the absence of Bax/Bak the outer membrane resists swelling and prevents organelle rupture to prevent cell death. DOI:http://dx.doi.org/10.7554/eLife.00772.001.
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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.