ArticleMolecular cell2016
An Autoinhibited Dimeric Form of BAX Regulates the BAX Activation Pathway.
Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 103 citations in OpenAlex.
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- YOD1 drives acute kidney injury by deubiquitinating Bax and promoting apoptosis in tubular epithelial cells.Theranostics · 2026Article
- Esketamine Enhances the Chemosensitivity of Colorectal Adenocarcinoma Cells to 5-Fluorouracil via AMPK/mTOR/HMMR Signaling Pathway.Oncology research · 2026Article
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- Optogenetic engineering of BAX to control mitochondrial permeabilization and attenuate apoptosis in cells.Experimental & molecular medicine · 2025Article
- Multifaceted Roles of Bcl-2 Family Proteins: Regulatory Roles in Apoptosis, Physiological Functions, and Therapeutic Potential.Current medical science · 2025Review
- 3-Hydroxy-β-ionone Suppresses Breast Cancer Progression by Inducing Apoptosis and Blocking EMT Through the TGF-β/Smad Signaling Pathway.International journal of molecular sciences · 2025Article
- Exploring the critical role of PANoptosis in the pathogenesis of intervertebral disc degeneration: mechanisms and potential therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Moschus ameliorates glutamate-induced cellular damage by regulating autophagy and apoptosis pathway.Scientific reports · 2023Article
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Microfluidic Generation of Near-Infrared Photothermal Vitexin/ICG Liposome with Amplified Photodynamic Therapy.AAPS PharmSciTech · 2023Article
- Anticancer Activities of Re(I) Tricarbonyl and Its Imidazole-Based Ligands: Insight from a Theoretical Approach.ACS omega · 2023Article
- A kinetic fluorescence polarization ligand assay for monitoring BAX early activation.Cell reports methods · 2022Article
- Physiological and pharmacological modulation of BAX.Trends in pharmacological sciences · 2022Review
- Bcl-2 Family Members and the Mitochondrial Import Machineries: The Roads to Death.Biomolecules · 2022Review
- Article
- BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021Review
- Protective and Anti-Inflammatory Effects of Protegrin-1 onInternational journal of molecular sciences · 2021Article
Corrections and comments
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- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pro-apoptotic BAX is a cell fate regulator playing an important role in cellular homeostasis and pathological cell death. BAX is predominantly localized in the cytosol, where it has a quiescent monomer conformation. Following a pro-apoptotic trigger, cytosolic BAX is activated and translocates to the mitochondria to initiate mitochondrial dysfunction and apoptosis. Here, cellular, biochemical, and structural data unexpectedly demonstrate that cytosolic BAX also has an inactive dimer conformation that regulates its activation. The full-length crystal structure of the inactive BAX dimer revealed an asymmetric interaction consistent with inhibition of the N-terminal conformational change of one protomer and the displacement of the C-terminal helix α9 of the second protomer. This autoinhibited BAX dimer dissociates to BAX monomers before BAX can be activated. Our data support a model whereby the degree of apoptosis induction is regulated by the conformation of cytosolic BAX and identify an unprecedented mechanism of cytosolic BAX inhibition.
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What OpenQuestion holds
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.