ArticleScience advances2023
Creation of distinctive Bax-lipid complexes at mitochondrial membrane surfaces drives pore formation to initiate apoptosis.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Neutron reflectometry instrumentation at the ISIS source: current state.Journal of applied crystallography · 2026Article
- Avoiding Mitochondrial Apoptosis by the Bcl-2-Driven Bax Oligomerization on Membrane Surfaces.ACS chemical biology · 2026Article
- UGT8 mediated sulfatide synthesis modulates BAX localization and dictates apoptosis sensitivity of colorectal cancer.Cell death and differentiation · 2025Article
- Extracellular Histones as Exosome Membrane Proteins Regulated by Cell Stress.Journal of extracellular vesicles · 2025Article
- Expression and Function of FAM72A Gene in Multiple MyelomaFAM72A.Current pharmaceutical biotechnology · 2025Article
- Types of cell death in diabetic cardiomyopathy: insights from animal models.Acta biochimica et biophysica Sinica · 2024Review
- The minimal membrane requirements for BAX-induced pore opening upon exposure to oxidative stress.Biophysical journal · 2024Article
- Review
- FBXO5-mediated RNF183 degradation prevents endoplasmic reticulum stress-induced apoptosis and promotes colon cancer progression.Cell death & disease · 2024Article
- An octameric PqiC toroid stabilises the outer-membrane interaction of the PqiABC transport system.EMBO reports · 2024Article
- The roles of long non-coding RNAs in ovarian cancer: from functions to therapeutic implications.Frontiers in oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apotosis is an essential process tightly regulated by the Bcl-2 protein family where proapoptotic Bax triggers cell death by perforating the mitochondrial outer membrane. Although intensively studied, the molecular mechanism by which these proteins create apoptotic pores remains elusive. Here, we show that Bax creates pores by extracting lipids from outer mitochondrial membrane mimics by formation of Bax/lipid clusters that are deposited on the membrane surface. Time-resolved neutron reflectometry and Fourier transform infrared spectroscopy revealed two kinetically distinct phases in the pore formation process, both of which were critically dependent on cardiolipin levels. The initially fast adsorption of Bax on the mitochondrial membrane surface is followed by a slower formation of pores and Bax-lipid clusters on the membrane surface. Our findings provide a robust molecular understanding of mitochondrial membrane perforation by cell-killing Bax protein and illuminate the initial phases of programmed cellular death.
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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.