ArticleCell reports2020
Site-Dependent Cysteine Lipidation Potentiates the Activation of Proapoptotic BAX.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 32 citations in OpenAlex.
- An enantioselective covalent inhibitor of BAX confers cytoprotection in vivo.Nature chemical biology · 2026Article
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- A gated hydrophobic funnel within BAX binds bioactive lipids to potentiate pro-apoptotic function.Nature communications · 2026Article
- ZDHHC-Mediated Protein S-Palmitoylation in Cancer: Epigenetic Interfaces, Structural Logic and Therapeutic Targeting.International journal of medical sciences · 2026Review
- Article
- Covalent inhibition of pro-apoptotic BAX.Nature chemical biology · 2024Article
- Plasmalogen oxidation induces the generation of excited molecules and electrophilic lipid species.PNAS nexus · 2024Article
- Directly targeting BAX for drug discovery: Therapeutic opportunities and challenges.Acta pharmaceutica Sinica. B · 2024Review
- A crosstalk between autophagy and apoptosis in intracerebral hemorrhage.Frontiers in cellular neuroscience · 2024Review
- Recent Insight into the Role of Sphingosine-1-Phosphate Lyase in Neurodegeneration.International journal of molecular sciences · 2023Review
- Apoptotic mitochondrial poration by a growing list of pore-forming BCL-2 family proteins.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- 2-Hexadecenal Regulates ROS Production and Induces Apoptosis in Polymorphonuclear Leucocytes.Cell biochemistry and biophysics · 2023Article
- Reduced ER-mitochondria connectivity promotes neuroblastoma multidrug resistance.The EMBO journal · 2022Article
- 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
- Protein cysteine palmitoylation in immunity and inflammation.The FEBS journal · 2021Review
- The conformational stability of pro-apoptotic BAX is dictated by discrete residues of the protein core.Nature communications · 2021Article
- A redox switch regulates the structure and function of anti-apoptotic BFL-1.Nature structural & molecular biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BCL-2 family proteins converge at the mitochondrial outer membrane to regulate apoptosis and maintain the critical balance between cellular life and death. This physiologic process is essential to organism homeostasis and relies on protein-protein and protein-lipid interactions among BCL-2 family proteins in the mitochondrial lipid environment. Here, we find that trans-2-hexadecenal (t-2-hex), previously implicated in regulating BAX-mediated apoptosis, does so by direct covalent reaction with C126, which is located on the surface of BAX at the junction of its α5/α6 core hydrophobic hairpin. The application of nuclear magnetic resonance spectroscopy, hydrogen-deuterium exchange mass spectrometry, specialized t-2-hex-containing liposomes, and BAX mutational studies in mitochondria and cells reveals structure-function insights into the mechanism by which covalent lipidation at the mitochondria sensitizes direct BAX activation. The functional role of BAX lipidation as a control point of mitochondrial apoptosis could provide a therapeutic strategy for BAX modulation by chemical modification of C126.
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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.