ReviewTrends in biochemical sciences2011
BAX unleashed: the biochemical transformation of an inactive cytosolic monomer into a toxic mitochondrial pore.
Review in Trends in biochemical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 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
103 citing papers in PubMed, 168 citations in OpenAlex.
- An enantioselective covalent inhibitor of BAX confers cytoprotection in vivo.Nature chemical biology · 2026Article
- A peptide-based screen for cell death inhibitors identifies the cytoprotective compound CDL36.bioRxiv : the preprint server for biology · 2026Article
- Alginate Oligosaccharide Alleviates Salmonella Typhimurium-Induced Liver Injury by Regulating Oxidative Stress, Apoptosis, and Inflammatory Signaling Pathway.Probiotics and antimicrobial proteins · 2026Article
- A metabolic cell death program downstream of SARM1 couples NADProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Review
- Interactome screening implicates BAG6 as a suppressor of UBQLN2 misfolding in ALS/FTD.Frontiers in molecular neuroscience · 2025Article
- Covalent inhibition of pro-apoptotic BAX.Nature chemical biology · 2024Article
- Chemical modulation of cytosolic BAX homodimer potentiates BAX activation and apoptosis.Nature communications · 2023Article
- Targeting MCL-1 triggers DNA damage and an anti-proliferative response independent from apoptosis induction.Cell reports · 2023Article
- Recent advances in targeting the "undruggable" proteins: from drug discovery to clinical trials.Signal transduction and targeted therapy · 2023Review
- Novel Chlorin e6-Curcumin Derivatives as a Potential Photosensitizer: Synthesis, Characterization, and Anticancer Activity.Pharmaceutics · 2023Article
- Membrane interactions of apoptotic inhibitor Bcl-xL: What can be learned using fluorescence spectroscopy.BBA advances · 2023Article
- Targeting protein conformations with small molecules to control protein complexes.Trends in biochemical sciences · 2022Review
- MCL-1 is a master regulator of cancer dependency on fatty acid oxidation.Cell reports · 2022Article
- Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer.Nature communications · 2022Article
- Novel Therapeutics for Anthracycline Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Extrinsic interactions in the microenvironment in vivo activate an antiapoptotic multidrug-resistant phenotype in CLL.Blood advances · 2021Article
- Lipids modulate the BH3-independent membrane targeting and activation of BAX and Bcl-xL.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The conformational stability of pro-apoptotic BAX is dictated by discrete residues of the protein core.Nature communications · 2021Article
43 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
BAX, the BCL-2-associated X protein, is a cardinal proapoptotic member of the BCL-2 family, which regulates the critical balance between cellular life and death. Because so many medical conditions can be categorized as diseases of either too many or too few cells, dissecting the biochemistry of BCL-2 family proteins and developing pharmacological strategies to target them have become high priority scientific objectives. Here, we focus on BAX, a latent, cytosolic and monomeric protein that transforms into a lethal mitochondrial oligomer in response to cellular stress. New insights into the structural location of BAX's 'on switch', and the multi-step conformational changes that ensue upon BAX activation, are providing fresh opportunities to modulate BAX for potential benefit in human diseases characterized by pathologic cell survival or unwanted cellular demise.
Indexed as
Identifiers
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.