ReviewOncogene2004
Toxic proteins released from mitochondria in cell death.
Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 320 papers, 1 of them a synthesis that pooled it.
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
320 citing papers in PubMed, 1 synthesis or guideline pooled it, 958 citations in OpenAlex.
- Cuproptosis: Mechanisms, biological significance, and advances in disease treatment-A systematic review.CNS neuroscience & therapeutics · 2024Pooled it
- Gene expression regulated by abatacept associated with methotrexate and correlation with disease activity in rheumatoid arthritis.PloS one · 2020Trial
- Molecular switches in cell death: the interplay of apoptosis and pyroptosis in cancer.Cell communication and signaling : CCS · 2026Review
- Investigating the Cellular and Tissue Response to Herbal Glucose/Cellulose-based Mesoporous Graphene Frameworks in a Rat Diabetic Wounds Model.Cell biochemistry and biophysics · 2026Article
- Assessment of Cellular Apoptosis Induced by Hydroxychalcones in MCC13 Merkel Cells.International journal of molecular sciences · 2026Article
- Review
- Dysregulated Cell Signaling Pathways in Prostate Tumoral Plasticity-Checkpoints.Oncology research · 2026Article
- Modulation of host cell pathways bymLife · 2025Review
- Organic Sonosensitizers-based SDT with enhanced ROS generation.Ultrasonics sonochemistry · 2025Review
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Structural Characterization of, and Protective Effects Against, CoClFoods (Basel, Switzerland) · 2025Article
- Quercetin Protects against Ethanol-induced Neurodegeneration in Adult Rat Cortex.Current neuropharmacology · 2025Article
- The role of cell death in the physiological and pathological processes of skeletal muscle.Frontiers in physiology · 2025Review
- The cyclophilin D (CypD) of Toxoplasma gondii is involved in the parasite's response to oxidative stress damage.Parasitology research · 2024Article
- Genetic insights into the role of cathepsins in cardiovascular diseases: a Mendelian randomization study.ESC heart failure · 2024Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- Apoptosis in post-streptococcal glomerulonephritis and mechanisms for failed of inflammation resolution.Pediatric nephrology (Berlin, Germany) · 2024Review
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
260 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
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A plethora of apoptotic stimuli converge on the mitochondria and affect their membrane integrity. As a consequence, multiple death-promoting factors residing in the mitochondrial intermembrane space are liberated in the cytosol. Pro- and antiapoptotic Bcl-2 family proteins control the release of these mitochondrial proteins by inducing or preventing permeabilization of the outer mitochondrial membrane. Once released into the cytosol, these mitochondrial proteins activate both caspase-dependent and -independent cell death pathways. Cytochrome c was the first protein shown to be released from the mitochondria into the cytosol, where it induces apoptosome formation. Other released mitochondrial proteins include apoptosis-inducing factor (AIF) and endonuclease G, both of which contribute to apoptotic nuclear DNA damage in a caspase-independent way. Other examples are Smac/DIABLO (second mitochondria-derived activator of caspase/direct IAP-binding protein with low PI) and the serine protease HtrA2/OMI (high-temperature requirement protein A2), which both promote caspase activation and instigate caspase-independent cytotoxicity. The precise mode of action and importance of cytochrome c in apoptosis in mammalian cells has become clear through biochemical, structural and genetic studies. More recently identified factors, for example HtrA2/OMI and Smac/DIABLO, are still being studied intensively in order to delineate their functions in apoptosis. A better understanding of these functions may help to develop new strategies to treat cancer.
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.