ArticleThe Biochemical journal2005
Suppression of the pro-apoptotic function of cytochrome c by singlet oxygen via a haem redox state-independent mechanism.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- Raman Monitoring ofInternational journal of molecular sciences · 2025Article
- Article
- Biological Action of Singlet Molecular Oxygen from the Standpoint of Cell Signaling, Injury and Death.Molecules (Basel, Switzerland) · 2023Review
- Electron transfer between cytochrome c and microsomal monooxygenase generates reactive oxygen species that accelerates apoptosis.Redox biology · 2022Article
- Superoxide Radicals in the Execution of Cell Death.Antioxidants (Basel, Switzerland) · 2022Review
- Effect of blueberry extract on energetic metabolism, levels of brain-derived neurotrophic factor, and CaMetabolic brain disease · 2022Article
- Protective effects of anthocyanins against brain ischemic damage.Journal of bioenergetics and biomembranes · 2020Article
- Exploring the Continuum of Hypertrophic Cardiomyopathy-From DNA to Clinical Expression.Medicina (Kaunas, Lithuania) · 2019Review
- Downregulation of cytochromeOncology letters · 2017Article
- Oxidized or Reduced Cytochrome c and Axial Ligand Variants All Form the Apoptosome in Vitro.Biochemistry · 2017Article
- Computational evidence support the hypothesis of neuroglobin also acting as an electron transfer species.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2017Article
- Overproduction of reactive oxygen species - obligatory or not for induction of apoptosis by anticancer drugs.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2016Article
- The NADPH oxidase NOX5 protects against apoptosis in ALK-positive anaplastic large-cell lymphoma cell lines.Free radical biology & medicine · 2015Article
- Ascorbate peroxidase, a key molecule regulating amphotericin B resistance in clinical isolates of Leishmania donovani.Antimicrobial agents and chemotherapy · 2014Article
- Regulation of the intrinsic apoptosis pathway by reactive oxygen species.Antioxidants & redox signaling · 2013Review
- Review
- The redox state of cytochrome c modulates resistance to methotrexate in human MCF7 breast cancer cells.PloS one · 2013Article
- Mitochondrial mechanisms of neuroglobin's neuroprotection.Oxidative medicine and cellular longevity · 2013Review
- UV-light effects on cytochrome c modulated by the aggregation state of phenothiazines.PloS one · 2013Article
- S. choloroleuca, S. mirzayanii and S. santolinifolia protect PC12 cells from H(2)O (2)-induced apoptosis by blocking the intrinsic pathway.Cytotechnology · 2012Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimuli for apoptotic signalling typically induce release of cyt c (cytochrome c) from mitochondria. Cyt c then initiates the formation of the apoptosome, comprising Apaf-1 (apoptotic protease-activating factor 1), caspase-9 and other cofactors. The issue of whether the redox state of the haem in cyt c affects the initiation of the apoptotic pathway is currently a subject of debate. In a cell-free reconstitution system, we found that only oxidized cyt c was capable of activating the caspase cascade. Oxidized cyt c was reduced by the physiological reductants cysteine and glutathione, after which it was unable to activate the caspase cascade. It is thus likely that cyt c with oxidized haem is in a conformation capable of interaction with Apaf-1 and forming apoptosomes. When either oxidized or reduced cyt c was treated with submillimolar concentrations of endoperoxide, which affected less than 3% of the redox state of haem, the ability of the oxidized cyt c to activate the caspase cascade was abolished. Higher amounts of singlet oxygen were required to affect the optical spectral change of haem, suggesting that the suppressed pro-apoptotic function of oxidized cyt c is a mechanism that is separate from the redox state of haem. Oxidative protein modification of cyt c by singlet oxygen was evident, on the basis of elevated contents of carbonyl compounds. Our data suggest that singlet oxygen eliminates the pro-apoptotic ability of oxidized cyt c not via the reduction of haem, but via the modification of amino acid residues that are required for apoptosome formation.
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.