ArticleKorean journal of biological sciences2003
Redox Regulation of Apoptosis before and after Cytochrome C Release.
Article in Korean journal of biological sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 31 citations in OpenAlex.
- Redox signalling and ageing: insights from Drosophila.Biochemical Society transactions · 2020Review
- Escaping Death: Mitochondrial Redox Homeostasis in Cancer Cells.Frontiers in oncology · 2017Review
- Cytotoxic effect of gambogic acid on SH-SY5Y neuroblastoma cells is mediated by intrinsic caspase-dependent signaling pathway.Molecular and cellular biochemistry · 2013Article
- A growth factor attenuates HIV-1 Tat and morphine induced damage to human neurons: implication in HIV/AIDS-drug abuse cases.PloS one · 2011Article
- Potential therapeutic benefits of strategies directed to mitochondria.Antioxidants & redox signaling · 2010Review
- Tropheryma whipplei, the Whipple's disease bacillus, induces macrophage apoptosis through the extrinsic pathway.Cell death & disease · 2010Article
- Combining 2-deoxy-D-glucose with electron transport chain blockers: a double-edged sword.Cancer biology & therapy · 2009Article
- Molecular mechanism of curcumin induced cytotoxicity in human cervical carcinoma cells.Molecular and cellular biochemistry · 2009Article
- Long-chain ceramide is a potent inhibitor of the mitochondrial permeability transition pore.The Journal of biological chemistry · 2008Article
- Mechanisms of neutrophil death in human immunodeficiency virus-infected patients: role of reactive oxygen species, caspases and map kinase pathways.Clinical and experimental immunology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Programmed cell death, or apoptosis, is one of the most studied areas of modern biology. Apoptosis is a genetically regulated process, which plays an essential role in the development and homeostasis of higher organisms. Mitochondria, known to play a central role in regulating cellular metabolism, was found to be critical for regulating apoptosis induced under both physiological and pathological conditions. Mitochondria are a major source of reactive oxygen species (ROS) but they can also serve as its target during the apoptosis process. Release of apoptogenic factors from mitochondria, the best known of which is cytochrome c, leads to assembly of a large apoptosis-inducing complex called the apoptosome. Cysteine proteases (called caspases) are recruited to this complex and, following their activation by proteolytic cleavage, activate other caspases, which in turn target for specific cleavage a large number of cellular proteins. The redox regulation of apoptosis during and after cytochrome c release is an area of intense investigation. This review summarizes what is known about the biological role of ROS and its targets in apoptosis with an emphasis on its intricate connections to mitochondria and the basic components of cell death.
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.