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Signal transduction by reactive oxygen species
Open accessAbstract
Although historically viewed as purely harmful, recent evidence suggests that reactive oxygen species (ROS) function as important physiological regulators of intracellular signaling pathways. The specific effects of ROS are modulated in large part through the covalent modification of specific cysteine residues found within redox-sensitive target proteins. Oxidation of these specific and reactive cysteine residues in turn can lead to the reversible modification of enzymatic activity. Emerging evidence suggests that ROS regulate diverse physiological parameters ranging from the response to growth factor stimulation to the generation of the inflammatory response, and that dysregulated ROS signaling may contribute to a host of human diseases.
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“high levels of ROS generated by ongoing aerobic glycolysis followed by pyruvate oxidation in mitochondria (the Warburg effect), increase receptor and oncogene activity, and the stimulation of growth factor-dependent pathways or oxidizing enzymes induce genetic instability3,4.”
From ROS in cancer therapy: the bright side of the moon (2020) · cites this paper as [4]
Experimental — accuracy not yet measuredIn the citing paper
“Indeed, the generation of superoxide and hydrogen peroxide, among others, has been shown to mediate critical processes such as angiogenesis, hypoxic adaptation, and energy homeostasis (96, 249, 291, 720, 778, 825, 960).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [291]
In the citing paper
“As outlined above, ROS have origin from two main sources: mitochondrial oxidative metabolism and processes of cellular response to xenobiotics, bacteria, and cytokines during which ROS are formed as a part of either signal transduction pathways or a cellular defense mechanism (Finkel 2011).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Finkel 2011
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Metadata
- Authors
- Finkel, T.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Finkel, Toren
- ORCID
- Finkel, Toren
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2011-07-11
- Volume
- 194
- Issue
- 1
- Pages
- 7-15
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC3135394
- OpenAlex
- W2115708356
- Cited by
- 2,322
- References
- 100
- Citations by year
- 2026: 90 · 2025: 120 · 2024: 134 · 2023: 166 · 2022: 187 · 2021: 223 · 2020: 187 · 2019: 188 · 2018: 130 · 2017: 168 · 2016: 161 · 2015: 164 · 2014: 155 · 2013: 129 · 2012: 107
- FWCI
- 11.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- reactive oxygen species, redox signaling, cysteine oxidation, post-translational modification, intracellular signaling, growth factor signaling, inflammation, disease
- MeSH terms
- Animals, Humans, Models, Biological, Oxidation-Reduction, Signal Transduction, Reactive Oxygen Species
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