ArticleOncogene2005
Regulation of reactive oxygen species, DNA damage, and c-Myc function by peroxiredoxin 1.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 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
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Who cites it
112 citing papers in PubMed, 228 citations in OpenAlex.
- Dual targeting of the DNA damage response pathway and BCL-2 in diffuse large B-cell lymphoma.Leukemia · 2022Trial
- Peroxiredoxin 1 safeguards the nucleolar genome from oxidative damage.Science advances · 2026Article
- Chemogenomic maps reveal a PRDX1-dependent iron-damage axis in the DNA damage response.Nature chemical biology · 2026Article
- Isoliensinine inhibits mitophagy and sensitizes T cell malignancies for STING-mediated NK clearance.Acta pharmacologica Sinica · 2026Article
- Peroxiredoxin 1 safeguards the nucleolar genome from oxidative damage.bioRxiv : the preprint server for biology · 2025Article
- Targeting PRDX1 impairs acute myeloid leukemic blasts and stem cells by disrupting redox homeostasis.Cell death & disease · 2025Article
- A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.Apoptosis : an international journal on programmed cell death · 2025Review
- PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling.Oncotarget · 2025Article
- Thioredoxin: a key factor in cold tumor formation and a promising biomarker for immunotherapy resistance in NSCLC.Respiratory research · 2025Article
- Article
- Modeling Melanoma Heterogeneity In Vitro: Redox, Resistance and Pigmentation Profiles.Antioxidants (Basel, Switzerland) · 2024Article
- Tigecycline Opposes Bortezomib Effect on Myeloma Cells Decreasing Mitochondrial Reactive Oxygen Species Production.International journal of molecular sciences · 2024Article
- Fracture healing on non-union fracture model promoted by non-thermal atmospheric-pressure plasma.PloS one · 2024Article
- PRDX1 inhibits ferroptosis by binding to Cullin-3 as a molecular chaperone in colorectal cancer.International journal of biological sciences · 2024Article
- Spatial transcriptome atlas reveals pulmonary microstructure-specific COVID-19 gene signatures in cynomolgus macaques.Communications biology · 2023Article
- A metabolic map of the DNA damage response identifies PRDX1 in the control of nuclear ROS scavenging and aspartate availability.Molecular systems biology · 2023Article
- Protective Effect and Mechanism of Kuntai Capsule on Angiotensin II -Induced Hypertension in Ovariectomized Rats.Chinese journal of integrative medicine · 2023Article
- Article
- Assessing the Formation of Purine Lesions in Mitochondrial DNA of Cockayne Syndrome Cells.Biomolecules · 2022Article
- Effects of Aging and Disease Conditions in Brain of Tumor-Bearing Mice: Evaluation of Purine DNA Damages and Fatty Acid Pool Changes.Biomolecules · 2022Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Overexpression of c-Myc results in transformation and multiple other phenotypes, and is accompanied by the deregulation of a large number of target genes. We previously demonstrated that peroxiredoxin 1 (Prdx1), a scavenger of reactive oxygen species (ROS), interacts with a region of the c-Myc transcriptional regulatory domain that is essential for transformation. This results either in the suppression or enhancement of some c-Myc functions and in the altered expression of select target genes. Most notably, c-Myc-mediated transformation is inhibited, implying a tumor suppressor role for Prdx1. Consistent with this, prdx1-/- mice develop age-dependent hemolytic anemias and/or malignancies. We now show that erythrocytes and embryonic fibroblasts from these animals contain higher levels of ROS, and that the latter cells show evidence of c-Myc activation, including the ability to be transformed by a ras oncogene alone. In contrast, other primary cells from prdx1-/- mice do not have elevated ROS, but nonetheless show increased oxidative DNA damage. This apparent paradox can be explained by the fact that ROS localize primarily to the cytoplasm of prdx1+/+ cells, whereas in prdx1-/- cells, much higher levels of nuclear ROS are seen. We suggest that increased DNA damage and tumor susceptibility in prdx1-/- animals results from this shift in intracellular ROS. prdx1-/- mice should be useful in studying the role of oxidative DNA damage in the causation of cancer and its prevention by antioxidants. They should also help in studying the relationship between oncogenes such as c-Myc and DNA damage.
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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.