ArticleProceedings of the National Academy of Sciences of the United States of America2002
The c-Myc target gene PRDX3 is required for mitochondrial homeostasis and neoplastic transformation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 196 citations in OpenAlex.
- Peroxiredoxins in the kidney: a Jekyll and Hyde existence in disease pathogenesis.Renal failure · 2026Review
- Machine learning-driven decoding of maternal immune signatures in repeated pregnancy loss.PLoS computational biology · 2026Article
- The Role of Peroxiredoxins in the Mechanisms of Oxidative Stress in Patients After Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2026Review
- Up-regulation of peroxiredoxin 3 by high-risk human papillomavirus in cervical cancer cells.Archives of medical science : AMS · 2026Article
- Identification of potential genes and candidate drugs for intrahepatic cholestasis of pregnancy based on bioinformatics.Annals of medicine and surgery (2012) · 2026Article
- Oxidant-Based Cytotoxic Agents During Aging: From Disturbed Energy Metabolism to Chronic Inflammation and Disease Progression.Biomolecules · 2025Review
- TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways.Communications biology · 2025Article
- m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.Briefings in functional genomics · 2025Review
- Recent advances in mitochondria-targeting theranostic agents.Exploration (Beijing, China) · 2024Review
- Diaphragm Fatigue in SMNΔ7 Mice and Its Molecular Determinants: An Underestimated Issue.International journal of molecular sciences · 2023Article
- A PPIX-binding probe facilitates discovery of PPIX-induced cell death modulation by peroxiredoxin.Communications biology · 2023Article
- Evaluation of Mitochondrial Function in Blood Samples Shows Distinct Patterns in Subjects with Thyroid Carcinoma from Those with Hyperplasia.International journal of molecular sciences · 2023Article
- Protein misfolding and clearance in the pathogenesis of a new infantile onset ataxia caused by mutations in PRDX3.Human molecular genetics · 2022Article
- The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis.Redox biology · 2022Article
- Proton export upregulates aerobic glycolysis.BMC biology · 2022Article
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- CCND3 is indispensable for the maintenance of B-cell acute lymphoblastic leukemia.Oncogenesis · 2022Article
- High mitochondrial content is associated with breast cancer aggressiveness.Molecular and clinical oncology · 2021Article
- Peroxiredoxins-The Underrated Actors during Virus-Induced Oxidative Stress.Antioxidants (Basel, Switzerland) · 2021Review
- Systems level profiling of arginine starvation reveals MYC and ERK adaptive metabolic reprogramming.Cell death & disease · 2020Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Deregulated expression of the c-Myc transcription factor is found in a wide variety of human tumors. Because of this significant role in oncogenesis, considerable effort has been devoted to elucidating the molecular program initiated by deregulated c-myc expression. The primary transforming activity of Myc is thought to arise through transcriptional regulation of numerous target genes. Thus far, Myc target genes involved in mitochondrial function have not been characterized in depth. Here, we describe a nuclear c-Myc target gene, PRDX3, which encodes a mitochondrial protein of the peroxiredoxin gene family. Expression of PRDX3 is induced by the mycER system and is reduced in c-myc(-/-) cells. Chromatin immunoprecipitation analysis spanning the entire PRDX3 genomic sequence reveals that Myc binds preferentially to a 930-bp region surrounding exon 1. We show that PRDX3 is required for Myc-mediated proliferation, transformation, and apoptosis after glucose withdrawal. Results using mitochondria-specific fluorescent probes demonstrate that PRDX3 is essential for maintaining mitochondrial mass and membrane potential in transformed rat and human cells. These data provide evidence that PRDX3 is a c-Myc target gene that is required to maintain normal mitochondrial function.
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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.