ArticleOncogene2010
The NADPH oxidases NOX4 and DUOX2 regulate cell cycle entry via a p53-dependent pathway.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 46 citations in OpenAlex.
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- NOX4 Suppresses Ferroptosis Through Regulation of the Pentose Phosphate Pathway in Colorectal Cancer.Current medical science · 2025Article
- Nicotinamide adenine dinucleotide phosphate oxidase in pancreatic diseases: Mechanisms and future perspectives.World journal of gastroenterology · 2024Review
- Multi-range ERK responses shape the proliferative trajectory of single cells following oncogene induction.Cell reports · 2023Article
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- G protein-coupled receptor kinase 2 modifies the cellular reaction to cisplatin through interactions with NADPH oxidase 4.Molecular and cellular biochemistry · 2021Article
- Effects of Functionalized Fullerenes on ROS Homeostasis Determine Their Cytoprotective or Cytotoxic Properties.Nanomaterials (Basel, Switzerland) · 2020Article
- Cytoplasm-localized SIRT1 downregulation attenuates apoptosis and cell cycle arrest in cisplatin-resistant lung cancer A549 cells.Journal of Cancer · 2020Article
- Review
- HAntioxidants (Basel, Switzerland) · 2019Review
- Poldip2 knockdown inhibits vascular smooth muscle proliferation and neointima formation by regulating the expression of PCNA and p21.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Induced Trf2 deletion leads to aging vascular phenotype in mice associated with arterial telomere uncapping, senescence signaling, and oxidative stress.Journal of molecular and cellular cardiology · 2019Article
- Sexual Dimorphism of NADPH Oxidase/H₂O₂ System in Rat Thyroid Cells; Effect of Exogenous 17β-Estradiol.International journal of molecular sciences · 2018Article
- The defense and signaling role of NADPH oxidases in eukaryotic cells : Review.Wiener medizinische Wochenschrift (1946) · 2018Review
- Selection scan reveals three new loci related to high altitude adaptation in Native Andeans.Scientific reports · 2018Article
- CRISPR-Cas9 Mediated NOX4 Knockout Inhibits Cell Proliferation and Invasion in HeLa Cells.PloS one · 2017Article
- DUOX2 Expression Is Increased in Barrett Esophagus and Cancerous Tissues of Stomach and Colon.Gastroenterology research and practice · 2016Article
- The proinflammatory LTB4/BLT1 signal axis confers resistance to TGF-β1-induced growth inhibition by targeting Smad3 linker region.Oncotarget · 2015Article
- Regulation of NADPH-dependent Nitric Oxide and reactive oxygen species signalling in endothelial and melanoma cells by a photoactive NADPH analogue.Oncotarget · 2014Article
- Dosage of Dyrk1a shifts cells within a p21-cyclin D1 signaling map to control the decision to enter the cell cycle.Molecular cell · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are produced in growth factor-signaling pathways leading to cell proliferation, but the mechanisms leading to ROS generation and the targets of ROS signals are not well understood. Using a focused siRNA screen to identify redox-related proteins required for growth factor-induced cell cycle entry, we show that two ROS-generating proteins, the NADPH oxidases NOX4 and DUOX2, are required for platelet-derived growth factor (PDGF) induced retinoblastoma protein (Rb) phosphorylation in normal human fibroblasts. Unexpectedly, NOX4 and DUOX2 knockdown did not inhibit the early signaling pathways leading to cyclin D1 upregulation. However, hours after growth factor stimulation, NOX4 and DUOX2 knockdown reduced ERK1 phosphorylation and increased levels of the tumor suppressor protein p53 and a cell cycle inhibitor protein p21 (Waf1/Cip1) that is transcriptionally regulated by p53. Co-knockdown of NOX4 or DUOX2 with either p53 or with p21 overcame the inhibition of Rb phosphorylation that occurred with NOX4 or DUOX2 knockdown alone. Our results argue that rather than primarily affecting growth factor receptor signaling, NOX4 and DUOX2 regulate cell cycle entry as part of a p53-dependent checkpoint for proliferation.
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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.