ArticleNucleic acids research2005
Activation of APE1/Ref-1 is dependent on reactive oxygen species generated after purinergic receptor stimulation by ATP.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 63 papers.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 127 citations in OpenAlex.
- Role of APE1/Ref-1 in hydrogen peroxide-induced apoptosis in human renal HK-2 cells.Kidney research and clinical practice · 2024Article
- Saengmaeksan, a traditional polyherbal formulation containing Panax ginseng, improves energy metabolism during exercise.PloS one · 2024Article
- Article
- Editorial Expression of Concern on 'Activation of APE1/Ref-1 is dependent on reactive oxygen species generated after purinergic receptor stimulation by ATP'.Nucleic acids research · 2021Article
- Cephalomannine inhibits hypoxia-induced cellular function via the suppression of APEX1/HIF-1α interaction in lung cancer.Cell death & disease · 2021Article
- Inhibition of APE1/Ref-1 Redox Signaling Alleviates Intestinal Dysfunction and Damage to Myenteric Neurons in a Mouse Model of Spontaneous Chronic Colitis.Inflammatory bowel diseases · 2021Article
- PTEN-mediated mitophagy and APE1 overexpression protects against cardiac hypoxia/reoxygenation injury.In vitro cellular & developmental biology. Animal · 2019Article
- Apurinic/apyrimidinic endonuclease/redox factor 1 (APE1) alleviates myocardial hypoxia-reoxygenation injury by inhibiting oxidative stress and ameliorating mitochondrial dysfunction.Experimental and therapeutic medicine · 2019Article
- Verapamil Inhibits Ser202/Thr205 Phosphorylation of Tau by Blocking TXNIP/ROS/p38 MAPK Pathway.Pharmaceutical research · 2018Article
- Profiles of Radioresistance Mechanisms in Prostate Cancer.Critical reviews in oncogenesis · 2018Review
- Article
- Mitochondrial DNA Integrity Is Maintained by APE1 in Carcinogen-Induced Colorectal Cancer.Molecular cancer research : MCR · 2017Article
- Paradoxical induction of growth arrest and apoptosis by EGF via the up-regulation of PTEN by activating Redox factor-1/Egr-1 in human lung cancer cells.Oncotarget · 2017Article
- Acetylation of hMOF Modulates H4K16ac to Regulate DNA Repair Genes in Response to Oxidative Stress.International journal of biological sciences · 2017Article
- Cancer drug resistance: redox resetting renders a way.Oncotarget · 2016Review
- High-Throughput Phenotypic Screening of Human Astrocytes to Identify Compounds That Protect Against Oxidative Stress.Stem cells translational medicine · 2016Article
- Dynamic Regulation of APE1/Ref-1 as a Therapeutic Target Protein.Chonnam medical journal · 2016Review
- Secreted APE1/Ref-1 inhibits TNF-α-stimulated endothelial inflammation via thiol-disulfide exchange in TNF receptor.Scientific reports · 2016Article
- A novel method for determining human ex vivo submaximal skeletal muscle mitochondrial function.The Journal of physiology · 2015Article
- Elevation of the Serum Apurinic/Apyrimidinic Endonuclease 1/Redox Factor-1 in Coronary Artery Disease.Korean circulation journal · 2015Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern · 2021-10-29Concerns/Issues about Image · Investigation by Journal/Publisher · Objections by Third Party · Original Data and/or Images not Provided and/or not Available · · see also: https://pubpeer.com/publications/7C031F16838075DFB339F62E1DEA91
- Erratum issued
- Expression of concern
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apurinic apyrimidinic endonuclease redox effector factor-1 (APE1/Ref-1) is involved both in the base excision repair (BER) of DNA lesions and in the eukaryotic transcriptional regulation. APE1/Ref-1 is regulated at both the transcriptional and post-translational levels, through control of subcellular localization and post-translational modification. In response to stress conditions, several cell types release ATP, which exerts stimulatory effects on eukaryotic cells via the purinergic receptors (P2) family. By using western blot and immunofluorescence analysis on a human tumour thyroid cell line (ARO), we demonstrate that purinergic stimulation by extracellular ATP induces quick cytoplasm to nucleus translocation of the protein at early times and its neosynthesis at later times. Continuous purinergic triggering by extracellular ATP released by ARO cells is responsible for the control of APE1/Ref-1 intracellular level. Interference with intracellular pathways activated by P2 triggering demonstrates that Ca2+ mobilization and intracellular reactive oxygen species (ROS) production are responsible for APE1/Ref-1 translocation. The APE1/Ref-1 activities on activator protein-1 (AP-1) DNA binding and DNA repair perfectly match its nuclear enrichment upon ATP stimulation. The biological relevance of our data is reinforced by the observation that APE1/Ref-1 stimulation by ATP protects ARO cells by H2O2-induced cell death. Our data provide new insights into the complex mechanisms regulating APE1/Ref-1 functions.
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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.