ArticleOncogene2013
The E6AP E3 ubiquitin ligase regulates the cellular response to oxidative stress.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 42 citations in OpenAlex.
- Arabidopsis Ubiquitin E3 Ligase AtCHYR1 Promotes ROS Production in Plant Responses to Sugar Availability.Plants (Basel, Switzerland) · 2025Article
- ROSBASE1.0: a comprehensive database of reactive oxygen species (ROS): categorization of cell organelles, proteins, taxonomy, and diseases based on ROS-related activities.Database : the journal of biological databases and curation · 2025Article
- Article
- Association of CUL4B with the pathogenesis of age-related cataract.International ophthalmology · 2024Article
- The ubiquitin codes in cellular stress responses.Protein & cell · 2024Review
- Article
- Elevated ROS levels during the early development of Angelman syndrome alter the apoptotic capacity of the developing neural precursor cells.Molecular psychiatry · 2023Article
- The ATM-E6AP-MASTL axis mediates DNA damage checkpoint recovery.bioRxiv : the preprint server for biology · 2023Article
- Siah2-GRP78 interaction regulates ROS and provides a proliferative advantage to Helicobacter pylori-infected gastric epithelial cancer cells.Cellular and molecular life sciences : CMLS · 2022Article
- Bioinformatics Analyses of the Transcriptome Reveal Ube3a-Dependent Effects on Mitochondrial-Related Pathways.International journal of molecular sciences · 2020Article
- Novel Insights into the Role of UBE3A in Regulating Apoptosis and Proliferation.Journal of clinical medicine · 2020Article
- Induction of E6AP by microRNA-302c dysregulation inhibits TGF-β-dependent fibrogenesis in hepatic stellate cells.Scientific reports · 2020Article
- Proteotranscriptomic Measurements of E6-Associated Protein (E6AP) Targets in DU145 Prostate Cancer Cells.Molecular & cellular proteomics : MCP · 2018Article
- Identifying the ubiquitination targets of E6AP by orthogonal ubiquitin transfer.Nature communications · 2017Article
- E6AP promotes prostate cancer by reducing p27 expression.Oncotarget · 2017Article
- ΔNp63 targets cytoglobin to inhibit oxidative stress-induced apoptosis in keratinocytes and lung cancer.Oncogene · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
The E6AP E3 ubiquitin ligase has been linked to the regulation of cell growth and to the cellular stress response. However, the specific stress conditions that are controlled by E6AP have not been defined. An important stress condition that controls cell growth is oxidative stress, where the levels of intracellular reactive oxygen species (ROS) regulate the appropriate cellular response. Here, we describe a novel role for E6AP in the control of oxidative stress response. Cells lacking E6AP expression have reduced capacity to accumulate ROS, and oxidative DNA damage, in response to 20% cell culture oxygen levels, treatment with hydrogen peroxide and expression of oncogenic RAS. This effect of E6AP is associated with the regulation of the anti-oxidant enzyme, Prx1, a previously identified target of E6AP, and can be corrected by downregulation of Prx1 or by reconstitution of E6AP expression. Consequently, cells with compromised E6AP have impaired senescent and apoptotic response to sub-lethal and lethal doses of oxidative stress, respectively. In a xenograft model, downregulation of E6AP renders transplanted tumours refractory to growth-suppressive effects of hydrogen peroxide. Our results provide the first demonstration that E6AP is an important regulator of ROS-mediated cellular senescence and cell death.
Indexed as
Identifiers
What OpenQuestion holds
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.