ArticlePLoS genetics2010
The E1A-associated p400 protein modulates cell fate decisions by the regulation of ROS homeostasis.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 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.
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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
19 citing papers in PubMed, 29 citations in OpenAlex.
- Chromatin Modifier EP400 Regulates Oocyte Quality and Zygotic Genome Activation in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- H2A.Z overexpression suppresses senescence and chemosensitivity in pancreatic ductal adenocarcinoma.Oncogene · 2021Article
- RNA-Seq transcriptome profiling in three liver regeneration models in rats: comparative analysis of partial hepatectomy, ALLPS, and PVL.Scientific reports · 2020Article
- Potential molecular mechanism of ACE gene at different time points in STEMI patients based on genome-wide microarray dataset.Lipids in health and disease · 2019Article
- The H2A.Z histone variant integrates Wnt signaling in intestinal epithelial homeostasis.Nature communications · 2019Article
- Control of alternative end joining by the chromatin remodeler p400 ATPase.Nucleic acids research · 2016Article
- EP400 Deposits H3.3 into Promoters and Enhancers during Gene Activation.Molecular cell · 2016Article
- Article
- Genomic analysis of host - Peste des petits ruminants vaccine viral transcriptome uncovers transcription factors modulating immune regulatory pathways.Veterinary research · 2015Article
- Oxidative stress preferentially induces a subtype of micronuclei and mediates the genomic instability caused by p53 dysfunction.Mutation research · 2014Article
- DNA repair: Chromatin remodeling without H2A.Z?Cell cycle (Georgetown, Tex.) · 2014Article
- Transcriptome profiling of the theca interna from bovine ovarian follicles during atresia.PloS one · 2014Article
- H2A.Z depletion impairs proliferation and viability but not DNA double-strand breaks repair in human immortalized and tumoral cell lines.Cell cycle (Georgetown, Tex.) · 2014Article
- H2A.Z-dependent crosstalk between enhancer and promoter regulates cyclin D1 expression.Oncogene · 2013Article
- The chromatin remodeler p400 ATPase facilitates Rad51-mediated repair of DNA double-strand breaks.The Journal of cell biology · 2012Article
- TP53 disruptive mutations lead to head and neck cancer treatment failure through inhibition of radiation-induced senescence.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- H3K27 demethylation by JMJD3 at a poised enhancer of anti-apoptotic gene BCL2 determines ERα ligand dependency.The EMBO journal · 2011Article
- ATP-dependent chromatin remodeling: genetics, genomics and mechanisms.Cell research · 2011Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p400 E1A-associated protein, which mediates H2A.Z incorporation at specific promoters, plays a major role in cell fate decisions: it promotes cell cycle progression and inhibits induction of apoptosis or senescence. Here, we show that p400 expression is required for the correct control of ROS metabolism. Depletion of p400 indeed increases intracellular ROS levels and causes the appearance of DNA damage, indicating that p400 maintains oxidative stress below a threshold at which DNA damages occur. Suppression of the DNA damage response using a siRNA against ATM inhibits the effects of p400 on cell cycle progression, apoptosis, or senescence, demonstrating the importance of ATM-dependent DDR pathways in cell fates control by p400. Finally, we show that these effects of p400 are dependent on direct transcriptional regulation of specific promoters and may also involve a positive feedback loop between oxidative stress and DNA breaks since we found that persistent DNA breaks are sufficient to increase ROS levels. Altogether, our results uncover an unexpected link between p400 and ROS metabolism and allow deciphering the molecular mechanisms largely responsible for cell proliferation control by p400.
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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.