ArticleCancer research2008
Differential p53 engagement in response to oxidative and oncogenic stresses in Fanconi anemia mice.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Insights and modulation of RNA polymerase-dependent R-loop and dsRNA in Fanconi anemia hematopoietic stem cells.JCI insight · 2026Article
- Distinct developmental outcomes in DNA repair-deficient FANCC c.67delG mutant and FANCCCell death and differentiation · 2025Article
- Transcriptome profiling of 3D co-cultured cardiomyocytes and endothelial cells under oxidative stress using a photocrosslinkable hydrogel system.Acta biomaterialia · 2017Article
- The Fanconi anemia pathway controls oncogenic response in hematopoietic stem and progenitor cells by regulating PRMT5-mediated p53 arginine methylation.Oncotarget · 2016Article
- Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo.Nucleic acids research · 2016Article
- Robust DNA Damage Response and Elevated Reactive Oxygen Species in TINF2-Mutated Dyskeratosis Congenita Cells.PloS one · 2016Article
- Oxidative stress-associated protein tyrosine kinases and phosphatases in Fanconi anemia.Antioxidants & redox signaling · 2014Review
- Evidence of mitochondrial dysfunction and impaired ROS detoxifying machinery in Fanconi anemia cells.Oncogene · 2014Article
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- Damaged mitochondria and overproduction of ROS in Fanconi anemia cells.Rare diseases (Austin, Tex.) · 2013Article
- Fanconi anemia links reactive oxygen species to insulin resistance and obesity.Antioxidants & redox signaling · 2012Article
- Bone marrow failure in Fanconi anemia is triggered by an exacerbated p53/p21 DNA damage response that impairs hematopoietic stem and progenitor cells.Cell stem cell · 2012Article
- Congenital bone marrow failure in DNA-PKcs mutant mice associated with deficiencies in DNA repair.The Journal of cell biology · 2011Article
- Spontaneous abrogation of the G₂DNA damage checkpoint has clinical benefits but promotes leukemogenesis in Fanconi anemia patients.The Journal of clinical investigation · 2011Article
- Hematopoietic stem cell defects in mice with deficiency of Fancd2 or Usp1.Stem cells (Dayton, Ohio) · 2010Article
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- Mouse models of Fanconi anemia.Mutation research · 2009Review
- Fanconi anemia proteins and endogenous stresses.Mutation research · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Members of the Fanconi anemia (FA) protein family are involved in repair of genetic damage caused by DNA cross-linkers. It is not clear whether the FA proteins function in oxidative DNA damage and oncogenic stress response. Here, we report that deficiency in the Fanca gene in mice elicits a p53-dependent growth arrest and DNA damage response to oxidative DNA damage and oncogenic stress. Using a Fanca-/-Trp53-/- double knockout model and a functionally switchable p53 retrovirus, we define the kinetics, dependence, and persistence of p53-mediated response to oxidative and oncogenic stresses in Fanca-/- cells. Notably, oxidative stress induces persistent p53 response in Fanca-/- cells, likely due to accumulation of unrepaired DNA damage. On the other hand, whereas wild-type cells exhibit prolonged response to oncogene activation, the p53-activating signals induced by oncogenic ras are short-lived in Fanca-/- cells, suggesting that Fanca may be required for the cell to engage p53 during constitutive ras activation. We propose that the FA proteins protect cells from stress-induced proliferative arrest and tumor evolution by acting as a modulator of the signaling pathways that link FA to p53.
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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.