ArticlePLoS genetics2013
Synergistic interaction of Rnf8 and p53 in the protection against genomic instability and tumorigenesis.
Article in PLoS genetics, 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, 22 citations in OpenAlex.
- Differential regulation of immunoglobulin class switch recombination by the tumor suppressor p53.Scientific reports · 2026Article
- Article
- ZSCAN4 interacts with PARP1 to promote DNA repair in mouse embryonic stem cells.Cell & bioscience · 2023Article
- RNF8 up-regulates AR/ARV7 action to contribute to advanced prostate cancer progression.Cell death & disease · 2022Article
- Urokinase Receptor uPAR Downregulation in Neuroblastoma Leads to Dormancy, Chemoresistance and Metastasis.Cancers · 2022Article
- Identification of the potential roles of ring finger protein 8 in TP53-mutant breast cancer.Oncology letters · 2021Article
- RNF8 promotes efficient DSB repair by inhibiting the pro-apoptotic activity of p53 through regulating the function of Tip60.Cell proliferation · 2020Article
- Spatiotemporal regulation of the Dma1-mediated mitotic checkpoint coordinates mitosis with cytokinesis.Current genetics · 2019Review
- The Functions of DNA Damage Factor RNF8 in the Pathogenesis and Progression of Cancer.International journal of biological sciences · 2019Review
- Ubiquitin ligase RNF8 suppresses Notch signaling to regulate mammary development and tumorigenesis.The Journal of clinical investigation · 2018Article
- Chiral ruthenium(ii) complex as potent radiosensitizer ofRSC advances · 2018Article
- Plumbagin shows anticancer activity in human osteosarcoma (MG-63) cells via the inhibition of S-Phase checkpoints and down-regulation of c-myc.International journal of clinical and experimental medicine · 2015Article
- Tight regulation of ubiquitin-mediated DNA damage response by USP3 preserves the functional integrity of hematopoietic stem cells.The Journal of experimental medicine · 2014Article
- Rapid analysis of chromosome aberrations in mouse B lymphocytes by PNA-FISH.Journal of visualized experiments : JoVE · 2014Article
- Ubiquitin-like (UBX)-domain-containing protein, UBXN2A, promotes cell death by interfering with the p53-Mortalin interactions in colon cancer cells.Cell death & disease · 2014Article
- Effect of a poly(ADP-ribose) polymerase-1 inhibitor against esophageal squamous cell carcinoma cell lines.Cancer science · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rnf8 is an E3 ubiquitin ligase that plays a key role in the DNA damage response as well as in the maintenance of telomeres and chromatin remodeling. Rnf8(-/-) mice exhibit developmental defects and increased susceptibility to tumorigenesis. We observed that levels of p53, a central regulator of the cellular response to DNA damage, increased in Rnf8(-/-) mice in a tissue- and cell type-specific manner. To investigate the role of the p53-pathway inactivation on the phenotype observed in Rnf8(-/-) mice, we have generated Rnf8(-/-)p53(-/-) mice. Double-knockout mice showed similar growth retardation defects and impaired class switch recombination compared to Rnf8(-/-) mice. In contrast, loss of p53 fully rescued the increased apoptosis and reduced number of thymocytes and splenocytes in Rnf8(-/-) mice. Similarly, the senescence phenotype of Rnf8(-/-) mouse embryonic fibroblasts was rescued in p53 null background. Rnf8(-/-)p53(-/-) cells displayed defective cell cycle checkpoints and DNA double-strand break repair. In addition, Rnf8(-/-)p53(-/-) mice had increased levels of genomic instability and a remarkably elevated tumor incidence compared to either Rnf8(-/-) or p53(-/-) mice. Altogether, the data in this study highlight the importance of p53-pathway activation upon loss of Rnf8, suggesting that Rnf8 and p53 functionally interact to protect against genomic instability and tumorigenesis.
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.