ArticleOncotarget2016
The dominant-negative interplay between p53, p63 and p73: A family affair.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 41 citations in OpenAlex.
- The p53-Associated Regulation of ATF4 mRNA Expression Involves p21 and p130 in a Stress-Dependent Manner.Cells · 2026Article
- GD3 synthase drives resistance to p53-induced apoptosis in breast cancer by modulating mitochondrial function.Oncogene · 2025Article
- p53 biology and reactivation for improved therapy in MDS and AML.Biomarker research · 2024Review
- Review
- Association ofmedRxiv : the preprint server for health sciences · 2023Article
- Multidimensional quantitative phenotypic and molecular analysis reveals neomorphic behaviors of p53 missense mutants.NPJ breast cancer · 2023Article
- Differences in somatic TP53 mutation type in breast tumors by race and receptor status.Breast cancer research and treatment · 2022Article
- Review
- ExploringMicrobial cell (Graz, Austria) · 2021Review
- Review
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- p53, A Victim of the Prion Fashion.Cancers · 2021Review
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- Synergetic Effects of Intronic Mature miR-944 and ΔNp63 Isoforms on Tumorigenesis in a Cervical Cancer Cell Line.International journal of molecular sciences · 2020Article
- Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020Review
- Mouse models of colorectal cancer: Past, present and future perspectives.World journal of gastroenterology · 2020Review
- Evaluation of p53 and Its Target Gene Expression as Potential Biomarkers of Cholangiocarcinoma in Thai Patients.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Homologs of the Tumor Suppressor Protein p53: A Bioinformatics Study for Drug Design.MOJ proteomics & bioinformatics · 2020Article
- Control of p53-dependent transcription and enhancer activity by the p53 family member p63.The Journal of biological chemistry · 2019Article
- Salvation of the fallen angel: Reactivating mutant p53.British journal of pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppression activity of p53 is frequently impaired in cancers even when a wild-type copy of the gene is still present, suggesting that a dominant-negative effect is exerted by some of p53 mutants and isoforms. p63 and p73, which are related to p53, have also been reported to be subjected to a similar loss of function, suggesting that a dominant-negative interplay might happen between p53, p63 and p73. However, to which extent p53 hotspot mutants and isoforms of p53, p63 and p73 are able to interfere with the tumor suppressive activity of their siblings as well as the underlying mechanisms remain undeciphered. Using yeast, we showed that a dominant-negative effect is widely spread within the p53/p63/p73 family as all p53 loss-of-function hotspot mutants and several of the isoforms of p53 and p73 tested exhibit a dominant-negative potential. In addition, we found that this dominant-negative effect over p53 wild-type is based on tetramer poisoning through the formation of inactive hetero-tetramers and does not rely on a prion-like mechanism contrary to what has been previously suggested. We also showed that mutant p53-R175H gains the ability to inhibit p63 and p73 activity by a mechanism that is only partially based on tetramerization.
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.