ArticleOncogene2003
Characterization of the p53 mutants ability to inhibit p73 beta transactivation using a yeast-based functional assay.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 43 citations in OpenAlex.
- Analytical Validation and Application of a Targeted Next-Generation Sequencing Mutation-Detection Assay for Use in Treatment Assignment in the NCI-MPACT Trial.The Journal of molecular diagnostics : JMD · 2016Trial
- Reactivation ofInternational journal of molecular sciences · 2026Article
- Association ofmedRxiv : the preprint server for health sciences · 2023Article
- The Spectrum of Germline Nucleotide Variants in Gastric Cancer Patients in the Kyrgyz Republic.Current issues in molecular biology · 2023Article
- ExploringMicrobial cell (Graz, Austria) · 2021Review
- Article
- Clinical aspects of TP53 gene inactivation in diffuse large B-cell lymphoma.BMC medical genomics · 2019Article
- p53, p63 and p73 in the wonderland ofOncotarget · 2017Review
- Article
- Gain of function of mutant p53: R282W on the peak?Oncogenesis · 2016Review
- Mutant p53 promotes ovarian cancer cell adhesion to mesothelial cells via integrin β4 and Akt signals.Scientific reports · 2015Article
- TP53 oncomorphic mutations predict resistance to platinum‑ and taxane‑based standard chemotherapy in patients diagnosed with advanced serous ovarian carcinoma.International journal of oncology · 2015Article
- Transactivation specificity is conserved among p53 family proteins and depends on a response element sequence code.Nucleic acids research · 2013Article
- Serine substitution of proline at codon 151 of TP53 confers gain of function activity leading to anoikis resistance and tumor progression of head and neck cancer cells.The Laryngoscope · 2013Article
- A comparison of multiscale methods for the analysis of molecular dynamics simulations.The journal of physical chemistry. B · 2012Article
- Structure of p73 DNA-binding domain tetramer modulates p73 transactivation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The prevalence of germ-line TP53 mutations in women diagnosed with breast cancer before age 30.Familial cancer · 2009Article
- Transcriptional functionality of germ line p53 mutants influences cancer phenotype.Clinical cancer research : an official journal of the American Association for Cancer Research · 2007Article
- Evaluation of p53 codon 72 polymorphism in adenocarcinomas of the colon and rectum in La Plata, Argentina.World journal of gastroenterology · 2006Article
- Homozygosity for Pro of p53 Arg72Pro as a potential risk factor for hepatocellular carcinoma in Chinese population.World journal of gastroenterology · 2005Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is the most frequently altered tumor suppressor gene in a wide spectrum of human tumors. The large majority of p53 mutations observed in tumors are missense mutations. The p73 gene, encoding a protein with significant sequence similarity to p53, expresses multiple transcription-competent spliced variants, or transcription-incompetent forms (i.e. DeltaNp73). It was clearly shown that p73 transactivation from a p53-responsive promoter is inhibited by some tumor-derived p53 mutants in eucaryotic cells. In this study, we adapted a yeast-based p53 functional assay for the analysis of the influences of different p53 mutants on the activity of one of the p73 isoforms, namely p73beta. We determined the ability of a panel of 61 p53 mutants to inhibit p73beta activity following the net transcription of the ADE2 color (red/white) reporter gene driven by a p53-responsive promoter. By analysing a large number of mutants, we could conclude that interference: (a) is a quite frequent phenomenon (more than 70% of p53 mutants analysed are interfering); (b) is not confined to p53 mutations located in particular topological regions of the DNA binding domain; (c) does not appear to be dependent on the kind of side chains introduced at a specific position; (d) appears to significantly correlate with evolutionary conservation of the mutated p53 codon, frequency of occurrence of the mutation in tumors. The influence of a common R/P polymorphism at codon 72 on the ability of p53 mutants to interfere with p73beta was also studied. Two sets of polymorphic variants (R and P) for 14 mutants were constructed and analysed. In all cases, the R/P 72 polymorphism was phenotypically irrelevant. In conclusion, our results suggest that the interpretation of the biological effects of p53 mutants should take into consideration the possibility that p53 mutants show loss or gain of function also through the interference with p53 family members.
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