ArticlePloS one2013
Preferential binding of hot spot mutant p53 proteins to supercoiled DNA in vitro and in cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- p53 hotspot mutants attenuate CTL-mediated tumor cell killing through a novel ALKBH5-YTHDF3-PD-L1 pathway.Oncogene · 2026Article
- The mutational spectrum in whole exon of p53 in oral squamous cell carcinoma and its clinical implications.Scientific reports · 2022Article
- Review
- The P72R Polymorphism in R248Q/W p53 Mutants Modifies the Mutant Effect on Epithelial to Mesenchymal Transition Phenotype and Cell Invasion via CXCL1 Expression.International journal of molecular sciences · 2020Article
- p53's Extended Reach: The Mutant p53 Secretome.Biomolecules · 2020Review
- Mutant p53 Gain-of-Function: Role in Cancer Development, Progression, and Therapeutic Approaches.Frontiers in cell and developmental biology · 2020Review
- The Rich World of p53 DNA Binding Targets: The Role of DNA Structure.International journal of molecular sciences · 2019Review
- p53 Binds Preferentially to Non-B DNA Structures Formed by the Pyrimidine-Rich Strands of GAA·TTC Trinucleotide Repeats Associated with Friedreich's Ataxia.Molecules (Basel, Switzerland) · 2019Article
- p53 overexpression is a prognosticator of poor outcome in esophageal cancer.Oncology letters · 2019Article
- Regulators of Oncogenic Mutant TP53 Gain of Function.Cancers · 2018Review
- The curcumin analog HO-3867 selectively kills cancer cells by converting mutant p53 protein to transcriptionally active wildtype p53.The Journal of biological chemistry · 2018Article
- Control of Nucleotide Metabolism Enables Mutant p53's Oncogenic Gain-of-Function Activity.International journal of molecular sciences · 2017Review
- Cancer-associated arginine-to-histidine mutations confer a gain in pH sensing to mutant proteins.Science signaling · 2017Article
- Recognition of Local DNA Structures by p53 Protein.International journal of molecular sciences · 2017Review
- TP53 mutations in epithelial ovarian cancer.Translational cancer research · 2016Article
- Oncogenic Mutant p53 Gain of Function Nourishes the Vicious Cycle of Tumor Development and Cancer Stem-Cell Formation.Cold Spring Harbor perspectives in medicine · 2016Review
- Wild-type p53 binds to MYC promoter G-quadruplex.Bioscience reports · 2016Article
- p53 Specifically Binds Triplex DNA In Vitro and in Cells.PloS one · 2016Article
- Proteome-wide analysis of mutant p53 targets in breast cancer identifies new levels of gain-of-function that influence PARP, PCNA, and MCM4.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Differential salt-induced dissociation of the p53 protein complexes with circular and linear plasmid DNA substrates suggest involvement of a sliding mechanism.International journal of molecular sciences · 2015Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hot spot mutant p53 (mutp53) proteins exert oncogenic gain-of-function activities. Binding of mutp53 to DNA is assumed to be involved in mutp53-mediated repression or activation of several mutp53 target genes. To investigate the importance of DNA topology on mutp53-DNA recognition in vitro and in cells, we analyzed the interaction of seven hot spot mutp53 proteins with topologically different DNA substrates (supercoiled, linear and relaxed) containing and/or lacking mutp53 binding sites (mutp53BS) using a variety of electrophoresis and immunoprecipitation based techniques. All seven hot spot mutp53 proteins (R175H, G245S, R248W, R249S, R273C, R273H and R282W) were found to have retained the ability of wild-type p53 to preferentially bind circular DNA at native negative superhelix density, while linear or relaxed circular DNA was a poor substrate. The preference of mutp53 proteins for supercoiled DNA (supercoil-selective binding) was further substantiated by competition experiments with linear DNA or relaxed DNA in vitro and ex vivo. Using chromatin immunoprecipitation, the preferential binding of mutp53 to a sc mutp53BS was detected also in cells. Furthermore, we have shown by luciferase reporter assay that the DNA topology influences p53 regulation of BAX and MSP/MST1 promoters. Possible modes of mutp53 binding to topologically constrained DNA substrates and their biological consequences are discussed.
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