ArticleNucleic acids research2008
Algorithm for prediction of tumour suppressor p53 affinity for binding sites in DNA.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 110 citations in OpenAlex.
- Revisiting the p53:Sirt1 interaction in light of controlling p53 acetylation levels.Communications chemistry · 2026Article
- Nucleosome binding by TP53, TP63, and TP73 is determined by the composition, accessibility, and helical orientation of their binding sites.Genome research · 2025Article
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Navigating the complexity of p53-DNA binding: implications for cancer therapy.Biophysical reviews · 2024Review
- Determinants of p53 DNA binding, gene regulation, and cell fate decisions.Cell death and differentiation · 2024Review
- Structural assessment of the full-length wild-type tumor suppressor protein p53 by mass spectrometry-guided computational modeling.Scientific reports · 2023Article
- Polymorphisms within DIO2 and GADD45A genes increase the risk of liver disease progression in chronic hepatitis b carriers.Scientific reports · 2023Article
- Improving Reporter Gene Assay Methodology for Evaluating the Ability of Compounds to Restore P53 Activity.International journal of molecular sciences · 2022Article
- Host-pathogen protein-nucleic acid interactions: A comprehensive review.Computational and structural biotechnology journal · 2022Review
- ΔNp63 is a pioneer factor that binds inaccessible chromatin and elicits chromatin remodeling.Epigenetics & chromatin · 2021Article
- Distinct mechanisms control genome recognition by p53 at its target genes linked to different cell fates.Nature communications · 2021Article
- Linker DNA and histone contributions in nucleosome binding by p53.Journal of biochemistry · 2020Article
- Article
- Stochastic transcription in the p53-mediated response to DNA damage is modulated by burst frequency.Molecular systems biology · 2019Article
- The Rich World of p53 DNA Binding Targets: The Role of DNA Structure.International journal of molecular sciences · 2019Review
- The multiple mechanisms that regulate p53 activity and cell fate.Nature reviews. Molecular cell biology · 2019Review
- Defining TP53 pioneering capabilities with competitive nucleosome binding assays.Genome research · 2019Article
- Revealing a human p53 universe.Nucleic acids research · 2018Article
- A novel molecular rotor facilitates detection of p53-DNA interactions using the Fluorescent Intercalator Displacement Assay.Scientific reports · 2018Article
- p53 positively regulates the expression of cancer stem cell marker CD133 in HCT116 colon cancer cells.Oncology letters · 2018Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The tumour suppressor p53 is a transcription factor that binds DNA in the vicinity of the genes it controls. The affinity of p53 for specific binding sites relative to other DNA sequences is an inherent driving force for specificity, all other things being equal. We measured the binding affinities of systematically mutated consensus p53 DNA-binding sequences using automated fluorescence anisotropy titrations. Based on measurements of the effects of every possible single base-pair substitution of a consensus sequence, we defined the DNA sequence with the highest affinity for full-length p53 and quantified the effects of deviation from it on the strength of protein-DNA interaction. The contributions of individual nucleotides were to a first approximation independent and additive. But, in some cases we observed significant deviations from additivity. Based on affinity data, we constructed a binding predictor that mirrored the existing p53 consensus sequence definition. We used it to search for high-affinity binding sites in the genome and to predict the effects of single-nucleotide polymorphisms in these sites. Although there was some correlation between the K(d) and biological function, the spread of the K(d)s by itself was not sufficient to explain the activation of different pathways by changes in p53 concentration alone.
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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.