ArticleNucleic acids research2013
Models incorporating chromatin modification data identify functionally important p53 binding sites.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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3 citing papers in PubMed, 5 citations in OpenAlex.
- Cluster Analysis of p53 Binding Site Sequences Reveals Subsets with Different Functions.Cancer informatics · 2016Article
- Inferring dynamic gene regulatory networks in cardiac differentiation through the integration of multi-dimensional data.BMC bioinformatics · 2015Article
- TP53 engagement with the genome occurs in distinct local chromatin environments via pioneer factor activity.Genome research · 2015Article
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3 authors at 3 institutions in 2 countries.
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Abstract
Genome-wide prediction of transcription factor binding sites is notoriously difficult. We have developed and applied a logistic regression approach for prediction of binding sites for the p53 transcription factor that incorporates sequence information and chromatin modification data. We tested this by comparison of predicted sites with known binding sites defined by chromatin immunoprecipitation (ChIP), by the location of predictions relative to genes, by the function of nearby genes and by analysis of gene expression data after p53 activation. We compared the predictions made by our novel model with predictions based only on matches to a sequence position weight matrix (PWM). In whole genome assays, the fraction of known sites identified by the two models was similar, suggesting that there was little to be gained from including chromatin modification data. In contrast, there were highly significant and biologically relevant differences between the two models in the location of the predicted binding sites relative to genes, in the function of nearby genes and in the responsiveness of nearby genes to p53 activation. We propose that these contradictory results can be explained by PWM and ChIP data reflecting primarily biophysical properties of protein-DNA interactions, whereas chromatin modification data capture biologically important functional information.
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