ArticleGenome research2025
Nucleosome binding by TP53, TP63, and TP73 is determined by the composition, accessibility, and helical orientation of their binding sites.
Article in Genome research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Genome-wide rotational and translational phasing of nucleosomes with human transcription factors.Molecular cell · 2026Article
- Evaluating high-fidelity CRISPR-Cas nucleases in nucleosomal contexts using a quantitative framework.Frontiers in genome editing · 2026Article
- E2F1 induces a G0-G1 reentry transcriptional program without changing chromatin accessibility.bioRxiv : the preprint server for biology · 2025Article
- p53 reveals principles of chromatin remodeling and enhancer activation.Nucleic acids research · 2025Article
Corrections and comments
- Update of
Authors and funding
4 authors.
Funding
Abstract
The TP53 family of transcription factors plays key roles in driving development and combating cancer by regulating gene expression. TP53, TP63, and TP73-the three members of the TP53 family-regulate gene expression by binding to their DNA binding sites, many of which are situated within nucleosomes. To thoroughly examine the nucleosome-binding abilities of the TP53 family, we used Pioneer-seq, a technique that assesses a transcription factor's binding affinity to its DNA-binding sites at all possible positions within the nucleosome core particle. Using Pioneer-seq, we analyzed the binding affinities of TP53, TP63, and TP73 to 10 TP53 family binding sites across the nucleosome core particle. We find that the affinities of TP53, TP63, and TP73 for nucleosomes are primarily determined by the positioning of TP53 family binding sites within nucleosomes; TP53 family members bind strongly to the more accessible edges of nucleosomes but weakly to the less accessible centers of nucleosomes. Our results further show that the DNA-helical orientation of TP53 family binding sites within nucleosomal DNA impacts the nucleosome-binding affinities of TP53 family members, with binding-site composition impacting the affinity of each TP53 family member only when the binding-site location is accessible. Taken together, our results show that the accessibility, composition, and helical orientation of TP53 family binding sites collectively determine the nucleosome-binding affinities of TP53, TP63, and TP73. These findings help explain the rules underlying TP53 family-nucleosome binding and thus provide requisite insight into how we may better control gene expression changes involved in development and tumor suppression.
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.