ArticleBMC molecular and cell biology2020
Identification of universal and cell-type specific p53 DNA binding.
Article in BMC molecular and cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 23 citations in OpenAlex.
- p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiated luminal identity in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Decoding stimulus-specific regulation of promoter activity of p53 target genes.Frontiers in cell and developmental biology · 2025Article
- Mouse models to investigate in situ cell fate decisions induced by p53.The EMBO journal · 2024Article
- Determinants of p53 DNA binding, gene regulation, and cell fate decisions.Cell death and differentiation · 2024Review
- Optimisation of TP53 reporters by systematic dissection of synthetic TP53 response elements.Nucleic acids research · 2023Article
- Transposable elements as tissue-specific enhancers in cancers of endodermal lineage.Nature communications · 2023Article
- Cell differentiation modifies the p53 transcriptional program through a combination of gene silencing and constitutive transactivation.Cell death and differentiation · 2023Article
- Integrative bioinformatic analysis of p53 and pathway alterations in two different lung cancer subtypes.Biochemistry and biophysics reports · 2023Article
- pTINCR microprotein promotes epithelial differentiation and suppresses tumor growth through CDC42 SUMOylation and activation.Nature communications · 2022Article
- Mutual exclusivity of ESR1 and TP53 mutations in endocrine resistant metastatic breast cancer.NPJ breast cancer · 2022Article
- Article
- The transcriptomic revolution and radiation biology.International journal of radiation biology · 2022Article
- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- Increased p53 signaling impairs neural differentiation in HUWE1-promoted intellectual disabilities.Cell reports. Medicine · 2021Article
- p53 dynamics vary between tissues and are linked with radiation sensitivity.Nature communications · 2021Article
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe tumor suppressor p53 is a major regulator of the DNA damage response and has been suggested to selectively bind and activate cell-type specific gene expression programs. However recent studies and meta-analyses of genomic data propose largely uniform, and condition independent p53 binding and thus question the selective and cell-type dependent function of p53.
resultsTo systematically assess the cell-type specificity of p53, we measured its association with DNA in 12 p53 wild-type cancer cell lines, from a range of epithelial linages, in response to ionizing radiation. We found that the majority of bound sites were occupied across all cell lines, however we also identified a subset of binding sites that were specific to one or a few cell lines. Unlike the shared p53-bound genome, which was not dependent on chromatin accessibility, the association of p53 with these atypical binding sites was well explained by chromatin accessibility and could be modulated by forcing cell state changes such as the epithelial-to-mesenchymal transition.
conclusionsOur study reconciles previous conflicting views in the p53 field, by demonstrating that although the majority of p53 DNA binding is conserved across cell types, there is a small set of cell line specific binding sites that depend on cell state.
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.