ArticlePloS one2010
Genome-wide mapping indicates that p73 and p63 co-occupy target sites and have similar dna-binding profiles in vivo.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- DARPins detect the formation of hetero-tetramers of p63 and p73 in epithelial tissues and in squamous cell carcinoma.Cell death & disease · 2023Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- Enhanced pro-apoptosis gene signature following the activation of TAp63α in oocytes upon γ irradiation.Cell death & disease · 2022Article
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Isoform-Specific Roles of Mutant p63 in Human Diseases.Cancers · 2021Review
- Review
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis.International journal of molecular sciences · 2019Review
- Article
- Mesenchymal stem cell-mediated Notch2 activation overcomes radiation-induced injury of the hematopoietic system.Scientific reports · 2018Article
- The Roles of P53 and Its Family Proteins, P63 and P73, in the DNA Damage Stress Response in Organogenesis-Stage Mouse Embryos.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Non-oncogenic roles of TAp73: from multiciliogenesis to metabolism.Cell death and differentiation · 2018Review
- Cell cycle arrest through indirect transcriptional repression by p53: I have a DREAM.Cell death and differentiation · 2018Review
- p53 binding sites in normal and cancer cells are characterized by distinct chromatin context.Cell cycle (Georgetown, Tex.) · 2017Article
- Mechanism of TAp73 inhibition by ΔNp63 and structural basis of p63/p73 hetero-tetramerization.Cell death and differentiation · 2016Article
- Article
- Novel p53 target gene FUCA1 encodes a fucosidase and regulates growth and survival of cancer cells.Cancer science · 2016Article
- p73 Is Required for Multiciliogenesis and Regulates the Foxj1-Associated Gene Network.Cell reports · 2016Article
- Analysis of the p53/CEP-1 regulated non-coding transcriptome in C. elegans by an NSR-seq strategy.Protein & cell · 2014Article
- ΔNp63 promotes pediatric neuroblastoma and osteosarcoma by regulating tumor angiogenesis.Cancer research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe p53 homologs, p63 and p73, share approximately 85% amino acid identity in their DNA-binding domains, but they have distinct biological functions. PRINCIPAL
findingsUsing chromatin immunoprecipitation and high-resolution tiling arrays covering the human genome, we identify p73 DNA binding sites on a genome-wide level in ME180 human cervical carcinoma cells. Strikingly, the p73 binding profile is indistinguishable from the previously described binding profile for p63 in the same cells. Moreover, the p73:p63 binding ratio is similar at all genomic loci tested, suggesting that there are few, if any, targets that are specific for one of these factors. As assayed by sequential chromatin immunoprecipitation, p63 and p73 co-occupy DNA target sites in vivo, suggesting that p63 and p73 bind primarily as heterotetrameric complexes in ME180 cells.
conclusionsThe observation that p63 and p73 associate with the same genomic targets suggest that their distinct biological functions are due to cell-type specific expression and/or protein domains that involve functions other than DNA binding.
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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.