ArticleEpigenetics & chromatin2021
ΔNp63 is a pioneer factor that binds inaccessible chromatin and elicits chromatin remodeling.
Article in Epigenetics & chromatin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- Defining transcription factor nucleosome binding with Pioneer-seq.PLoS genetics · 2025Article
- p63 co-opts the skin Krt8-to-Krt5 transition for enamel organ development.bioRxiv : the preprint server for biology · 2025Article
- Nucleosome binding by TP53, TP63, and TP73 is determined by the composition, accessibility, and helical orientation of their binding sites.Genome research · 2025Article
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- Crosstalk between paralogs and isoforms influences p63-dependent regulatory element activity.Nucleic acids research · 2024Article
- ΔNp63 bookmarks and creates an accessible epigenetic environment for TGFβ-induced cancer cell stemness and invasiveness.Cell communication and signaling : CCS · 2024Article
- Identification of HTRA4 as a Transcriptional Target of p63 in Trophoblast.The American journal of pathology · 2024Article
- Context dependent activity of p63-bound gene regulatory elements.bioRxiv : the preprint server for biology · 2024Article
- Detection of new pioneer transcription factors as cell-type-specific nucleosome binders.eLife · 2024Article
- ΔNp63α-mediated epigenetic regulation in keratinocyte senescence.Epigenetics · 2023Article
- ΔNp63α facilitates proliferation and migration, and modulates the chromatin landscape in intrahepatic cholangiocarcinoma cells.Cell death & disease · 2023Article
- Lola-I is a promoter pioneer factor that establishes de novo Pol II pausing during development.Nature communications · 2023Article
- Direct Lineage Reprogramming for Induced Keratinocyte Stem Cells: A Potential Approach for Skin Repair.Stem cells translational medicine · 2023Review
- The impact of nucleosome structure on CRISPR/Cas9 fidelity.Nucleic acids research · 2023Article
- A Kaleidoscope of Keratin Gene Expression and the Mosaic of Its Regulatory Mechanisms.International journal of molecular sciences · 2023Review
- A novel ΔNp63-dependent immune mechanism improves prognosis of HPV-related head and neck cancer.Frontiers in immunology · 2023Article
- ΔNp63 drives dysplastic alveolar remodeling and restricts epithelial plasticity upon severe lung injury.Cell reports · 2022Article
- The TΑp63/BCL2 axis represents a novel mechanism of clinical aggressiveness in chronic lymphocytic leukemia.Blood advances · 2022Article
- p63 and p53: Collaborative Partners or Dueling Rivals?Frontiers in cell and developmental biology · 2021Review
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundΔNp63 is a master transcriptional regulator playing critical roles in epidermal development and other cellular processes. Recent studies suggest that ΔNp63 functions as a pioneer factor that can target its binding sites within inaccessible chromatin and induce chromatin remodeling.
methodsIn order to examine if ΔNp63 can bind to inaccessible chromatin and to determine if specific histone modifications are required for binding, we induced ΔNp63 expression in two p63-naïve cell lines. ΔNp63 binding was then examined by ChIP-seq and the chromatin at ΔNp63 targets sites was examined before and after binding. Further analysis with competitive nucleosome binding assays was used to determine how ΔNp63 directly interacts with nucleosomes.
resultsOur results show that before ΔNp63 binding, targeted sites lack histone modifications, indicating ΔNp63's capability to bind at unmodified chromatin. Moreover, the majority of the sites that are bound by ectopic ΔNp63 expression exist in an inaccessible state. Once bound, ΔNp63 induces acetylation of the histone and the repositioning of nucleosomes at its binding sites. Further analysis with competitive nucleosome binding assays reveal that ΔNp63 can bind directly to nucleosome edges with significant binding inhibition occurring within 50 bp of the nucleosome dyad.
conclusionOverall, our results demonstrate that ΔNp63 is a pioneer factor that binds nucleosome edges at inaccessible and unmodified chromatin sites and induces histone acetylation and nucleosome repositioning.
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