ArticleNucleic acids research2006
Mechanisms of transcriptional repression of cell-cycle G2/M promoters by p63.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 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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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- ΔNp63α‑mediated regulation of tumor‑associated genes and pathways in hepatocellular carcinoma progression.Molecular medicine reports · 2026Article
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- Synergistic inhibition of TNBC by USP33 and TAP63 through autophagy and ferroptosis activation.Cellular and molecular life sciences : CMLS · 2025Article
- Promoter Hypermethylation Downregulates MiR-125b-5p and MiR-199b-5p Targeting of ΔNp63, Resulting in PI3K/AKT/mTOR Pathway Activation and Keratinocyte Differentiation.Combinatorial chemistry & high throughput screening · 2025Article
- TIP60 enhances cisplatin resistance via regulating ΔNp63α acetylation in SCC.Cell death & disease · 2024Article
- ΔNp63 bookmarks and creates an accessible epigenetic environment for TGFβ-induced cancer cell stemness and invasiveness.Cell communication and signaling : CCS · 2024Article
- ΔNp63α facilitates proliferation and migration, and modulates the chromatin landscape in intrahepatic cholangiocarcinoma cells.Cell death & disease · 2023Article
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
- C-terminal α Domain of p63 Binds to p300 to Coactivate β-Catenin.Neoplasia (New York, N.Y.) · 2019Article
- Human papillomavirus E7 induces p63 expression to modulate DNA damage response.Cell death & disease · 2018Article
- Molecular and cytoskeletal regulations in epidermal development.Seminars in cell & developmental biology · 2017Review
- p63 exerts spatio-temporal control of palatal epithelial cell fate to prevent cleft palate.PLoS genetics · 2017Article
- Transcription factor p63 controls the reserve status but not the stemness of horizontal basal cells in the olfactory epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Modeling AEC-New approaches to study rare genetic disorders.American journal of medical genetics. Part A · 2014Review
- Integrating animal models and in vitro tissue models to elucidate the role of desmosomal proteins in diseases.Cell communication & adhesion · 2014Review
- Diverse p63 and p73 isoforms regulate Δ133p53 expression through modulation of the internal TP53 promoter activity.Cell death and differentiation · 2012Article
- p63 regulates human keratinocyte proliferation via MYC-regulated gene network and differentiation commitment through cell adhesion-related gene network.The Journal of biological chemistry · 2012Article
- Chromatin dynamics of gene activation and repression in response to interferon alpha (IFN(alpha)) reveal new roles for phosphorylated and unphosphorylated forms of the transcription factor STAT2.The Journal of biological chemistry · 2011Article
- NF-Y joins E2Fs, p53 and other stress transcription factors at the apoptosis table.Cell death & disease · 2011Article
- Phospho-ΔNp63α/Rpn13-dependent regulation of LKB1 degradation modulates autophagy in cancer cells.Aging · 2010Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
p63 is a developmentally regulated transcription factor related to p53, which activates and represses specific genes. The human AEC (Ankyloblepharon-Ectodermal dysplasia-Clefting) and EEC (Ectrodactyly-Ectodermal dysplasia-Cleft lip/palate) syndromes are caused by missense mutations of p63, within the DNA-binding domain (EEC) or in the C-terminal sterile alpha motif domain (AEC). We show here that p63 represses transcription of cell-cycle G(2)/M genes by binding to multiple CCAAT core promoters in immortalized and primary keratinocytes. The CCAAT-activator NF-Y and DeltaNp63alpha are associated in vivo and a conserved alpha-helix of the NF-YC histone fold is required. p63 AEC mutants, but not an EEC mutant, are incapable to bind NF-Y. DeltaNp63alpha, but not the AEC mutants repress CCAAT-dependent transcription of G(2)/M genes. Chromatin immunoprecipitation recruitment assays establish that the AEC mutants are not recruited to G(2)/M promoters, while normally present on 14-3-3sigma, which contains a sequence-specific binding site. Surprisingly, the EEC C306R mutant activates transcription. Upon keratinocytes differentiation, NF-Y and p63 remain bound to G(2)/M promoters, while HDACs are recruited, histones deacetylated, Pol II displaced and transcription repressed. Our data indicate that NF-Y is a molecular target of p63 and that inhibition of growth activating genes upon differentiation is compromised by AEC missense mutations.
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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.