ArticleGenes & development2012
E2F7, a novel target, is up-regulated by p53 and mediates DNA damage-dependent transcriptional repression.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 2 of them syntheses that pooled it.
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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
99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.
- Conservation and divergence of the p53 gene regulatory network between mice and humans.Oncogene · 2019Pooled it
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Targeted therapies plus radiotherapy for diffuse intrinsic pontine glioma: the randomized phase 2 BIOMEDE trial.Nature medicine · 2026Trial
- Whole genome analyses of a well-differentiated liposarcoma reveals novel SYT1 and DDR2 rearrangements.PloS one · 2014Trial
- Advancing genotoxicity assessment with transcriptomic biomarkers: from 2D to 3D HepaRG spheroid models.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- EIF3B is associated with mBMC cancer · 2026Article
- RNAseq analysis demonstrates polarization state-dependent responses to ambient particulate matter in a particle composition-specific manner.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Injury-induced paracrine effects on the podocyte's transcriptome.American journal of physiology. Renal physiology · 2026Article
- Silencing Ubiquitin-Specific Peptidase 10 Alleviates Persistent Corneal Epithelial Defect in Mice.The American journal of pathology · 2026Article
- Dissecting glioblastoma risk signatures in the tumor immune microenvironment based on multi-dimensional transcriptomics.GigaScience · 2026Article
- KCTD10 as a selective cancer dependency from transcription-replication conflicts (TRCs).Ageing and cancer research & treatment · 2026Article
- Decoding the germline genetic architecture of prostate cancer at a single cell resolution.PLoS genetics · 2025Article
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- RNA Sequencing Reveals Candidate Genes and Pathways Associated with Resistance to MDM2 Antagonist Idasanutlin inBiomedicines · 2024Article
- The crosstalk between non-coding RNAs and cell-cycle events: A new frontier in cancer therapy.Molecular therapy. Oncology · 2024Review
- p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response.Nature communications · 2024Article
- Unlocking the Power of Transcriptomic Biomarkers in Qualitative and Quantitative Genotoxicity Assessment of Chemicals.Chemical research in toxicology · 2024Article
- Article
- CircPOFUT1 fosters colorectal cancer metastasis and chemoresistance via decoying miR-653-5p/E2F7/WDR66 axis and stabilizing BMI1.iScience · 2024Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor protein is a transcription factor that exerts its effects on the cell cycle via regulation of gene expression. Although the mechanism of p53-dependent transcriptional activation has been well-studied, the molecular basis for p53-mediated repression has been elusive. The E2F family of transcription factors has been implicated in regulation of cell cycle-related genes, with E2F6, E2F7, and E2F8 playing key roles in repression. In response to cellular DNA damage, E2F7, but not E2F6 or E2F8, is up-regulated in a p53-dependent manner, with p53 being sufficient to increase expression of E2F7. Indeed, p53 occupies the promoter of the E2F7 gene after genotoxic stress, consistent with E2F7 being a novel p53 target. Ablation of E2F7 expression abrogates p53-dependent repression of a subset of its targets, including E2F1 and DHFR, in response to DNA damage. Furthermore, E2F7 occupancy of the E2F1 and DHFR promoters is detected, and expression of E2F7 is sufficient to inhibit cell proliferation. Taken together, these results show that p53-dependent transcriptional up-regulation of its target, E2F7, leads to repression of relevant gene expression. In turn, this E2F7-dependent mechanism contributes to p53-dependent cell cycle arrest in response to DNA damage.
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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.