ArticleeLife2014
Global analysis of p53-regulated transcription identifies its direct targets and unexpected regulatory mechanisms.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
187 citing papers in PubMed, 2 syntheses or guidelines pooled it, 250 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Dual contributions of Xrp1 to genome integrity through the DNA damage response and cell competition.PLoS genetics · 2026Article
- SMARCA4 loss reprograms p300 chromatin occupancy to subvert p53-mediated transcriptional repression in ovarian small cell carcinoma.Nature communications · 2026Article
- Article
- Differential regulation of immunoglobulin class switch recombination by the tumor suppressor p53.Scientific reports · 2026Article
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Asymmetric division in a two-cell-like state rejuvenates embryonic stem cells.Cell research · 2026Article
- APOBEC3C coordinates DDX5 in R-loop resolution and dynamic control of Chk1-mediated stress-responsive circuitry as a prerequisite for gemcitabine resistance in p53-deficient cells.Cell death & disease · 2026Article
- Improving calls of differentially transcribed enhancers and their upstream regulators.Bioinformatics advances · 2026Article
- Impact of Low-Dose CT Radiation on Gene Expression and DNA Integrity.International journal of molecular sciences · 2025Article
- Pharmacological activation of p53 induces dose-dependent changes in endothelial cell fate during angiogenic sprouting.Cell death & disease · 2025Article
- Improving confidence of differential transcription calls in enhancers.bioRxiv : the preprint server for biology · 2025Article
- The role of long non-coding RNAs in lung cancer metastasis: Molecular mechanisms, pathogenesis and clinical implications.Clinical and translational medicine · 2025Review
- Activation of Pvt1b isoform contributes to local Pvt1 abundance to repress Myc during stress.PLoS genetics · 2025Article
- Restoration of the Tumor Suppressor Function of Y220C-Mutant p53 by Rezatapopt, a Small-Molecule Reactivator.Cancer discovery · 2025Article
- TF Profiler: a transcription factor inference method that broadly measures transcription factor activity and identifies mechanistically distinct networks.Genome biology · 2025Article
- p53 regulates DREAM complex-mediated repression in a p21-independent manner.The EMBO journal · 2025Article
- Routine CT Diagnostics Cause Dose-Dependent Gene Expression Changes in Peripheral Blood Cells.International journal of molecular sciences · 2025Article
- Review
127 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The p53 transcription factor is a potent suppressor of tumor growth. We report here an analysis of its direct transcriptional program using Global Run-On sequencing (GRO-seq). Shortly after MDM2 inhibition by Nutlin-3, low levels of p53 rapidly activate ∼200 genes, most of them not previously established as direct targets. This immediate response involves all canonical p53 effector pathways, including apoptosis. Comparative global analysis of RNA synthesis vs steady state levels revealed that microarray profiling fails to identify low abundance transcripts directly activated by p53. Interestingly, p53 represses a subset of its activation targets before MDM2 inhibition. GRO-seq uncovered a plethora of gene-specific regulatory features affecting key survival and apoptotic genes within the p53 network. p53 regulates hundreds of enhancer-derived RNAs. Strikingly, direct p53 targets harbor pre-activated enhancers highly transcribed in p53 null cells. Altogether, these results enable the study of many uncharacterized p53 target genes and unexpected regulatory mechanisms.DOI: http://dx.doi.org/10.7554/eLife.02200.001.
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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.