ArticleNucleic acids research2014
Critical role for p53-serine 15 phosphorylation in stimulating transactivation at p53-responsive promoters.
Article in Nucleic acids research, 2014. 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 189 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.
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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
189 citing papers in PubMed, 304 citations in OpenAlex.
- Expression of p53 protein isoforms predicts survival in patients with multiple myeloma.American journal of hematology · 2022Trial
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- A Toxoplasma gondii-derived ROP38 protein engages Ser15/Thr18-linked p53 activation and DNA damage-associated apoptotic signaling in human cancer cells.Cell communication and signaling : CCS · 2026Article
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- TTC33 forms a complex with WDR61 and PHF5A to recruit factors relevant to genomic integrity.Nature communications · 2026Article
- Study of post-translational modifications of p53 in multiple myeloma.Blood cancer journal · 2026Article
- Osimertinib-induced cardiotoxicity is driven by HDAC-dependent epigenetic repression and rescued by vorinostat.Signal transduction and targeted therapy · 2026Article
- Apoptosis signaling and cancer targeted therapy: from bench to bespoke.Translational cancer research · 2026Review
- A ZNF-nanobody fusion reveals SUMOylation-dependent changes in p53 protein localization.iScience · 2026Article
- Targeting oncogene-induced senescence in ETV6::RUNX1 pre-leukemic cells.Cell death discovery · 2026Article
- Mutant KRAS Heterogeneity Shapes Nuclear Architecture During Pancreatic Cancer Initiation.Epigenomes · 2026Article
- DNA damage and cell death induced by exposure to ultra-high dose rate low-dose pulsed X-rays emitted from a kilojoule plasma focus device.Biological research · 2026Article
- Inhibition of Autophagy Reveals ATR Protein Kinase as a Key Mediator of Cisplatin Sensitivity in Osteosarcoma.Cancer medicine · 2026Article
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- Evaluation of the effects of silver nanoparticles and ciprofloxacin on apoptotic gene expression (BAX, Bcl-2, and caspase-3) in NALM-6 acute lymphoblastic leukemia progenitor B cells.Medical oncology (Northwood, London, England) · 2026Article
- Targeting the p53 pathway to treat atypical teratoid rhabdoid tumors.Neuro-oncology pediatrics · 2026Article
- Biomarkers for Recurrence and Prognosis in Metastatic Urothelial Cancer: Emerging Clinical Applications.Journal of Cancer · 2026Review
- Nanoscale Analysis beyond Imaging by Atomic Force Microscopy: Molecular Perspectives on Oncology and Neurodegeneration.Small science · 2025Review
- Sustainable Grape Antioxidant Dietary Fiber Preserves Proximal Colonic Homeostasis via Hsp27 and AMPK Signaling.International journal of molecular sciences · 2025Article
129 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 tumour suppressor is induced by various stress stimuli and coordinates an adaptive gene expression programme leading to growth arrest or cell death. Some stimuli, such as DNA damage, lead to rapid and substantial multisite phosphorylation of p53, nucleated initially through phosphorylation of serine 15. Other stimuli, such as hyper-proliferation, do not stimulate p53-phosphorylation, raising questions regarding the physiological role for phosphorylation. Here, we show that a basal level of Ser15 phosphorylation occurs in both unstimulated cells and cells stimulated pharmacologically to induce p53. p53 in which Ser15 is substituted by alanine (S15A) fails to mediate p53-dependent transcription or growth arrest but can be rescued by substitution with aspartate (S15D: a phospho-mimic). Chromatin immunoprecipitation (ChIP) analyses show that, while wt- and S15A-p53 are detectable on the CDKN1A (p21) promoter (as a representative p53-responsive promoter), S15A-p53 does not stimulate histone acetylation (a measure of chromatin relaxation), nor is its recruitment stimulated, in response to a DNA damage or pharmacological stimulus. These data demonstrate that Ser15 phosphorylation is required for p53 function in the physiological context of p53-responsive promoters and suggest a key and possibly universal role even for low levels of this modification in promoting p53-transcription function.
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What OpenQuestion holds
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.