ArticleAging2009
The regulation of p53 by phosphorylation: a model for how distinct signals integrate into the p53 pathway.
Article in Aging, 2009. 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 76 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
76 citing papers in PubMed, 26 citations in OpenAlex.
- A Tailored Phospho-p53 Library Probes Antibody Specificity and Recognition Limitations.Chembiochem : a European journal of chemical biology · 2025Article
- The hydroxamate based HDAC inhibitor WMJ-J-09 induces colorectal cancer cell death by targeting tubulin and downregulating survivin.Scientific reports · 2025Article
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- The therapeutic potential of repurposed mebendazole, alone and in synergistic combination with ONC201, in the treatment of diffuse midline glioma.American journal of cancer research · 2025Article
- Exploring the Functional Landscape of the p53 Regulatory Domain: The Stabilizing Role of Post-Translational Modifications.Journal of chemical theory and computation · 2024Article
- MDM2 inhibitor APG-115 synergizes with ABT-199 to induce cell apoptosis in chronic lymphocytic leukemia.Frontiers in pharmacology · 2024Article
- Aspergillus Carneus metabolite Averufanin induced cell cycle arrest and apoptotic cell death on cancer cell lines via inducing DNA damage.Scientific reports · 2023Article
- VprBP/DCAF1 regulates p53 function and stability through site-specific phosphorylation.Oncogene · 2023Article
- Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress.World journal of diabetes · 2023Review
- The prognostic role of p53 and its correlation with CDK9 in urothelial carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Activation of p53: How phosphorylated Ser15 triggers sequential phosphorylation of p53 at Thr18 by CK1δ.Proteins · 2022Article
- CRISPR-based kinome-screening revealed MINK1 as a druggable player to rewire 5FU-resistance in OSCC through AKT/MDM2/p53 axis.Oncogene · 2022Article
- Regulation of Stress-Activated Kinases in Response to Tacaribe Virus Infection and Its Implications for Viral Replication.Viruses · 2022Article
- Kinase-Catalyzed Crosslinking and Immunoprecipitation (K-CLIP) to Explore Kinase-Substrate Pairs.Current protocols · 2022Article
- Small-Molecule Gankyrin Inhibition as a Therapeutic Strategy for Breast and Lung Cancer.Journal of medicinal chemistry · 2022Article
- Mammalian eIF4E2-GSK3β maintains basal phosphorylation of p53 to resist senescence under hypoxia.Cell death & disease · 2022Article
- The Complex Interaction between P53 and miRNAs Joins New Awareness in Physiological Stress Responses.Cells · 2022Review
- The role of T-cells in head and neck squamous cell carcinoma: From immunity to immunotherapy.Frontiers in oncology · 2022Review
- Loss of peptidase D binding restores the tumor suppressor functions of oncogenic p53 mutants.Communications biology · 2021Article
- Structural and Drug Targeting Insights on Mutant p53.Cancers · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The tumour suppressor p53 is a transcription factor that has evolved the ability to integrate distinct environmental signals including DNA damage, virus infection, and cytokine signaling into a common biological outcome that maintains normal cellular control. Mutations in p53 switch the cellular transcription program resulting in deregulation of the stress responses that normally maintain cell and tissue integrity. Transgenic studies in mice have indicated that changes in the specific activity of p53 can have profound effects not only on cancer development, but also on organism aging. As the specific activity of p53 is regulated at a post-translational level by sets of enzymes that mediate phosphorylation, acetylation, methylation, and ubiquitin-like modifications, it is likely that physiological modifiers of the aging function of p53 would be enzymes that catalyze such covalent modifications. We demonstrate that distinct stress-activated kinases, including ataxia telangiectasia mutated (ATM), casein kinase 1 (CK1) and AMP-activated protein kinase (AMPK), mediate phosphorylation of a key phospho-acceptor site in the p53 transactivation domain in response to diverse stresses including ionizing radiation, DNA virus infection, and elevation in the intracellular AMP/ATP ratio. As diseases linked to aging can involve activation of p53-dependent changes in cellular protective pathways, the development of specific physiological models might further shed light on the role of p53 kinases in modifying age-related diseases.
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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.