ReviewHuman mutation2014
Mutant TP53 posttranslational modifications: challenges and opportunities.
Review in Human mutation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 70 citations in OpenAlex.
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Targeted citrullination enables p53 binding to non-canonical sites.Molecular cell · 2025Article
- Smad1 Promotes Tumorigenicity and Chemoresistance of Glioblastoma by Sequestering p300 From p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular characterization, function, tissue differential expression, and single-nucleotide polymorphism of buffaloArchives animal breeding · 2024Article
- Acetylation halts missense mutant p53 aggregation and rescues tumor suppression in non-small cell lung cancers.iScience · 2023Article
- Targeting p53 misfolding conundrum by stabilizing agents and their analogs in breast cancer therapy: a comprehensive computational analysis.Frontiers in pharmacology · 2023Article
- Review
- The role of p53 in liver fibrosis.Frontiers in pharmacology · 2022Review
- Evaluation of the Role of p53 Tumour Suppressor Posttranslational Modifications and TTC5 Cofactor in Lung Cancer.International journal of molecular sciences · 2021Article
- p53 Forms Redox-Dependent Protein-Protein Interactions through Cysteine 277.Antioxidants (Basel, Switzerland) · 2021Article
- Genetic regressive trajectories in colorectal cancer: A new hallmark of oligo-metastatic disease?Translational oncology · 2021Review
- The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3.Nature communications · 2021Article
- Structural insights into the role of DNA-PK as a master regulator in NHEJ.Genome instability & disease · 2021Review
- Making Connections: p53 and the Cathepsin Proteases as Co-Regulators of Cancer and Apoptosis.Cancers · 2020Review
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- A Protein in the YeastBiomolecules · 2020Article
- How p53 Molecules Solve the Target DNA Search Problem: A Review.International journal of molecular sciences · 2020Review
- Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas.Cell reports · 2019Article
- p53 modifications: exquisite decorations of the powerful guardian.Journal of molecular cell biology · 2019Review
- Cytarabine-ResistantInternational journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The wild-type (WT) human p53 (TP53) tumor suppressor can be posttranslationally modified at over 60 of its 393 residues. These modifications contribute to changes in TP53 stability and in its activity as a transcription factor in response to a wide variety of intrinsic and extrinsic stresses in part through regulation of protein-protein and protein-DNA interactions. The TP53 gene frequently is mutated in cancers, and in contrast to most other tumor suppressors, the mutations are mostly missense often resulting in the accumulation of mutant (MUT) protein, which may have novel or altered functions. Most MUT TP53s can be posttranslationally modified at the same residues as in WT TP53. Strikingly, however, codons for modified residues are rarely mutated in human tumors, suggesting that TP53 modifications are not essential for tumor suppression activity. Nevertheless, these modifications might alter MUT TP53 activity and contribute to a gain-of-function leading to increased metastasis and tumor progression. Furthermore, many of the signal transduction pathways that result in TP53 modifications are altered or disrupted in cancers. Understanding the signaling pathways that result in TP53 modification and the functions of these modifications in both WT TP53 and its many MUT forms may contribute to more effective cancer therapies.
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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.