ReviewCell death discovery2020
Regulation of p53 by the 14-3-3 protein interaction network: new opportunities for drug discovery in cancer.
Review in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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
33 citing papers in PubMed, 54 citations in OpenAlex.
- Mutant p53 gains RNA-binding activity to reprogram translation and mitochondrial function.Cell reports · 2026Article
- A cigarette compound-induced tumor microenvironment promotes sorafenib resistance in hepatocellular carcinoma via the 14-3-3η-modified tumor-associated proteome.Chinese medical journal · 2026Article
- Interplay between NRF2 post-translational modifications and protein-protein interactions: Perspectives from emerging structural and functional evidence.Archives of biochemistry and biophysics · 2026Review
- Discovery of Dimer-Dependent Aminoacrylamide Molecular Glues for 14-3-3 Protein-Protein Interactions.ACS medicinal chemistry letters · 2026Article
- 14-3-3ε-dependent deubiquitination and translocation of NLRP3 activates the inflammasome during sepsis.JCI insight · 2026Article
- Study on the mechanism of TP53 degradation by SFN ubiquitination affecting locally advanced TC progression.Frontiers in chemistry · 2026Article
- Mutant p53 binds RNA to drive mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Targeted Degradation of Class 1 HDACs With PROTACs is Highly Effective at Inducing DLBCL Cell Death.EJHaem · 2025Article
- Exploring molecular targets in cancer: Unveiling the anticancer potential of Paeoniflorin through a comprehensive analysis of diverse signaling pathways and recent advances.Journal of biological methods · 2024Review
- Review
- Infiltrating macrophages amplify doxorubicin-induced cardiac damage: role of catecholamines.Cellular and molecular life sciences : CMLS · 2023Article
- It Takes Two to Tango! Protein-Protein Interactions behind cAMP-Mediated CFTR Regulation.International journal of molecular sciences · 2023Review
- The Role of MEF2 Transcription Factor Family in Neuronal Survival and Degeneration.International journal of molecular sciences · 2023Review
- 14-3-3 proteins regulate cullin 7-mediated Eag1 degradation.Cell & bioscience · 2023Article
- Molecular Mechanisms and Targeted Therapies of Advanced Basal Cell Carcinoma.International journal of molecular sciences · 2022Review
- Understanding the interaction of 14-3-3 proteins with hDMX and hDM2: a structural and biophysical study.The FEBS journal · 2022Article
- Peptide and protein chemistry approaches to study the tumor suppressor protein p53.Organic & biomolecular chemistry · 2022Review
- ZLM-7 Blocks Breast Cancer Progression by Inhibiting MDM2 via Upregulation of 14-3-3 Sigma.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Review
- 14-3-3 Proteins are Potential Regulators of Liquid-Liquid Phase Separation.Cell biochemistry and biophysics · 2022Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cancers evolve to disable the p53 pathway, a key tumour suppressor mechanism that prevents transformation and malignant cell growth. However, only ~50% exhibit inactivating mutations of p53, while in the rest its activity is suppressed by changes in the proteins that modulate the pathway. Therefore, restoring p53 activity in cells in which it is still wild type is a highly attractive therapeutic strategy that could be effective in many different cancer types. To this end, drugs can be used to stabilise p53 levels by modulating its regulatory pathways. However, despite the emergence of promising strategies, drug development has stalled in clinical trials. The need for alternative approaches has shifted the spotlight to the 14-3-3 family of proteins, which strongly influence p53 stability and transcriptional activity through direct and indirect interactions. Here, we present the first detailed review of how 14-3-3 proteins regulate p53, with special emphasis on the mechanisms involved in their binding to different members of the pathway. This information will be important to design new compounds that can reactivate p53 in cancer cells by influencing protein-protein interactions. The intricate relationship between the 14-3-3 isoforms and the p53 pathway suggests that many potential drug targets for p53 reactivation could be identified and exploited to design novel antineoplastic therapies with a wide range of applications.
Identifiers
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.