ReviewTrends in biochemical sciences2025
How does p53 work? Regulation by the intrinsically disordered domains.
Review in Trends in biochemical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Using Organoids to Unlock the Potential of Human Torpor for Spaceflight.Current stem cell reports · 2026Article
- Deubiquitinating enzymes in cervical cancer: Molecular mechanisms and therapeutic implications (Review).International journal of oncology · 2026Review
- Evidence for dual pathways of Tc1/mariner domestication in Drosophila.BMC biology · 2026Article
- Disordered N-Terminal Tail "Wags the Dog" in Human Thymidylate Synthase.Biochemistry · 2026Article
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- HtrA2/Omi: potential therapeutic targets for neurodegenerative diseases.Frontiers in pharmacology · 2026Review
- Quantum chemical profiling of protein mutations via fragment-based DFT.Frontiers in molecular biosciences · 2026Article
- The molecular mechanisms and therapeutic potential of p53 in kidney injury repair: a perspective on the p53alpha/delta133p53alpha signaling axis.Renal failure · 2025Review
- Article
- Functional characteristics of fresh antitumor immune interferer GDF-15 in multiple cancers.Scientific reports · 2025Article
- Competition between Nucleic Acids and Intrinsically Disordered Regions within Proteins.Accounts of chemical research · 2025Article
- GnomAD Missense Variants of Uncertain Significance: Implications for p53 Stability and Phosphorylation.International journal of molecular sciences · 2025Article
- Opto-p53: A light-controllable activation of p53 signaling pathway.Cell structure and function · 2025Article
- A Truncated Mutation of TP53 Promotes Chemoresistance in Tongue Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- Sex Disparities in P53 Regulation and Functions: Novel Insights for Personalized Cancer Therapies.Cells · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Defects in the tumor suppressor protein p53 are found in the majority of cancers. The p53 protein (393 amino acids long) contains the folded DNA-binding domain (DBD) and tetramerization domain (TET), with the remainder of the sequence being intrinsically disordered. Since cancer-causing mutations occur primarily in the DBD, this has been the focus of most of the research on p53. However, recent reports show that the disordered N-terminal activation domain (NTAD) and C-terminal regulatory domain (CTD) function synergistically with the DBD to regulate p53 activity. We propose a mechanistic model in which intermolecular and intramolecular interactions of the disordered regions, modulated by post-translational modifications, perform a central role in the regulation and activation of p53 in response to cellular stress.
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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.