ReviewCell death and differentiation2022
The genotypes and phenotypes of missense mutations in the proline domain of the p53 protein.
Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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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Who cites it
36 citing papers in PubMed, 43 citations in OpenAlex.
- The TP53 gene contains a diversity box that makes it more than a tumor suppressor.Cell death and differentiation · 2026Review
- Associative memory plays a role in ER-1α positive breast cancers.Cell death and differentiation · 2026Review
- Conformational flexibility and transient structure of the proline-rich domain in p53.Biophysical journal · 2026Article
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Genetic landscape of cancer: mechanisms, key genes, and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Multi-omic characterization of consensus molecular subtype 1 (CMS1) colorectal cancer with dampened immune response improves precision medicine.Molecular oncology · 2025Article
- The molecular mechanisms and therapeutic potential of p53 in kidney injury repair: a perspective on the p53alpha/delta133p53alpha signaling axis.Renal failure · 2025Review
- Distinct functional heterogeneity of TP53 R175 mutations in platinum-resistant ovarian cancer: unveiling molecular mechanisms and therapeutic targets.Cell death & disease · 2025Article
- Article
- Life Factors and Melanoma: From the Macroscopic State to the Molecular Mechanism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Personalized screening strategies forLancet regional health. Americas · 2025Article
- Proline-Selective Electrochemiluminescence Detecting a Single Amino Acid Variation Between A1 and A2 β-Casein Containing Milks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- How does p53 work? Regulation by the intrinsically disordered domains.Trends in biochemical sciences · 2025Review
- Deciphering the ghost proteome in ovarian cancer cells by deep proteogenomic characterization.Cell death & disease · 2024Article
- p53 Genetics and Biology in Lung Carcinomas: Insights, Implications and Clinical Applications.Biomedicines · 2024Review
- Understanding the complexity of p53 in a new era of tumor suppression.Cancer cell · 2024Review
- Computational Characterization of Membrane Proteins as Anticancer Targets: Current Challenges and Opportunities.International journal of molecular sciences · 2024Review
- Improving T cell killing and understanding senescence: Possible roles forProceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 protein is structurally and functionally divided into five domains. The proline-rich domain is localized at amino acids 55-100. 319 missense mutations were identified solely in the proline domain from human cancers. Six hotspot mutations were identified at amino acids 72, 73, 82, 84, 89, and 98. Codon 72 contains a polymorphism that changes from proline (and African descent) to arginine (with Caucasian descent) with increasing latitudes northward and is under natural selection for pigmentation and protection from UV light exposure. Cancers associated with mutations in the proline domain were considerably enriched for melanomas and skin cancers compared to mutations in other p53 domains. These hotspot mutations are enriched at UV mutational signatures disrupting amino acid signals for binding SH-3-containing proteins important for p53 function. Among the protein-protein interaction sites identified by hotspot mutations were MDM-2, a negative regulator of p53, XAF-1, promoting p53 mediated apoptosis, and PIN-1, a proline isomerase essential for structural folding of this domain.
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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.