ArticleThe Journal of biological chemistry2011
Cancer-associated p53 tetramerization domain mutants: quantitative analysis reveals a low threshold for tumor suppressor inactivation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 74 citations in OpenAlex.
- ROWVA: A Structure-Based Metric for Predicting the Pathogenicity of Protein Variants Using Alphafold2.Cancer science · 2026Article
- Evaluation of non-canonical p53 functions in DNA replication and recombination for variant classification.Cell death & disease · 2026Article
- Mutant p53 and TP53 mutations in esophageal squamous cell carcinoma: consistency and diagnostic significance.Frontiers in genetics · 2026Article
- Dominant-Negative Effects of p53 R337 Variants in Li-Fraumeni Syndrome: Impact on Tetramer Formation and Transcriptional Activity.Chembiochem : a European journal of chemical biology · 2025Article
- A quantitative, Bayesian-informed approach to gene-specific variant classification: Updated Expert Panel recommendations improve classification of TP53 germline variants for Li-Fraumeni syndrome.Genome medicine · 2025Review
- GnomAD Missense Variants of Uncertain Significance: Implications for p53 Stability and Phosphorylation.International journal of molecular sciences · 2025Article
- Transcription Factors and Methods for the Pharmacological Correction of Their Activity.International journal of molecular sciences · 2025Review
- Germline variant affecting p53β isoforms predisposes to familial cancer.Nature communications · 2024Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Novel Antineoplastic Inducers of Mitochondrial Apoptosis in Human Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- Highly Similar Tetramerization Domains from the p53 Protein of Different Mammalian Species Possess Varying Biophysical, Functional and Structural Properties.International journal of molecular sciences · 2023Article
- How Do Cancer-Related Mutations Affect the Oligomerisation State of the p53 Tetramerisation Domain?Current issues in molecular biology · 2023Article
- Dimeric p53 Mutant Elicits Unique Tumor-Suppressive Activities through an Altered Metabolic Program.Cancer discovery · 2023Article
- A tetramerization domain in prokaryotic and eukaryotic transcription regulators homologous to p53.Acta crystallographica. Section D, Structural biology · 2023Article
- Structural Basis of Mutation-Dependent p53 Tetramerization Deficiency.International journal of molecular sciences · 2022Article
- Soft Tissue Sarcoma Study: Association of Genetic Alterations in the Apoptosis Pathways with Chemoresistance to Doxorubicin.Cancers · 2022Article
- Molecular Characterization of the Tumor Microenvironment in Renal Medullary Carcinoma.Frontiers in oncology · 2022Article
- Article
- p53 tetramerization: at the center of the dominant-negative effect of mutant p53.Genes & development · 2020Review
- A RareCancer research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53, a 393-amino acid transcription factor, induces cell cycle arrest and apoptosis in response to genotoxic stress. Its inactivation via the mutation of its gene is a key step in tumor progression, and tetramer formation is critical for p53 post-translational modification and its ability to activate or repress the transcription of target genes vital in inhibiting tumor growth. About 50% of human tumors have TP53 gene mutations; most are missense ones that presumably lower the tumor suppressor activity of p53. In this study, we explored the effects of known tumor-derived missense mutations on the stability and oligomeric structure of p53; our comprehensive, quantitative analyses encompassed the tetramerization domain peptides representing 49 such substitutions in humans. Their effects on tetrameric structure were broad, and the stability of the mutant peptides varied widely (ΔT(m) = 4.8 ∼ -46.8 °C). Because formation of a tetrameric structure is critical for protein-protein interactions, DNA binding, and the post-translational modification of p53, a small destabilization of the tetrameric structure could result in dysfunction of tumor suppressor activity. We suggest that the threshold for loss of tumor suppressor activity in terms of the disruption of the tetrameric structure of p53 could be extremely low. However, other properties of the tetramerization domain, such as electrostatic surface potential and its ability to bind partner proteins, also may be important.
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