ArticleCell death & disease2023
Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Inverse Association of p63 Expression with Hormone Receptor Status in Invasive Breast Cancer.Journal of personalized medicine · 2026Article
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- COCOMAPS 2.0: a web server for identifying, analyzing, and visualizing atomic interactions at the interface of biomolecular complexes.Bioinformatics (Oxford, England) · 2025Article
- Article
- A Novel TP63 Missense Mutation in the Sumoylation Motif Causes Isolated Split-Hand/Foot Malformation 4: A Pedigree Report and Literature Review.Molecular genetics & genomic medicine · 2025Review
- Alternative splicing in the DBD linker region of p63 modulates binding to DNA and iASPP in vitro.Cell death & disease · 2025Article
- Case report: Artificial thymic organoids facilitate clinical decisions for a patient with aFrontiers in immunology · 2024Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor p63 shares a high sequence identity with the tumour suppressor p53 which manifests itself in high structural similarity and preference for DNA sequences. Mutations in the DNA binding domain (DBD) of p53 have been studied in great detail, enabling a general mechanism-based classification. In this study we provide a detailed investigation of all currently known mutations in the p63 DBD, which are associated with developmental syndromes, by measuring their impact on transcriptional activity, DNA binding affinity, zinc binding capacity and thermodynamic stability. Some of the mutations we have further characterized with respect to their ability to convert human dermal fibroblasts into induced keratinocytes. Here we propose a classification of the p63 DBD mutations based on the four different mechanisms of DNA binding impairment which we identified: direct DNA contact, zinc finger region, H2 region, and dimer interface mutations. The data also demonstrate that, in contrast to p53 cancer mutations, no p63 mutation induces global unfolding and subsequent aggregation of the domain. The dimer interface mutations that affect the DNA binding affinity by disturbing the interaction between the individual DBDs retain partial DNA binding capacity which correlates with a milder patient phenotype.
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