ArticleMolecules (Basel, Switzerland)2017
Insights into the Effect of the G245S Single Point Mutation on the Structure of p53 and the Binding of the Protein to DNA.
Article in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Clinico-Morphological and Genetic Features of Colorectal Cancer in Multiple Primary Cancers Cases.Biochemical genetics · 2026Article
- mTORC1 suppression by Trp53 mutation drives resistance to immune checkpoint blockade.Cell death & disease · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- PEGASUS: Prediction of MD-derived protein flexibility from sequence.Protein science : a publication of the Protein Society · 2025Article
- p53 aberrant expression is pervasive in pleomorphic carcinomas of the lung and a sensitive diagnostic adjunct for biopsy specimens.Diagnostic pathology · 2025Article
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Review
- Review
- Complete Models of p53 Better Inform the Impact of Hotspot Mutations.International journal of molecular sciences · 2022Article
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- Computational Prediction and Experimental Validation of the Unique Molecular Mode of Action of Scoulerine.Molecules (Basel, Switzerland) · 2022Article
- High Tumor Mutation Burden and DNA Repair Gene Mutations are Associated with Primary Resistance to Crizotinib inOncoTargets and therapy · 2021Article
- [Research Progress in the Pathogenesis of Idiopathic Pulmonary Fibrosis with Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Article
- A novel hotspot and rare somatic mutation p.A138V, at TP53 is associated with poor survival of pancreatic ductal and periampullary adenocarcinoma patients.Molecular medicine (Cambridge, Mass.) · 2020Article
- When Stiffness Matters: Mechanosensing in Heart Development and Disease.Frontiers in cell and developmental biology · 2020Review
- Article
- Genomic stratification and liquid biopsy in a rare adrenocortical carcinoma (ACC) case, with dual lung metastases.Cold Spring Harbor molecular case studies · 2019Article
- The molecular mechanism of action of methylene quinuclidinone and its effects on the structure of p53 mutants.Oncotarget · 2018Article
- Frontiers in Computational Chemistry for Drug Discovery.Molecules (Basel, Switzerland) · 2018Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor p53 is a potent tumor suppressor dubbed as the "guardian of the genome" because of its ability to orchestrate protective biological outputs in response to a variety of oncogenic stresses. Mutation and thus inactivation of p53 can be found in 50% of human tumors. The majority are missense mutations located in the DNA binding region. Among them, G245S is known to be a structural hotspot mutation. To understand the behaviors and differences between the wild-type and mutant, both a dimer of the wild type p53 (wt-p53) and its G245S mutant (G245S-mp53), complexed with DNA, were simulated using molecular dynamics for more than 1 μs. wt-p53 and G245S-mp53 apo monomers were simulated for 1 μs as well. Conformational analyses and binding energy evaluations performed underline important differences and therefore provide insights to understand the G245S-mp53 loss of function. Our results indicate that the G245S mutation destabilizes several structural regions in the protein that are crucial for DNA binding when found in its apo form and highlight differences in the mutant-DNA complex structure compared to the wt protein. These findings not only provide means that can be applied to other p53 mutants but also serve as structural basis for further studies aimed at the development of cancer therapies based on restoring the function of p53.
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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.