ArticlePloS one2013
Structure and stability insights into tumour suppressor p53 evolutionary related proteins.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.Cell death & disease · 2023Article
- Conformational Heterogeneity and Frustration of the Tumor Suppressor p53 as Tuned by Punctual Mutations.International journal of molecular sciences · 2022Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- Hidden electrostatic energy contributions define dynamic allosteric communications within p53 during molecular recognition.Biophysical journal · 2021Article
- TRIM3 inhibits P53 signaling in breast cancer cells.Cancer cell international · 2020Article
- Raman Evidence of p53-DBD Disorder Decrease upon Interaction with the Anticancer Protein Azurin.International journal of molecular sciences · 2019Article
- Analysis of theInternational journal of molecular sciences · 2019Article
- Roles of computational modelling in understanding p53 structure, biology, and its therapeutic targeting.Journal of molecular cell biology · 2019Review
- Simulations of mutant p53 DNA binding domains reveal a novel druggable pocket.Nucleic acids research · 2019Article
- Aggregation tendencies in the p53 family are modulated by backbone hydrogen bonds.Scientific reports · 2016Article
- Identification of p53-target genes in Danio rerio.Scientific reports · 2016Article
- Evolution of p53 transactivation specificity through the lens of a yeast-based functional assay.PloS one · 2015Article
- Bioinformatics study of cancer-related mutations within p53 phosphorylation site motifs.International journal of molecular sciences · 2014Article
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Authors and funding
8 authors.
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Abstract
The p53 family of genes and their protein products, namely, p53, p63 and p73, have over one billion years of evolutionary history. Advances in computational biology and genomics are enabling studies of the complexities of the molecular evolution of p53 protein family to decipher the underpinnings of key biological conditions spanning from cancer through to various metabolic and developmental disorders and facilitate the design of personalised medicines. However, a complete understanding of the inherent nature of the thermodynamic and structural stability of the p53 protein family is still lacking. This is due, to a degree, to the lack of comprehensive structural information for a large number of homologous proteins and to an incomplete knowledge of the intrinsic factors responsible for their stability and how these might influence function. Here we investigate the thermal stability, secondary structure and folding properties of the DNA-binding domains (DBDs) of a range of proteins from the p53 family using biophysical methods. While the N- and the C-terminal domains of the p53 family show sequence diversity and are normally targets for post-translational modifications and alternative splicing, the central DBD is highly conserved. Together with data obtained from Molecular Dynamics simulations in solution and with structure based homology modelling, our results provide further insights into the molecular properties of evolutionary related p53 proteins. We identify some marked structural differences within the p53 family, which could account for the divergence in biological functions as well as the subtleties manifested in the oligomerization properties of this family.
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