ArticleThe Journal of biological chemistry2013
Crystal structures of the DNA-binding domain tetramer of the p53 tumor suppressor family member p73 bound to different full-site response elements.
Article in The Journal of biological chemistry, 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.
- Advances in cyclotide research: bioactivity to cyclotide-based therapeutics.Molecular diversity · 2025Review
- UV-C Exposure Enhanced the CdMicroorganisms · 2024Article
- Structural assessment of the full-length wild-type tumor suppressor protein p53 by mass spectrometry-guided computational modeling.Scientific reports · 2023Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- MCL1 binds and negatively regulates the transcriptional function of tumor suppressor p73.Cell death & disease · 2020Article
- Review
- Defining TP53 pioneering capabilities with competitive nucleosome binding assays.Genome research · 2019Article
- Quantification of Cooperativity in Heterodimer-DNA Binding Improves the Accuracy of Binding Specificity Models.The Journal of biological chemistry · 2016Article
- Integrated transcriptional profiling and genomic analyses reveal RPN2 and HMGB1 as promising biomarkers in colorectal cancer.Cell & bioscience · 2015Article
- Evolution of p53 transactivation specificity through the lens of a yeast-based functional assay.PloS one · 2015Article
- ∆N-P63α and TA-P63α exhibit intrinsic differences in transactivation specificities that depend on distinct features of DNA target sites.Oncotarget · 2014Article
- p53 Family and Cellular Stress Responses in Cancer.Frontiers in oncology · 2014Review
- Transactivation specificity is conserved among p53 family proteins and depends on a response element sequence code.Nucleic acids research · 2013Article
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Authors and funding
3 authors.
Funding
Abstract
How cells choose between developmental pathways remains a fundamental biological question. In the case of the p53 protein family, its three transcription factors (p73, p63, and p53) each trigger a gene expression pattern that leads to specific cellular pathways. At the same time, these transcription factors recognize the same response element (RE) consensus sequences, and their transactivation of target genes overlaps. We aimed to understand target gene selectivity at the molecular level by determining the crystal structures of the p73 DNA-binding domain (DBD) in complex with full-site REs that vary in sequence. We report two structures of the p73 DBD bound as a tetramer to 20-bp full-site REs based on two distinct quarter-sites: GAACA and GAACC. Our study confirms that the DNA-binding residues are conserved within the p53 family, whereas the dimerization and tetramerization interfaces diverge. Moreover, a conserved lysine residue in loop L1 of the DBD senses the presence of guanines in positions 2 and 3 of the quarter-site RE, whereas a conserved arginine in loop 3 adapts to changes in position 5. Sequence variations in the RE elicit a p73 conformational response that might explain target gene specificity.
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