ArticleOncogene2017
Full-length p53 tetramer bound to DNA and its quaternary dynamics.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- A Tale of Two Mechanisms: The p53 Modulator COTI-2 Is a Zn Metallochaperone.Drug development research · 2026Article
- TowardsbioRxiv : the preprint server for biology · 2025Article
- Mitochondrially Targeted p53-Bad* Fusion Gene Therapy Promotes Apoptosis in Hepatocellular Carcinoma by Pan-Bcl-2 Inhibition.Molecular pharmaceutics · 2025Article
- How does p53 work? Regulation by the intrinsically disordered domains.Trends in biochemical sciences · 2025Review
- Covalent Modification of p53 by (ACS pharmacology & translational science · 2024Article
- Structural assessment of the full-length wild-type tumor suppressor protein p53 by mass spectrometry-guided computational modeling.Scientific reports · 2023Article
- Mapping Interactions of the Intrinsically Disordered C-Terminal Regions of Tetrameric p53 by Segmental Isotope Labeling and NMR.Biochemistry · 2022Article
- Sequence Properties of An Intramolecular Interaction That Inhibits p53 DNA Binding.Biomolecules · 2022Article
- Structural Basis of Mutation-Dependent p53 Tetramerization Deficiency.International journal of molecular sciences · 2022Article
- Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.Frontiers in molecular biosciences · 2022Review
- Allosteric conformational ensembles have unlimited capacity for integrating information.eLife · 2021Article
- An integrated view of p53 dynamics, function, and reactivation.Current opinion in structural biology · 2021Review
- A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Investigating Conformational Dynamics and Allostery in the p53 DNA-Binding Domain Using Molecular Simulations.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Markov state models and NMR uncover an overlooked allosteric loop in p53.Chemical science · 2020Article
- Review
- Li-Fraumeni syndrome heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- Roles of computational modelling in understanding p53 structure, biology, and its therapeutic targeting.Journal of molecular cell biology · 2019Review
- Salvation of the fallen angel: Reactivating mutant p53.British journal of pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
P53 is a major tumor suppressor that is mutated and inactivated in ~50% of all human cancers. Thus, reactivation of mutant p53 using small molecules has been a long sought-after anticancer therapeutic strategy. Full structural characterization of the full-length oligomeric p53 is challenging because of its complex architecture and multiple highly flexible regions. To explore p53 structural dynamics, here we developed a series of atomistic integrative models with available crystal structures of the full-length p53 (fl-p53) tetramer bound to three different DNA sequences: a p21 response element, a puma response element and a nonspecific DNA sequence. Explicitly solvated, all-atom molecular dynamics simulations of the three complexes (totaling nearly 1 μs of aggregate simulation time) yield final structures consistent with electron microscopy maps and, for the first time, show the direct interactions of the p53 C-terminal with DNA. Through a collective principal component analysis, we identify sequence-dependent differential quaternary binding modes of the p53 tetramer interfacing with DNA. Additionally, L1 loop dynamics of fl-p53 in the presence of DNA is revealed, and druggable pockets of p53 are identified via solvent mapping to aid future drug discovery studies.
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What OpenQuestion holds
Registered trials
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.