ArticlePLoS computational biology2015
Modulation of the disordered conformational ensembles of the p53 transactivation domain by cancer-associated mutations.
Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Likely Overstabilization of Charge-Charge Interactions in CHARMM36m(w): A Case for a99SB-disp Water.The journal of physical chemistry. B · 2024Article
- Binding-and-Folding Recognition of an Intrinsically Disordered Protein Using Online Learning Molecular Dynamics.Journal of chemical theory and computation · 2023Article
- Toward Accurate Coarse-Grained Simulations of Disordered Proteins and Their Dynamic Interactions.Journal of chemical information and modeling · 2022Article
- The Elephant Evolved p53 Isoforms that Escape MDM2-Mediated Repression and Cancer.Molecular biology and evolution · 2022Article
- Replica exchange molecular dynamics simulations reveal self-association sites in M-crystallin caused by mutations provide insights of cataract.Scientific reports · 2021Article
- Advanced Sampling Methods for Multiscale Simulation of Disordered Proteins and Dynamic Interactions.Biomolecules · 2021Review
- Cancer-Associated Mutations Perturb the Disordered Ensemble and Interactions of the Intrinsically Disordered p53 Transactivation Domain.Journal of molecular biology · 2021Article
- Connecting Coil-to-Globule Transitions to Full Phase Diagrams for Intrinsically Disordered Proteins.Biophysical journal · 2020Article
- Targeting Intrinsically Disordered Proteins through Dynamic Interactions.Biomolecules · 2020Review
- Modulation of p53 Transactivation Domain Conformations by Ligand Binding and Cancer-Associated Mutations.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2020Article
- Sequence specificity despite intrinsic disorder: How a disease-associated Val/Met polymorphism rearranges tertiary interactions in a long disordered protein.PLoS computational biology · 2019Article
- Residual Structures and Transient Long-Range Interactions of p53 Transactivation Domain: Assessment of Explicit Solvent Protein Force Fields.Journal of chemical theory and computation · 2019Article
- Gain-of-Function Mutations: An Emerging Advantage for Cancer Biology.Trends in biochemical sciences · 2019Review
- Roles of computational modelling in understanding p53 structure, biology, and its therapeutic targeting.Journal of molecular cell biology · 2019Review
- Improvements to the ABSINTH Force Field for Proteins Based on Experimentally Derived Amino Acid Specific Backbone Conformational Statistics.Journal of chemical theory and computation · 2019Article
- Atomistic Peptide Folding Simulations Reveal Interplay of Entropy and Long-Range Interactions in Folding Cooperativity.Scientific reports · 2018Article
- Emergence of Alternative Structures in Amyloid Beta 1-42 Monomeric Landscape by N-terminal Hexapeptide Amyloid Inhibitors.Scientific reports · 2017Article
- Optimization of the GBMV2 implicit solvent force field for accurate simulation of protein conformational equilibria.Journal of computational chemistry · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrinsically disordered proteins (IDPs) are frequently associated with human diseases such as cancers, and about one-fourth of disease-associated missense mutations have been mapped into predicted disordered regions. Understanding how these mutations affect the structure-function relationship of IDPs is a formidable task that requires detailed characterization of the disordered conformational ensembles. Implicit solvent coupled with enhanced sampling has been proposed to provide a balance between accuracy and efficiency necessary for systematic and comparative assessments of the effects of mutations as well as post-translational modifications on IDP structure and interaction. Here, we utilize a recently developed replica exchange with guided annealing enhanced sampling technique to calculate well-converged atomistic conformational ensembles of the intrinsically disordered transactivation domain (TAD) of tumor suppressor p53 and several cancer-associated mutants in implicit solvent. The simulations are critically assessed by quantitative comparisons with several types of experimental data that provide structural information on both secondary and tertiary levels. The results show that the calculated ensembles reproduce local structural features of wild-type p53-TAD and the effects of K24N mutation quantitatively. On the tertiary level, the simulated ensembles are overly compact, even though they appear to recapitulate the overall features of transient long-range contacts qualitatively. A key finding is that, while p53-TAD and its cancer mutants sample a similar set of conformational states, cancer mutants could introduce both local and long-range structural modulations to potentially perturb the balance of p53 binding to various regulatory proteins and further alter how this balance is regulated by multisite phosphorylation of p53-TAD. The current study clearly demonstrates the promise of atomistic simulations for detailed characterization of IDP conformations, and at the same time reveals important limitations in the current implicit solvent protein force field that must be sufficiently addressed for reliable description of long-range structural features of the disordered ensembles.
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