Cargando…

Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2

Numerous biomolecular interactions involve unstructured protein regions, but how to exploit such interactions to enhance the affinity of a lead molecule in the context of rational drug design remains uncertain. Here clarification was sought for cases where interactions of different ligands with the...

Descripción completa

Detalles Bibliográficos
Autores principales: Bueren-Calabuig, Juan A., Michel, Julien
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457491/
https://www.ncbi.nlm.nih.gov/pubmed/26046940
http://dx.doi.org/10.1371/journal.pcbi.1004282
_version_ 1782374978386132992
author Bueren-Calabuig, Juan A.
Michel, Julien
author_facet Bueren-Calabuig, Juan A.
Michel, Julien
author_sort Bueren-Calabuig, Juan A.
collection PubMed
description Numerous biomolecular interactions involve unstructured protein regions, but how to exploit such interactions to enhance the affinity of a lead molecule in the context of rational drug design remains uncertain. Here clarification was sought for cases where interactions of different ligands with the same disordered protein region yield qualitatively different results. Specifically, conformational ensembles for the disordered lid region of the N-terminal domain of the oncoprotein MDM2 in the presence of different ligands were computed by means of a novel combination of accelerated molecular dynamics, umbrella sampling, and variational free energy profile methodologies. The resulting conformational ensembles for MDM2, free and bound to p53 TAD (17-29) peptide identify lid states compatible with previous NMR measurements. Remarkably, the MDM2 lid region is shown to adopt distinct conformational states in the presence of different small-molecule ligands. Detailed analyses of small-molecule bound ensembles reveal that the ca. 25-fold affinity improvement of the piperidinone family of inhibitors for MDM2 constructs that include the full lid correlates with interactions between ligand hydrophobic groups and the C-terminal lid region that is already partially ordered in apo MDM2. By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2.
format Online
Article
Text
id pubmed-4457491
institution National Center for Biotechnology Information
language English
publishDate 2015
publisher Public Library of Science
record_format MEDLINE/PubMed
spelling pubmed-44574912015-06-09 Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2 Bueren-Calabuig, Juan A. Michel, Julien PLoS Comput Biol Research Article Numerous biomolecular interactions involve unstructured protein regions, but how to exploit such interactions to enhance the affinity of a lead molecule in the context of rational drug design remains uncertain. Here clarification was sought for cases where interactions of different ligands with the same disordered protein region yield qualitatively different results. Specifically, conformational ensembles for the disordered lid region of the N-terminal domain of the oncoprotein MDM2 in the presence of different ligands were computed by means of a novel combination of accelerated molecular dynamics, umbrella sampling, and variational free energy profile methodologies. The resulting conformational ensembles for MDM2, free and bound to p53 TAD (17-29) peptide identify lid states compatible with previous NMR measurements. Remarkably, the MDM2 lid region is shown to adopt distinct conformational states in the presence of different small-molecule ligands. Detailed analyses of small-molecule bound ensembles reveal that the ca. 25-fold affinity improvement of the piperidinone family of inhibitors for MDM2 constructs that include the full lid correlates with interactions between ligand hydrophobic groups and the C-terminal lid region that is already partially ordered in apo MDM2. By contrast, Nutlin or benzodiazepinedione inhibitors, that bind with similar affinity to full lid and lid-truncated MDM2 constructs, interact additionally through their solubilizing groups with N-terminal lid residues that are more disordered in apo MDM2. Public Library of Science 2015-06-05 /pmc/articles/PMC4457491/ /pubmed/26046940 http://dx.doi.org/10.1371/journal.pcbi.1004282 Text en © 2015 Bueren-Calabuig, Michel http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Bueren-Calabuig, Juan A.
Michel, Julien
Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title_full Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title_fullStr Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title_full_unstemmed Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title_short Elucidation of Ligand-Dependent Modulation of Disorder-Order Transitions in the Oncoprotein MDM2
title_sort elucidation of ligand-dependent modulation of disorder-order transitions in the oncoprotein mdm2
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457491/
https://www.ncbi.nlm.nih.gov/pubmed/26046940
http://dx.doi.org/10.1371/journal.pcbi.1004282
work_keys_str_mv AT buerencalabuigjuana elucidationofliganddependentmodulationofdisorderordertransitionsintheoncoproteinmdm2
AT micheljulien elucidationofliganddependentmodulationofdisorderordertransitionsintheoncoproteinmdm2