Evidence map›Paper›PMID 37001021›Full record

ArticleThe journal of physical chemistry. B2023

Binding of Venezuelan Equine Encephalitis Virus Inhibitors to Importin-α Receptors Explored with All-Atom Replica Exchange Molecular Dynamics.

Bryan M Delfing, Audrey Olson, Xavier E Laracuente, Kenneth W Foreman, Mikell Paige, Kylene Kehn-Hall, Christopher Lockhart, Dmitri K Klimov

Open access · greenAbstract read
In one paragraph

Article in The journal of physical chemistry. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 28% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Bryan M DelfingSchool of Systems Biology, George Mason University, Manassas, Virginia 20110, United States.
Audrey OlsonSchool of Systems Biology, George Mason University, Manassas, Virginia 20110, United States.
Xavier E LaracuenteSchool of Systems Biology, George Mason University, Manassas, Virginia 20110, United States.
Kenneth W ForemanDepartment of Chemistry and Biochemistry, George Mason University, Manassas, Virginia 20110, United States.ORCID 0000-0002-4908-6576
Mikell PaigeDepartment of Chemistry and Biochemistry, George Mason University, Manassas, Virginia 20110, United States.
Kylene Kehn-HallDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061, United States.
Christopher LockhartSchool of Systems Biology, George Mason University, Manassas, Virginia 20110, United States.
Dmitri K KlimovSchool of Systems Biology, George Mason University, Manassas, Virginia 20110, United States.ORCID 0000-0002-2893-867X
George Mason University · USVirginia–Maryland College of Veterinary Medicine · US

Funding

Developing capsid-importin alpha inhibitors for the treatment of VEEV infectionR01AI143817 · NIAID · GEORGE MASON UNIVERSITY · PI KEHN-HALL, KYLENE, KLIMOV, DMITRI KONSTANTINOVICH · 2020 to 2024
$3.6M
NIAID NIH HHS R01 AI143817
6 · The paper itself

Abstract

Although Venezuelan equine encephalitis virus (VEEV) is a life-threatening pathogen with a capacity for epidemic outbreaks, there are no FDA-approved VEEV antivirals for humans. VEEV cytotoxicity is partially attributed to the formation of a tetrameric complex between the VEEV capsid protein, the nuclear import proteins importin-α and importin-β, and the nuclear export protein CRM1, which together block trafficking through the nuclear pore complex. Experimental studies have identified small molecules from the CL6662 scaffold as potential inhibitors of the viral nuclear localization signal (NLS) sequence binding to importin-α. However, little is known about the molecular mechanism of CL6662 inhibition. To address this issue, we employed all-atom replica exchange molecular dynamics simulations to probe, in atomistic detail, the binding mechanism of CL6662 ligands to importin-α. Three ligands, including G281-1485 and two congeners with varying hydrophobicities, were considered. We investigated the distribution of ligand binding poses, their locations, and ligand specificities measured by the strength of binding interactions. We found that G281-1485 binds nonspecifically without forming well-defined binding poses throughout the NLS binding site. Binding of the less hydrophobic congener becomes strongly on-target with respect to the NLS binding site but remains nonspecific. However, a more hydrophobic congener is a strongly specific binder and the only ligand out of three to form a well-defined binding pose, while partially overlapping with the NLS binding site. On the basis of free energy estimates, we argue that all three ligands weakly compete with the viral NLS sequence for binding to importin-α in an apparent compromise to preserve host NLS binding. We further show that all-atom replica exchange binding simulations are a viable tool for studying ligands binding nonspecifically without forming well-defined binding poses.

Indexed as

alpha KaryopherinsEncephalitis Virus, Venezuelan EquineAnimalsBinding SitesCell NucleusHorsesHumansLigandsMolecular Dynamics SimulationNuclear Localization SignalsProtein Bindingalpha KaryopherinsLigandsNuclear Localization Signals

Identifiers

PMID37001021
PMCPMC10358320
OpenAlexW4362458548

What OpenQuestion holds

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Registered trials

None linked

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.