ArticleJournal of molecular modeling2021
Modelling of an autonomous Nav1.5 channel system as a part of in silico pharmacology study.
Article in Journal of molecular modeling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- 4-(Azolyl)-Benzamidines as a Novel Chemotype for ASIC1a Inhibitors.International journal of molecular sciences · 2024Article
- Antiepileptic Drug Tiagabine Does Not Directly Target Key Cardiac Ion Channels Kv11.1, Nav1.5 and Cav1.2.Molecules (Basel, Switzerland) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
A homology model of Nav1.5, based mainly on the crystal structures of Nav1.2/1.5 was built, optimized and successfully inserted into the membrane bilayer. We applied steered and free MD simulation protocols for the visualization of the mechanism of Nav1.5 activation. We constrained dihedrals of S4 trigger to introduce a structural tension with further rearrangement and movement of secondary structure elements. From these, we observed an intracellular gate opening and movement of the Lys1419 residue caused by a gradual displacement of the distal S6 α-helix with the extended S4 3-10 helix of voltage-sensing domains (VSD). A construction containing the Lys1419 residue in P-loop also changed its position due to the extension of this helix and subsequent induction of the pore-forming helixes motion. From this point, a double membrane system was generated, implying a free of ligand Nav1.5 protein and on the opposite side its copy containing a docked bupivacaine molecule inside the pore channel. The system can be used for the design of selective inhibitors against the Nav1.7 channel, instead of mixed effect on both channels.
Indexed as
Identifiers
34031769What 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.