Evidence map›Paper›PMID 35325302›Full record

ArticleJournal of molecular modeling2022

Molecular docking studies of natural immunomodulators indicate their interactions with the CD40L of CD40/CD40L pathway and CSF1R kinase domain of microglia.

Shashank Kumar Maurya, Rajnikant Mishra

Abstract read
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In one paragraph

Article in Journal of molecular modeling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. Review
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

2 authors at 2 institutions in 1 country.

Shashank Kumar MauryaDepartment of Zoology, Ramjas College, University of Delhi, 110007, Delhi, India.
Rajnikant MishraBiochemistry and Molecular Biology Laboratory, Department of Zoology, Banaras Hindu University, 221005, Varanasi, India. rmishraa@bhu.ac.in.ORCID http://orcid.org/0000-0002-6714-1460
Banaras Hindu University · INUniversity of Delhi · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural products have proved beneficial in reducing neuroinflammation in neurological diseases. Their impacts have also been associated with the activities of microglia, responsible for brain-specific immunity. Recent studies have shown the involvement of the number of microglia-specific proteins in the regulation of brain-specific immunity. However, molecular targets of natural products and their mechanism of interaction with microglia-specific proteins are elusive. Since the genetic signature of microglia offers many potential targets for drug discovery, molecular docking followed by molecular dynamics (MD) simulations of cluster of differentiation 40 ligand (CD40L) and colony-stimulating factor 1 receptor (CSF1R) kinase domain protein with some known neuro-immunomodulators (Curcumin, Cannabidiol, Ginsenoside Rg1, Resveratrol, and Sulforaphane) has been evaluated. Curcumin and cannabidiol were observed likely to modulate CD40L and expression of cytokines and entry of inflammatory cells. Resveratrol and cannabidiol may affect the CSF1R kinase domain and activation of microglia. Our finding suggests that curcumin, cannabidiol, and resveratrol may serve specific drug ligands in regulating microglia-mediated brain immunity.

Indexed as

CD40 LigandMicrogliaImmunologic FactorsLigandsMolecular Docking SimulationCD40 LigandImmunologic FactorsLigandsDrug targetMD simulationMicrogliaMolecular dockingNatural productsProtein–ligand interaction

Identifiers

PMID35325302
OpenAlexW4220947328

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.