Evidence map›Paper›PMID 35924852›Full record

ArticlemBio2022

Genistein Targets STING-Driven Antiviral Responses.

Tomalika R Ullah, Katherine R Balka, Rebecca L Ambrose, Geneviève Pépin, Matthew C J Wilce, Jacqueline A Wilce, Belinda J Thomas, Dominic De Nardo, Bryan R G Williams, Michael P Gantier

Open access · goldAbstract read
In one paragraph

Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  10. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
    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

10 authors at 3 institutions in 1 country.

Tomalika R UllahCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Researchgrid.452824.d, Clayton, Victoria, Australia.ORCID 0000-0002-5935-6939
Katherine R BalkaDepartment of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash Universitygrid.1002.3, Clayton, Victoria, Australia.
Rebecca L AmbroseCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Researchgrid.452824.d, Clayton, Victoria, Australia.
Geneviève PépinCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Researchgrid.452824.d, Clayton, Victoria, Australia.
Matthew C J WilceDepartment of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash Universitygrid.1002.3, Clayton, Victoria, Australia.
Jacqueline A WilceDepartment of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash Universitygrid.1002.3, Clayton, Victoria, Australia.
Belinda J ThomasCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Researchgrid.452824.d, Clayton, Victoria, Australia.
Dominic De NardoDepartment of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash Universitygrid.1002.3, Clayton, Victoria, Australia.
Bryan R G WilliamsDepartment of Molecular and Translational Science, Monash Universitygrid.1002.3, Clayton, Victoria, Australia.
Michael P GantierCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Researchgrid.452824.d, Clayton, Victoria, Australia.ORCID 0000-0003-3740-698X
Hudson Institute of Medical Research · AUAustralian Regenerative Medicine Institute · AUMonash Medical Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytoplasmic detection of DNA by cyclic GMP-AMP (cGAMP) synthase (cGAS) is an essential component of antiviral responses. Upon synthesis, cGAMP binds to the stimulator of interferon (IFN) genes (STING) in infected and adjacent cells through intercellular transfer by connexins forming gap-junctions, eliciting a strong IFN-β-driven antiviral response. We demonstrate here that Genistein, a flavonoid compound naturally occurring in soy-based foods, inhibits cGAS-STING antiviral signaling at two levels. First, Genistein pretreatment of cGAMP-producing cells inhibited gap-junction intercellular communication, resulting in reduced STING responses in adjacent cells. In addition, Genistein directly blocked STING activation by the murine agonist DMXAA, by decreasing the interaction of STING with TBK1 and IKKε. As a result, Genistein attenuated STING signaling in human and mouse cells, dampening antiviral activity against Semliki Forest Virus infection. Collectively, our findings identify a previously unrecognized proviral activity of Genistein mediated via its inhibitory effects at two levels of cGAS-STING signaling.

Indexed as

GenisteinMembrane ProteinsAnimalsAntiviral AgentsHumansImmunity, InnateInterferon-betaMiceNucleotidyltransferasesAntiviral AgentsGenisteinInterferon-betaMembrane ProteinsNucleotidyltransferasescGAMPgap junctionGenisteinSTING inhibitor

Identifiers

PMID35924852
PMCPMC9426420
OpenAlexW4289774638

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.