Evidence map›Paper›PMID 36793726›Full record

ArticleFrontiers in immunology2023

Interferon alpha inducible protein 6 is a negative regulator of innate immune responses by modulating RIG-I activation.

Laura Villamayor, Vanessa Rivero, Darío López-García, David J Topham, Luis Martínez-Sobrido, Aitor Nogales, Marta L DeDiego

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Human long noncoding RNAJournal of virology · 2025
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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

7 authors at 4 institutions in 2 countries.

Laura VillamayorDepartment of Molecular and Cell Biology. Centro Nacional de Biotecnología (CNB-CSIC), Madrid, Spain.
Vanessa RiveroDepartment of Molecular and Cell Biology. Centro Nacional de Biotecnología (CNB-CSIC), Madrid, Spain.
Darío López-GarcíaDepartment of Molecular and Cell Biology. Centro Nacional de Biotecnología (CNB-CSIC), Madrid, Spain.
David J TophamDavid H. Smith Center for Vaccine Biology and Immunology, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY, United States.
Luis Martínez-SobridoDisease Intervention and Prevention and Population Health Programs, Texas Biomedical Research Institute, San Antonio, TX, United States.
Aitor NogalesCenter for Animal Health Research, CISA-INIA-CSIC, Valdeolmos, Madrid, Spain.
Marta L DeDiegoDepartment of Molecular and Cell Biology. Centro Nacional de Biotecnología (CNB-CSIC), Madrid, Spain.
Centro Nacional de Biotecnología · ESCentre de Recerca en Sanitat Animal · ESTexas Biomedical Research Institute · USUniversity of Rochester Medical Center · US

Funding

Dynamics of the protective vaccine-induced human influenza neuraminidase B cell responseR01AI145332 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KOBIE, JAMES J, MARTINEZ-SOBRIDO, LUIS · 2019 to 2022
$3.0M
The origin and future protective activity of SARS-CoV-2 RBD specific neutralizing antibodiesR01AI161175 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KOBIE, JAMES J, MARTINEZ-SOBRIDO, LUIS · 2021 to 2024
$2.5M
NIAID NIH HHS R01 AI145332NIAID NIH HHS R01 AI161175
6 · The paper itself

Abstract

Interferons (IFNs), IFN-stimulated genes (ISGs), and inflammatory cytokines mediate innate immune responses, and are essential to establish an antiviral response. Within the innate immune responses, retinoic acid-inducible gene I (RIG-I) is a key sensor of virus infections, mediating the transcriptional induction of IFNs and inflammatory proteins. Nevertheless, since excessive responses could be detrimental to the host, these responses need to be tightly regulated. In this work, we describe, for the first time, how knocking-down or knocking-out the expression of IFN alpha-inducible protein 6 (IFI6) increases IFN, ISG, and pro-inflammatory cytokine expression after the infections with Influenza A Virus (IAV), Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), and Sendai Virus (SeV), or poly(I:C) transfection. We also show how overexpression of IFI6 produces the opposite effect,

Indexed as

Immunity, InnateMitochondrial ProteinsReceptors, ImmunologicVirus DiseasesCytokinesDEAD Box Protein 58HumansInfluenza, HumanSARS-CoV-2CytokinesDEAD Box Protein 58IFI6 protein, humanMitochondrial ProteinsReceptors, ImmunologicRIGI protein, humancoronavirusIFI6inflammationinfluenza virusinnate immunityinterferonRIG-IRNA binding

Identifiers

PMID36793726
PMCPMC9923010
OpenAlexW4318464708

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.