Evidence map›Paper›PMID 34257104›Full record

ArticleScience signaling2021

ETV7 limits antiviral gene expression and control of influenza viruses.

Heather M Froggatt, Alfred T Harding, Ryan R Chaparian, Nicholas S Heaton

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  14. CELLULAR RNA INTERACTS WITH MAVS TO PROMOTE ANTIVIRAL SIGNALING.bioRxiv : the preprint server for biology · 2023
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  20. Journal of virology · 2022
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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

4 authors at 1 institution in 1 country.

Heather M FroggattDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.ORCID 0000-0001-7785-0976
Alfred T HardingDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.ORCID 0000-0002-1446-2359
Ryan R ChaparianDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Nicholas S HeatonDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA. nicholas.heaton@duke.edu.ORCID 0000-0002-5307-3428
Duke University · US

Funding

Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
The pathogenic effects of epithelial cells surviving direct influenza virus infectionR01AI137031 · NIAID · DUKE UNIVERSITY · PI Nicholas S Heaton · 2019 to 2026
$4.5M
Loss of cellular identity after influenza virus infection and effects on pulmonary functionR01HL142985 · NHLBI · DUKE UNIVERSITY · PI HEATON, NICHOLAS S · 2018 to 2022
$2.8M
NCI NIH HHS T32 CA009111NHLBI NIH HHS R01 HL142985NIAID NIH HHS R01 AI137031
6 · The paper itself

Abstract

The type I interferon (IFN) response is an important component of the innate immune response to viral infection. Precise control of IFN responses is critical because insufficient expression of IFN-stimulated genes (ISGs) can lead to a failure to restrict viral spread, whereas excessive ISG activation can result in IFN-related pathologies. Although both positive and negative regulatory factors control the magnitude and duration of IFN signaling, it is also appreciated that several ISGs regulate aspects of the IFN response themselves. In this study, we performed a CRISPR activation screen to identify previously unknown regulators of the type I IFN response. We identified the strongly induced ISG encoding ETS variant transcription factor 7 (ETV7) as a negative regulator of the type I IFN response. However, ETV7 did not uniformly suppress ISG transcription. Instead, ETV7 preferentially targeted a subset of antiviral ISGs that were particularly important for IFN-mediated control of influenza viruses. Together, our data assign a function for ETV7 as an IFN response regulator and also identify ETV7 as a potential therapeutic target to increase innate antiviral responses and enhance IFN-based antiviral therapies.

Indexed as

Interferon Type IOrthomyxoviridaeAntiviral Restriction FactorsGene ExpressionImmunity, InnateProto-Oncogene Proteins c-etsAntiviral Restriction FactorsInterferon Type IProto-Oncogene Proteins c-ets

Identifiers

PMID34257104
PMCPMC8630980
OpenAlexW3180516240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.