Evidence map›Paper›PMID 32571931›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Spatiotemporal dynamics of innate immune signaling via RIG-I-like receptors.

Katharina Esser-Nobis, Lauren D Hatfield, Michael Gale

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 74 citations in OpenAlex.

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  14. The Essential Role of Mitochondrial Dynamics in Viral Infections.International journal of molecular sciences · 2025
    Review
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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

3 authors at 1 institution in 1 country.

Katharina Esser-NobisCenter for Innate Immunity and Immune Disease, Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109.ORCID 0000-0002-9027-0391
Lauren D HatfieldCenter for Innate Immunity and Immune Disease, Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109.ORCID 0000-0003-0095-9863
Michael GaleCenter for Innate Immunity and Immune Disease, Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109 mgale@uw.edu.
University of Washington · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
Innate Immune Regulation of Zika Virus InfectionR01AI145296 · NIAID · UNIVERSITY OF WASHINGTON · PI COYNE, CAROLYN B, DIAMOND, MICHAEL S · 2019 to 2023
$4.1M
Mechanisms of hepatic innate immune activation by HCVR01AI127463 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL, ROSEN, HUGO RAMON · 2017 to 2021
$2.8M
The Host Response to Hepatitis C VirusR01AI118916 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2016 to 2020
$2.5M
NCI NIH HHS P30 CA015704NIAID NIH HHS R01 AI118916NIAID NIH HHS R01 AI127463NIAID NIH HHS R01 AI145296
6 · The paper itself

Abstract

RIG-I, MDA5, and LGP2 comprise the RIG-I-like receptors (RLRs). RIG-I and MDA5 are essential pathogen recognition receptors sensing viral infections while LGP2 has been described as both RLR cofactor and negative regulator. After sensing and binding to viral RNA, including double-stranded RNA (dsRNA), RIG-I and MDA5 undergo cytosol-to-membrane relocalization to bind and signal through the MAVS adaptor protein on intracellular membranes, thus directing downstream activation of IRF3 and innate immunity. Here, we report examination of the dynamic subcellular localization of all three RLRs within the intracellular response to dsRNA and RNA virus infection. Observations from high resolution biochemical fractionation and electron microscopy, coupled with analysis of protein interactions and IRF3 activation, show that, in resting cells, microsome but not mitochondrial fractions harbor the central components to initiate innate immune signaling. LGP2 interacts with MAVS in microsomes, blocking the RIG-I/MAVS interaction. Remarkably, in response to dsRNA treatment or RNA virus infection, LGP2 is rapidly released from MAVS and redistributed to mitochondria, temporally correlating with IRF3 activation. We reveal that IRF3 activation does not take place on mitochondria but instead occurs at endoplasmic reticulum (ER)-derived membranes. Our observations suggest ER-derived membranes as key RLR signaling platforms controlled through inhibitory actions of LGP2 binding to MAVS wherein LGP2 translocation to mitochondria releases MAVS inhibition to facilitate RLR-mediated signaling of innate immunity.

Indexed as

DEAD Box Protein 58HumansImmunity, InnateInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-3MitochondriaRNA, Double-StrandedRNA HelicasesRNA, ViralSignal TransductionVirus DiseasesDEAD Box Protein 58DHX58 protein, humanIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-3IRF3 protein, humanRNA, Double-StrandedRNA HelicasesRNA, Viralinnate immunityIRF3LGP2MAVSRIG-I

Identifiers

PMID32571931
PMCPMC7354926
OpenAlexW3037362093

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.