Evidence map›Paper›PMID 25734423›Full record

ArticlePloS one2015

Proteomic analysis of mitochondrial-associated ER membranes (MAM) during RNA virus infection reveals dynamic changes in protein and organelle trafficking.

Stacy M Horner, Courtney Wilkins, Samantha Badil, Jason Iskarpatyoti, Michael Gale

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  16. The Golgi Apparatus: A Key Player in Innate Immunity.International journal of molecular sciences · 2024
    Review
  17. MITOCHONDRIA-ASSOCIATED MEMBRANES ARE NOT ALTERED IN IMMUNE CELLS IN T2D.bioRxiv : the preprint server for biology · 2024
    Article
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Stacy M HornerDepartment of Immunology, University of Washington, Seattle, Washington, United States of America; Department of Medicine, Duke University Medical Center, Durham, North Carolina, United States of America.
Courtney WilkinsDepartment of Immunology, University of Washington, Seattle, Washington, United States of America.
Samantha BadilDepartment of Immunology, University of Washington, Seattle, Washington, United States of America.
Jason IskarpatyotiDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, United States of America.
Michael GaleDepartment of Immunology, University of Washington, Seattle, Washington, United States of America.
University of Washington · USDuke Medical Center · USDuke University Hospital · US

Funding

West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
Mechanisms Of Pathogen Recognition And Innate Immune Control Of Hepatitis C VirusU19AI088778 · NIAID · UNIVERSITY OF WASHINGTON · PI LAU, DARYL T · 2010 to 2014
$4.2M
The Host Response to Hepatitis C VirusR01AI060389 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI GALE, MICHAEL · 2003 to 2012
$3.4M
Innate immune regulation during hepatitis C virus infectionK22AI100935 · NIAID · DUKE UNIVERSITY · PI HORNER, STACY MICHELLE · 2014 to 2015
$269k
Inhibition of Hepatitis C Virus Infection by Interferon-induced Transmembrane ProF32AI088856 · NIAID · UNIVERSITY OF WASHINGTON · PI WILKINS, COURTNEY · 2012 to 2014
$169k
NIAID NIH HHS F32 AI088856NIAID NIH HHS F32AI088856NIAID NIH HHS K22 AI100935NIAID NIH HHS R01 AI060389NIAID NIH HHS R01AI060389NIAID NIH HHS U19 AI083019NIAID NIH HHS U19 AI088778NIAID NIH HHS U19AI88778
6 · The paper itself

Abstract

RIG-I pathway signaling of innate immunity against RNA virus infection is organized between the ER and mitochondria on a subdomain of the ER called the mitochondrial-associated ER membrane (MAM). The RIG-I adaptor protein MAVS transmits downstream signaling of antiviral immunity, with signaling complexes assembling on the MAM in association with mitochondria and peroxisomes. To identify components that regulate MAVS signalosome assembly on the MAM, we characterized the proteome of MAM, ER, and cytosol from cells infected with either chronic (hepatitis C) or acute (Sendai) RNA virus infections, as well as mock-infected cells. Comparative analysis of protein trafficking dynamics during both chronic and acute viral infection reveals differential protein profiles in the MAM during RIG-I pathway activation. We identified proteins and biochemical pathways recruited into and out of the MAM in both chronic and acute RNA viral infections, representing proteins that drive immunity and/or regulate viral replication. In addition, by using this comparative proteomics approach, we identified 3 new MAVS-interacting proteins, RAB1B, VTN, and LONP1, and defined LONP1 as a positive regulator of the RIG-I pathway. Our proteomic analysis also reveals a dynamic cross-talk between subcellular compartments during both acute and chronic RNA virus infection, and demonstrates the importance of the MAM as a central platform that coordinates innate immune signaling to initiate immunity against RNA virus infection.

Indexed as

Tandem Mass SpectrometryCell LineChromatography, High Pressure LiquidEndoplasmic ReticulumHepacivirusHumansMetabolic Networks and PathwaysMicrosomesMitochondriaPrincipal Component AnalysisProteomeSendai virusVirus ReplicationProteome

Identifiers

PMID25734423
PMCPMC4348417
OpenAlexW2050937759

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.