Evidence map›Paper›PMID 23077300›Full record

ArticleJournal of virology2013

TRIM protein-mediated regulation of inflammatory and innate immune signaling and its association with antiretroviral activity.

Pradeep D Uchil, Angelika Hinz, Steven Siegel, Anna Coenen-Stass, Thomas Pertel, Jeremy Luban, Walther Mothes

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 1 pooled it
6.8field-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

133 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. Identification ofFrontiers in immunology · 2018
    Trial
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  18. Microglial P2YNeuron · 2024
    Article
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73 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Pradeep D UchilDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut, USA.
Angelika Hinz
Steven Siegel
Anna Coenen-Stass
Thomas Pertel
Jeremy Luban
Walther Mothes
Yale University · USUniversity of Geneva · CH

Funding

Retrovirus cell-to-cell transmissionR01CA098727 · NCI · YALE UNIVERSITY · PI MOTHES, WALTHER H · 2003 to 2017
$4.5M
Human Genes that Influence HIV-1 Replication, Pathogenesis, and Immunity in IVDUsDP1DA034990 · NIDA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUBAN, JEREMY · 2012 to 2016
$4.1M
A novel TRIM protein involved in innate immunityR21AI087467 · NIAID · YALE UNIVERSITY · PI MOTHES, WALTHER H · 2010 to 2011
$453k
NCI NIH HHS R01 CA098727NCI NIH HHS R01-CA098727NIAID NIH HHS R21 AI087467NIAID NIH HHS R21-AI087467NIDA NIH HHS DP1 DA034990
6 · The paper itself

Abstract

Members of the tripartite interaction motif (TRIM) family of E3 ligases are emerging as critical regulators of innate immunity. To identify new regulators, we carried out a screen of 43 human TRIM proteins for the ability to activate NF-κB, AP-1, and interferon, hallmarks of many innate immune signaling pathways. We identified 16 TRIM proteins that induced NF-κB and/or AP-1. We found that one of these, TRIM62, functions in the TRIF branch of the TLR4 signaling pathway. Knockdown of TRIM62 in primary macrophages led to a defect in TRIF-mediated late NF-κB, AP-1, and interferon production after lipopolysaccharide challenge. We also discovered a role for TRIM15 in the RIG-I-mediated interferon pathway upstream of MAVS. Knockdown of TRIM15 limited virus/RIG-I ligand-induced interferon production and enhanced vesicular stomatitis virus replication. In addition, most TRIM proteins previously identified to inhibit murine leukemia virus (MLV) demonstrated an ability to induce NF-κB/AP-1. Interfering with the NF-κB and AP-1 signaling induced by the antiretroviral TRIM1 and TRIM62 proteins rescued MLV release. In contrast, human immunodeficiency virus type 1 (HIV-1) gene expression was increased by TRIM proteins that induce NF-κB. HIV-1 resistance to inflammatory TRIM proteins mapped to the NF-κB sites in the HIV-1 long terminal repeat (LTR) U3 and could be transferred to MLV. Thus, our work identifies new TRIM proteins involved in innate immune signaling and reinforces the striking ability of HIV-1 to exploit innate immune signaling for the purpose of viral replication.

Indexed as

Immunity, InnateSignal TransductionAdaptor Proteins, Signal TransducingGene Knockdown TechniquesHIV-1HumansInterferonsLeukemia Virus, MurineMembrane ProteinsNF-kappa BTranscription Factor AP-1VesiculovirusAdaptor Proteins, Signal TransducingInterferonsMembrane ProteinsNF-kappa BTranscription Factor AP-1TRAT1 protein, human

Identifiers

PMID23077300
PMCPMC3536418
OpenAlexW2126018392

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.