Evidence map›Paper›PMID 36045682›Full record

ArticleFrontiers in immunology2022

Human metapneumovirus M2-2 protein inhibits RIG-I signaling by preventing TRIM25-mediated RIG-I ubiquitination.

Yukie Tanaka, Naoko Morita, Yoshinori Kitagawa, Bin Gotoh, Takayuki Komatsu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Yukie TanakaDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.
Naoko MoritaDepartment of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan.
Yoshinori KitagawaDivision of Microbiology and Infectious Diseases, Department of Pathology, Shiga University of Medical Science, Shiga, Japan.
Bin GotohDivision of Microbiology and Infectious Diseases, Department of Pathology, Shiga University of Medical Science, Shiga, Japan.
Takayuki KomatsuDepartment of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan.
Aichi Medical University · JPShiga University of Medical Science · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid-inducible gene I (RIG-I) is a receptor that senses viral RNA and interacts with mitochondrial antiviral signaling (MAVS) protein, leading to the production of type I interferons and inflammatory cytokines to establish an antiviral state. This signaling axis is initiated by the K63-linked RIG-I ubiquitination, mediated by E3 ubiquitin ligases such as TRIM25. However, many viruses, including several members of the family

Indexed as

Interferon Type IMetapneumovirusAntiviral AgentsDEAD Box Protein 58HEK293 CellsHumansImmunity, InnateInterferon-betaParamyxoviridaeParamyxoviridae InfectionsReceptors, ImmunologicTranscription FactorsTripartite Motif ProteinsUbiquitinationUbiquitin-Protein LigasesAntiviral AgentsDEAD Box Protein 58Interferon-betaInterferon Type IReceptors, ImmunologicTranscription FactorsTRIM25 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligaseshuman metapneumovirushuman respiratory syncytial virusinterferonM2-2 proteinmavsparamyxoviridaerig-itrim25

Identifiers

PMID36045682
PMCPMC9421128
OpenAlexW4291465398

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.