Evidence map›Paper›PMID 29948782›Full record

ArticleVirus genes2018

Sec13 is a positive regulator of VISA-mediated antiviral signaling.

Tian Chen, Dandan Wang, Tao Xie, Liang-Guo Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Virus genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
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  8. BovineFrontiers in immunology · 2021
    Article
  9. Review
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.

Tian ChenKey Laboratory of Functional Small Organic Molecule, Ministry of Education and College of Life Science, Jiangxi Normal University, 99 Ziyang Road, Nanchang, 330022, Jiangxi, China.
Dandan WangKey Laboratory of Functional Small Organic Molecule, Ministry of Education and College of Life Science, Jiangxi Normal University, 99 Ziyang Road, Nanchang, 330022, Jiangxi, China.
Tao XieKey Laboratory of Functional Small Organic Molecule, Ministry of Education and College of Life Science, Jiangxi Normal University, 99 Ziyang Road, Nanchang, 330022, Jiangxi, China.
Liang-Guo XuKey Laboratory of Functional Small Organic Molecule, Ministry of Education and College of Life Science, Jiangxi Normal University, 99 Ziyang Road, Nanchang, 330022, Jiangxi, China. xul@jxnu.edu.cn.ORCID http://orcid.org/0000-0003-1991-2889
Jiangxi Normal University · CN

Funding

Postdoctoral Start Fund of Jiangxi Normal University 2014AThe National Natural Science Foundation of Chi 31370876The National Natural Science Foundation of China 31570876The Natural Science Foundation of Jiangxi Province 20143ACB20004The Open Project Program of Key Laboratory of Functional Small Organic Molecule, Ministry of Education, and Jiangxi Normal University KLFS-KF-201407
6 · The paper itself

Abstract

Viral infection triggers the innate antiviral immune response that rapidly produces type I interferons in most cell types to combat viruses invading. Upon viral infection, the cytoplasmic RNA sensors RIG-I/MDA5 recognize viral RNA, and then RIG-I/MDA5 is transported to mitochondria interacting with VISA through the CARD domain. From there, VISA recruits downstream antiviral signaling pathways molecules, such as TRAFs and TBK1. Eventually, IRF3 is phosphorylated and type I IFNs are induced to fight as the first line of defense against viruses. However, it remains unclear how VISA acts as a scaffold to assemble the signalosome in RIG-I-mediated antiviral signaling. Here, we demonstrated Sec13 as a novel component that was involved in VISA-mediated antiviral signaling pathway. The co-immunoprecipitation assays showed that Sec13 specifically interacts with VISA. Overexpression of Sec13 increases VISA's aggregation and ubiquitination and significantly enhances the phosphorylation and dimerization of IRF3, facilitating the IFN-β production. Conversely, the knockdown of Sec13 attenuates Sendai virus-induced and VISA-mediated IRF3 activation and the production of IFNβ, thus weakens antiviral immune activity.

Indexed as

Disease ResistanceHost-Pathogen InteractionsSignal TransductionAdaptor Proteins, Signal TransducingCarrier ProteinsCell LineGene ExpressionGene Knockdown TechniquesHumansImmunity, InnateInterferon-betaProtein AggregatesProtein BindingReceptors, Pattern RecognitionRespirovirus InfectionsSendai virusAdaptor Proteins, Signal TransducingCarrier ProteinsInterferon-betaMAVS protein, humanProtein AggregatesReceptors, Pattern RecognitionSEC13 protein, humanInterferonIRF3RLR antiviral signalingSec13VISA/MAVS

Identifiers

PMID29948782
OpenAlexW2808117546

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.