Evidence map›Paper›PMID 28414768›Full record

ArticlePLoS pathogens2017

GPATCH3 negatively regulates RLR-mediated innate antiviral responses by disrupting the assembly of VISA signalosome.

Ying Nie, Yong Ran, Hong-Yan Zhang, Zhe-Fu Huang, Zhao-Yi Pan, Su-Yun Wang, Yan-Yi Wang

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 29 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

7 authors at 1 institution in 1 country.

Ying NieWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.
Yong RanWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.
Hong-Yan ZhangWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.
Zhe-Fu HuangWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.
Zhao-Yi PanWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.ORCID http://orcid.org/0000-0002-2183-6654
Su-Yun WangWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.
Yan-Yi WangWuhan Institute of Virology, Key Laboratory of Special Pathogens and Biosafety, Chinese Academy of Sciences, Wuhan, Hubei, China.ORCID http://orcid.org/0000-0002-9316-2417
Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon viral infection, retinoic acid-inducible gene I-like receptors (RLRs) recognize viral RNA and trigger a series of signaling events, leading to the induction of type I interferons (IFNs). These processes are delicately regulated to prevent excessive and harmful immune responses. In this study, we identified G patch domain-containing protein 3 (GPATCH3) as a negative regulator of RLR-mediated antiviral signaling pathways. Overexpression of GPATCH3 impaired RNA virus- triggered induction of downstream antiviral genes, whereas its knockdown had opposite effects and attenuated viral replication. In addition, GPATCH3-deficient cells had higher IFNB1 mRNA level compared with control cells after RNA virus infection. Mechanistically, GPATCH3 was recruited to VISA in a viral infection dependent manner and the assembly of VISA/TRAF6/TBK1 signalosome was impaired in GPATCH3-overexpressing cells. In contrast, upon viral infection, the recruitment of TRAF6 and TBK1 to VISA was enhanced in GPATCH3 deficient cells. Taking together, our findings demonstrate that GPATCH3 interacts with VISA and disrupts the assembly of virus-induced VISA signalosome therefore acts as a negative regulator of RLR-mediated innate antiviral immune responses.

Indexed as

Adaptor Proteins, Signal TransducingCarrier ProteinsCell LineHumansInterferon-Induced Helicase, IFIH1Interferon Type IMitochondriaProtein BindingReceptors, Retinoic AcidSignal TransductionVirus DiseasesAdaptor Proteins, Signal TransducingCarrier ProteinsGPATCH3 protein, humanIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon Type IMAVS protein, humanPLAAT4 protein, humanReceptors, Retinoic Acid

Identifiers

PMID28414768
PMCPMC5407853
OpenAlexW2606637443

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.