Evidence map›Paper›PMID 34512666›Full record

ArticleFrontiers in immunology2021

Negative Regulation of RNF90 on RNA Virus-Triggered Antiviral Immune Responses Targeting MAVS.

Bo Yang, Ge Zhang, Xiao Qin, Yulu Huang, Xiaowen Ren, Jingliang Sun, Shujun Ma, Yanzi Liu, Di Song, Yue Liu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  16. Interplay between TRIM7 and antiviral immunity.Frontiers in cellular and infection microbiology · 2023
    Review
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  18. Article
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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

13 authors at 2 institutions in 1 country.

Bo YangHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Ge ZhangHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Xiao QinHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Yulu HuangHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Xiaowen RenHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Jingliang SunHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Shujun MaHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Yanzi LiuDepartment of Laboratory Medicine, the Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Di SongHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Yue LiuHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Yuhan CuiHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Hui WangHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Jie WangHenan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Xinxiang Medical University · CNFu Wai Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antiviral innate immunity is the first line of host defense against viral infection. Mitochondrial antiviral signaling protein (MAVS, also named Cardif/IPS-1/VISA) is a critical protein in RNA virus-induced antiviral signaling pathways. Our previous research suggested that E3 ubiquitin-protein ligases RING-finger protein (RNF90) negatively regulate cellular antiviral responses by targeting STING for degradation, though its role in RNA virus infection remains unknown. This study demonstrated that RNF90 negatively regulated RNA virus-triggered antiviral innate immune responses in RNF90-silenced PMA-THP1 cells, RNF90-deficient cells (including HaCaTs, MEFs, and BMDMs), and RNF90-deficient mice. However, RNF90 regulated RNA virus-triggered antiviral innate immune responses independent of STING. RNF90 promoted K48-linked ubiquitination of MAVS and its proteasome-dependent degradation, leading to the inhibition of innate immune responses. Altogether, our findings suggested a novel function and mechanism of RNF90 in antiviral innate immunity.

Indexed as

Immunity, InnateAdaptor Proteins, Signal TransducingAnimalsChlorocebus aethiopsCytokinesHaCaT CellsHEK293 CellsHost-Pathogen InteractionsHumansMiceMice, KnockoutProteasome Endopeptidase ComplexProteolysisSignal TransductionTHP-1 CellsTripartite Motif ProteinsAdaptor Proteins, Signal TransducingCytokinesMAVS protein, humanMAVS protein, mouseProteasome Endopeptidase ComplexTRIM7 protein, humanTrim7 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligasesantiviral innate immune responsesdegradationMAVSRNF90signaling pathwayubiquitination

Identifiers

PMID34512666
PMCPMC8429505
OpenAlexW3197868426

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.