Evidence map›Paper›PMID 37978243›Full record

ArticleCellular & molecular immunology2023

CD97 negatively regulates the innate immune response against RNA viruses by promoting RNF125-mediated RIG-I degradation.

Huasong Chang, Peili Hou, Xuefeng Wang, Aibiao Xiang, Hao Wu, Wenjing Qi, Rukun Yang, Xue Wang, Xingyu Li, Wenqi He and 7 more

Open access · greenAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2023. 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
3.6field-weighted citation impact, top 7% 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, 22 citations in OpenAlex.

  1. Article
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  3. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
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  14. PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
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

17 authors at 4 institutions in 2 countries.

Huasong Chang *Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Peili Hou *Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Xuefeng Wang *Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, Jilin, 130122, China.
Aibiao XiangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Hao WuRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Wenjing QiRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Rukun YangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Xue WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Xingyu LiRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Wenqi HeKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, China.
Guimin ZhaoRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
Weiyang SunChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, Jilin, 130122, China.
Tiecheng WangChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, Jilin, 130122, China.ORCID http://orcid.org/0000-0002-5037-4911
Daniel Chang HeThe College of Arts and Sciences, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Hongmei WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China. hongmeiwang@sdnu.edu.cn.
Yuwei GaoChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, Jilin, 130122, China. yuwei0901@outlook.com.
Hongbin HeRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China. hongbinhe@sdnu.edu.cn.
Shandong Normal University · CNJilin Academy of Agricultural Sciences · CNJilin University · CNUniversity of North Carolina at Chapel Hill · US

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31972665National Natural Science Foundation of China (National Science Foundation of China) 32072834Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2021MC050Taishan Scholar Project of Shandong Province tspd20181207
6 · The paper itself

Abstract

The G protein-coupled receptor ADGRE5 (CD97) binds to various metabolites that play crucial regulatory roles in metabolism. However, its function in the antiviral innate immune response remains to be determined. In this study, we report that CD97 inhibits virus-induced type-I interferon (IFN-I) release and enhances RNA virus replication in cells and mice. CD97 was identified as a new negative regulator of the innate immune receptor RIG-I, and RIG-1 degradation led to the suppression of the IFN-I signaling pathway. Furthermore, overexpression of CD97 promoted the ubiquitination of RIG-I, resulting in its degradation, but did not impact its mRNA expression. Mechanistically, CD97 upregulates RNF125 expression to induce RNF125-mediated RIG-I degradation via K48-linked ubiquitination at Lys181 after RNA virus infection. Most importantly, CD97-deficient mice are more resistant than wild-type mice to RNA virus infection. We also found that sanguinarine-mediated inhibition of CD97 effectively blocks VSV and SARS-CoV-2 replication. These findings elucidate a previously unknown mechanism through which CD97 negatively regulates RIG-I in the antiviral innate immune response and provide a molecular basis for the development of new therapeutic strategies and the design of targeted antiviral agents.

Indexed as

RNA VirusesRNA Virus InfectionsAnimalsAntiviral AgentsDEAD Box Protein 58Immunity, InnateMiceReceptors, G-Protein-CoupledUbiquitinationUbiquitin-Protein LigasesAdgre5 protein, mouseAntiviral AgentsDdx58 protein, mouseDEAD Box Protein 58Receptors, G-Protein-CoupledRNF125 protein, mouseUbiquitin-Protein LigasesCD97IFN-IRIG-IRNA virusUbiquitination

Identifiers

PMID37978243
PMCPMC10687259
OpenAlexW4388764408

What OpenQuestion holds

Textmetadata
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Registered trials

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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.