Evidence map›Paper›PMID 31849979›Full record

ArticleFrontiers in immunology2019

Zebrafish TRIM25 Promotes Innate Immune Response to RGNNV Infection by Targeting 2CARD and RD Regions of RIG-I for K63-Linked Ubiquitination.

Yilin Jin, Kuntong Jia, Wanwan Zhang, Yangxi Xiang, Peng Jia, Wei Liu, Meisheng Yi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Pathogenic Characterization and Host Immune Response toAnimals : an open access journal from MDPI · 2026
    Article
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  5. Article
  6. Slc43a2Science China. Life sciences · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The lncRNAs involved in regulating the RIG-I signaling pathway.Frontiers in cellular and infection microbiology · 2022
    Review
  12. Article
  13. Advances in aquatic animal RIG-I-like receptors.Fish and shellfish immunology reports · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. 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

7 authors at 4 institutions in 1 country.

Yilin JinSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Kuntong JiaSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Wanwan ZhangSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Yangxi XiangSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Peng JiaSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Wei LiuSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Meisheng YiSchool of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNKey Laboratory of Guangdong Province · CNSouthern Marine Science and Engineering Guangdong Laboratory (Guangzhou) · CNSouthern Marine Science and Engineering Guangdong Laboratory (Zhuhai)

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RIG-I-like receptors (RLRs) play important roles in response to virus infection by regulating host innate immune signaling pathways. Meanwhile, the RLR signaling pathway is also tightly regulated by host and virus to achieve the immune homeostasis between antiviral responses and virus survival. Here, we found that zebrafish TRIM25 (zbTRIM25) functioned as a positive regulator of RLR signaling pathway during red spotted grouper nervous necrosis virus (RGNNV) infection. Post-RGNNV infection, zbTRIM25 expression was obviously inhibited and ectopic expression of zbTRIM25 led to enhanced expression of RLR signaling pathway-related genes. Overexpression and knockdown analysis revealed that zbTRIM25 promoted zebrafish RIG-I (zbRIG-I)-mediated IFN signaling and inhibited RGNNV replication. Mechanistically, zbTRIM25 bound to zbRIG-I; in particular, the SPRY domain of zbTRIM25 interacted with the tandem caspase activation and recruitment domains (2CARD) and repressor domain (RD) regions of zbRIG-I. zbTRIM25 promoted the K63 polyubiquitination of 2CARD and RD regions of zbRIG-I. Furthermore, zbTRIM25-mediated zbRIG-I activation of IFN production was enhanced by K63-linked ubiquitin, indicating that zbTRIM25-mediated zbRIG-I polyubiquitination was essential for RIG-I-triggered IFN induction. In conclusion, these findings reveal a novel mechanism that zbTRIM25 positively regulates the innate immune response by targeting and promoting the K63-linked polyubiquitination of zbRIG-I.

Indexed as

NodaviridaeAnimalsCell LineFish DiseasesHumansImmunity, InnateRNA, Small InterferingRNA Virus InfectionsTripartite Motif ProteinsUbiquitinationZebrafishZebrafish Proteinsddx58 protein, zebrafishRNA, Small InterferingTripartite Motif ProteinsZebrafish Proteinsred spotted grouper nervous necrosis virusRIG-ITRIM25ubiquitinationzebrafish

Identifiers

PMID31849979
PMCPMC6901795
OpenAlexW2991052053

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LicenceCC BY
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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.