Evidence map›Paper›PMID 34110282›Full record

ArticleeLife2021

Ubiquitination and degradation of NF90 by Tim-3 inhibits antiviral innate immunity.

Shuaijie Dou, Guoxian Li, Ge Li, Chunmei Hou, Yang Zheng, Lili Tang, Yang Gao, Rongliang Mo, Yuxiang Li, Renxi Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Roles of the E3 Ubiquitin Ligase TRIM47 in Inflammation, Organ Injury, and Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. 5-HTJournal of advanced research · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Tim-3Cell death & disease · 2022
    Article
  18. 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

13 authors at 3 institutions in 1 country.

Shuaijie Dou *Beijing Institute of Basic Medical Sciences, Beijing, China.
Guoxian Li *Beijing Institute of Basic Medical Sciences, Beijing, China.
Ge Li *Beijing Institute of Basic Medical Sciences, Beijing, China.
Chunmei HouBeijing Institute of Basic Medical Sciences, Beijing, China.
Yang ZhengDepartment of Oncology, First Hospital of Jilin University, Changchun, China.
Lili TangBeijing Institute of Basic Medical Sciences, Beijing, China.
Yang GaoBeijing Institute of Basic Medical Sciences, Beijing, China.
Rongliang MoBeijing Institute of Basic Medical Sciences, Beijing, China.
Yuxiang LiBeijing Institute of Basic Medical Sciences, Beijing, China.
Renxi WangBeijing Institute of Basic Medical Sciences, Beijing, China.
Beifen ShenBeijing Institute of Basic Medical Sciences, Beijing, China.
Jun ZhangInstitute of Immunology, Medical School of Henan University, Kaifeng, China.
Gencheng HanBeijing Institute of Basic Medical Sciences, Beijing, China.ORCID 0000-0003-1408-878X
Beijing Institute of Education · CNHenan University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor 90 (NF90) is a novel virus sensor that serves to initiate antiviral innate immunity by triggering stress granule (SG) formation. However, the regulation of the NF90-SG pathway remains largely unclear. We found that Tim-3, an immune checkpoint inhibitor, promotes the ubiquitination and degradation of NF90 and inhibits NF90-SG-mediated antiviral immunity. Vesicular stomatitis virus (VSV) infection induces the up-regulation and activation of Tim-3 in macrophages, which in turn recruit the E3 ubiquitin ligase TRIM47 to the zinc finger domain of NF90 and initiate a proteasome-dependent degradation via K48-linked ubiquitination at Lys297. Targeted inactivation of Tim-3 enhances the NF90 downstream SG formation by selectively increasing the phosphorylation of protein kinase R and eukaryotic translation initiation factor 2α, the expression of SG markers G3BP1 and TIA-1, and protecting mice from VSV challenge. These findings provide insights into the crosstalk between Tim-3 and other receptors in antiviral innate immunity and its related clinical significance.

Indexed as

Hepatitis A Virus Cellular Receptor 2Nuclear Factor 90 ProteinsAnimalsCytoplasmic GranulesImmunity, InnateMacrophagesMiceRhabdoviridae InfectionsUbiquitinationVesiculovirusVirus DiseasesHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2Nuclear Factor 90 Proteinsantiviral innate immunityimmunologyinflammationmouseNF90Tim-3ubiquitinationvirus sensor

Identifiers

PMID34110282
PMCPMC8225388
OpenAlexW3172133104

What OpenQuestion holds

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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.