Evidence map›Paper›PMID 42043255›Full record

ArticleViruses2026

TRIM13 Positively Regulates the NF-κB Signaling Pathway Induced by Encephalomyocarditis Virus.

Xiaolan Ji, Donglin Bi, Mingqi Liu, Xiangru Du, Zhiqi Wang, Haiqing Li, Jinluan Wang, Yiyang Fan, Hao Gao, Derong Zhang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Xiaolan JiKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Donglin BiKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Mingqi LiuKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Xiangru DuKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Zhiqi WangCollege of Life Science and Engineering, Northwest Minzu University, Lanzhou 730030, China.
Haiqing LiCollege of Life Science and Engineering, Northwest Minzu University, Lanzhou 730030, China.
Jinluan WangKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Yiyang FanCollege of Life Science and Engineering, Northwest Minzu University, Lanzhou 730030, China.
Hao GaoKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Derong ZhangKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.
Jialin BaiCollege of Life Science and Engineering, Northwest Minzu University, Lanzhou 730030, China.
Qiongyi LiKey Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China.

Funding

Fundamental Research Funds for the Central Universities in Northwest Minzu University 31920230154Natural Science Foundation of Gansu Province 23JRRA720
6 · The paper itself

Abstract

Encephalomyocarditis virus (EMCV) belongs to the genus Cardiovirus of the family Picornaviridae. It is a non-enveloped, positive-sense, single-stranded RNA virus and an important pathogen causing encephalomyocarditis (EMC). Tripartite motif 13 (TRIM13) is a member of the tripartite motif (TRIM) family and serves as an important effector molecule in antiviral innate immunity. However, its antiviral activity and underlying molecular mechanisms during EMCV infection remain unknown. In this study, we identified TRIM13 as a regulator of NF-κB activation. TRIM13, dependent on its E3 ubiquitin ligase activity, directly binds to IκBα and dose-dependently increases its phosphorylation level. To determine the chain type of IκBα polyubiquitination, antibodies specific for K48-linked and K63-linked ubiquitin were used. Our data indicated that IκBα was subjected to polyubiquitination independent of K48 and K63 linkages. This interaction promotes non-K48/K63-linked polyubiquitination of IκBα, thereby inducing NF-κB nuclear translocation. Subsequently, nuclear NF-κB activates the secretion of pro-inflammatory cytokines, exacerbating inflammatory responses and ultimately facilitating EMCV infection.

Indexed as

Cardiovirus InfectionsEncephalomyocarditis virusHost-Pathogen InteractionsNF-kappa BSignal TransductionTripartite Motif ProteinsAnimalsCell LineHumansImmunity, InnateNF-KappaB Inhibitor alphaPhosphorylationProtein BindingUbiquitinationUbiquitin-Protein LigasesNF-kappa BNF-KappaB Inhibitor alphaTripartite Motif ProteinsUbiquitin-Protein Ligasesencephalomyocarditis virusIκBαnuclear factor-κBtripartite motif 13

Identifiers

PMID42043255
PMCPMC13120059

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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.