Evidence map›Paper›PMID 42358943›Full record

ArticleFrontiers in immunology2026

OLFML3 negatively regulates RIG-I signaling in RNA virus infection.

Qian Gu, Hong Mei, Qijun Yu, Peihong Yu, Junjie Zhang, Pengfei Hu, Jieming Qu, Jia Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 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
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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

8 authors.

Qian Gu *Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Hong Mei *Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Qijun YuDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Peihong YuShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Junjie ZhangShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Pengfei HuShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Jieming QuDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jia LiuShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Olfactomedin-like protein 3 (OLFML3) is a secreted glycoprotein that is primarily deemed to be associated with embryonic development, angiogenesis, and tumorigenesis. Recent studies have highlighted the function of OLFML3 as an important regulatory protein in viral and bacterial infections. This study explores the role of OLFML3 in type I interferon (IFN-I) signaling in RNA virus infection and related mechanism of action. Methods: RT-qPCR was used to determine the effects of OLFML3 on IFN-I production in the RNA virus infection. Results: OLFML3 can inhibit IFN-I production in RNA virus infection by suppressing RIG-I signaling. OLFML3 interacts with the PRY/SPRY domain of TRIM21, an E3 ubiquitinligase. OLFML3 can disrupt TRIM21-mediated RIG-I K63-ubiquitination, leading to the destabilization of RIG-I and suppressed IFN-I signaling. Conclusion: OLFML3 functions as a general immunosuppressor in RNA virus infection. These results may help developing OLFML3-targeted antiviral therapeutics for the re-activation of IFN-I signaling.

Indexed as

DEAD Box Protein 58RNA VirusesRNA Virus InfectionsSignal TransductionAnimalsHumansInterferon Type IMiceMice, KnockoutTRIM21 ProteinDdx58 protein, mouseDEAD Box Protein 58Interferon Type ITRIM21 Proteinantiviral immunityIFN-I signalingOLFML3RIG-ITRIM21

Identifiers

PMID42358943
PMCPMC13290906

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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.