Evidence map›Paper›PMID 33640899›Full record

ArticleSignal transduction and targeted therapy2021

TRIM41 is required to innate antiviral response by polyubiquitinating BCL10 and recruiting NEMO.

Zhou Yu, Xuelian Li, Mingjin Yang, Jiaying Huang, Qian Fang, Jianjun Jia, Zheng Li, Yan Gu, Taoyong Chen, Xuetao Cao

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  14. Emerging Roles of Non-proteolytic Ubiquitination in Tumorigenesis.Frontiers in cell and developmental biology · 2022
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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

10 authors at 3 institutions in 1 country.

Zhou Yu *Center for Systems Medicine, Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100005, China.
Xuelian Li *National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Mingjin Yang *National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Jiaying HuangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Qian FangNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Jianjun JiaNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Zheng LiNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Yan GuNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Taoyong ChenNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China. chenty@immunol.org.
Xuetao CaoCenter for Systems Medicine, Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100005, China. caoxt@immunol.org.
Second Military Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sensing of pathogenic nucleic acids by pattern recognition receptors (PRR) not only initiates anti-microbe defense but causes inflammatory and autoimmune diseases. E3 ubiquitin ligase(s) critical in innate response need to be further identified. Here we report that the tripartite motif-containing E3 ubiquitin ligase TRIM41 is required to innate antiviral response through facilitating pathogenic nucleic acids-triggered signaling pathway. TRIM41 deficiency impairs the production of inflammatory cytokines and type I interferons in macrophages after transfection with nucleic acid-mimics and infection with both DNA and RNA viruses. In vivo, TRIM41 deficiency leads to impaired innate response against viruses. Mechanistically, TRIM41 directly interacts with BCL10 (B cell lymphoma 10), a core component of CARD proteins-BCL10 - MALT1 (CBM) complex, and modifies the Lys63-linked polyubiquitylation of BCL10, which, in turn, hubs NEMO for activation of NF-κB and TANK-binding kinase 1 (TBK1) - interferon regulatory factor 3 (IRF3) pathways. Our study suggests that TRIM41 is the potential universal E3 ubiquitin ligase responsible for Lys63 linkage of BCL10 during innate antiviral response, adding new insight into the molecular mechanism for the control of innate antiviral response.

Indexed as

B-Cell CLL-Lymphoma 10 ProteinDNA VirusesHost-Pathogen InteractionsHumansI-kappa B KinaseImmunity, InnateInterferon Regulatory Factor-3Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNucleic AcidsProtein Serine-Threonine KinasesReceptors, Pattern RecognitionRNA VirusesUbiquitin-Protein LigasesVirus DiseasesB-Cell CLL-Lymphoma 10 ProteinBCL10 protein, humanI-kappa B KinaseIKBKG protein, humanInterferon Regulatory Factor-3IRF3 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNucleic AcidsProtein Serine-Threonine KinasesReceptors, Pattern RecognitionTBK1 protein, humanTRIM41 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID33640899
PMCPMC7914255
OpenAlexW3133864950

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.