Evidence map›Paper›PMID 34161773›Full record

ArticleCell reports2021

Riok3 inhibits the antiviral immune response by facilitating TRIM40-mediated RIG-I and MDA5 degradation.

Yong Shen, Kejun Tang, Dongdong Chen, Mengying Hong, Fangfang Sun, SaiSai Wang, Yuehai Ke, Tingting Wu, Ren Sun, Jing Qian and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. TRIM40 Drives Pathological Cardiac Hypertrophy and Heart Failure via Ubiquitination of PKN2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. USP8-Governed MDA5 Homeostasis Promotes Innate Immunity and Autoimmunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Viruses · 2023
    Article
  20. 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

11 authors at 3 institutions in 2 countries.

Yong ShenCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China; Department of Breast Surgery, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, P.R. China.
Kejun TangCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China; Department of Surgery, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China.
Dongdong ChenCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China.
Mengying HongCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China.
Fangfang SunCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China.
SaiSai WangDepartment of Colorectal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China.
Yuehai KeDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, Hangzhou, China.
Tingting WuDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Ren SunCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; School of Biomedical Sciences, LKS Faculty of Medicine, The Hongkong University, Hongkong, China. Electronic address: rensun@hku.hk.
Jing QianPharmaceutical Informatics Institute, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, P.R. China. Electronic address: jingqian@zju.edu.cn.
Yushen DuCancer Institute, ZJU-UCLA Joint Center for Medical Education and Research, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P.R. China; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Electronic address: lilyduyushen@zju.edu.cn.
Second Affiliated Hospital of Zhejiang University · CNUniversity of California, Los Angeles · USZhejiang University · CN

Funding

ORF36 Viral Kinase as a Transcriptional Regulator of KSHVP01DE019085 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SUN, REN · 2008 to 2012
$6.4M
Reactivation of Kaposi's Sarcoma-Associated HerpesvirusR01CA091791 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SUN, REN · 2001 to 2017
$4.4M
NCI NIH HHS R01 CA091791NIDCR NIH HHS P01 DE019085
6 · The paper itself

Abstract

The type I interferon (IFN) pathway is a key component of innate immune response upon invasion of foreign pathogens. It is also under precise control to prevent excessive upregulation and undesired inflammation cascade. In the present study, we report that Riok3, an atypical kinase, negatively regulates retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) sensing-induced type I IFN signaling. Riok3 deficiency selectively inhibits RNA viral replication in vitro, resulting from an upregulated type I IFN pathway. Mice with myeloid-specific Riok3 knockout also show a more robust induction of type I IFN upon RNA virus infection and are more resistant to RNA virus-induced pathogenesis. Mechanistically, Riok3 recruits and interacts with the E3 ubiquitin ligase TRIM40, leading to the degradation of RIG-I and melanoma differentiation-associated gene-5 (MDA5) via K48- and K27-linked ubiquitination. Collectively, our data reveal the mechanism that Riok3 employs to be a negative regulator of antiviral innate immunity.

Indexed as

DEAD Box Protein 58ImmunityInterferon-Induced Helicase, IFIH1Protein Serine-Threonine KinasesProteolysisUbiquitin-Protein LigasesAnimalsCells, CulturedCytokinesFemaleFibroblastsMacrophages, PeritonealMaleMiceMice, Inbred C57BLProtein BindingCytokinesDEAD Box Protein 58Ifih1 protein, mouseInterferon-Induced Helicase, IFIH1Protein Serine-Threonine KinasesRiok3 protein, mouseTrim40 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID34161773
PMCPMC8363743
OpenAlexW3174374769

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.