Evidence map›Paper›PMID 32126128›Full record

ArticlePLoS pathogens2020

RNF90 negatively regulates cellular antiviral responses by targeting MITA for degradation.

Bo Yang, Yue Liu, Yuhan Cui, Di Song, Ge Zhang, Shujun Ma, Yanzi Liu, Mengmeng Chen, Fan Chen, Hui Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. The STING signaling pathways and bacterial infection.Apoptosis : an international journal on programmed cell death · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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 1 institution in 1 country.

Bo YangHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Yue LiuHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Yuhan CuiHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Di SongHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Ge ZhangHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Shujun MaHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Yanzi LiuDepartment of Laboratory Medicine, the Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan Province, China.
Mengmeng ChenHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Fan ChenHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.
Hui WangHenan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan Province, China.
Jie WangHenan Key Laboratory of immunology and targeted drug, Xinxiang Medical University, Xinxiang, Henan Province, China.ORCID 0000-0003-4495-8862
Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is essential to DNA virus- or cytosolic DNA-triggered innate immune responses. In this study, we demonstrated the negative regulatory role of RING-finger protein (RNF) 90 in innate immune responses targeting MITA. RNF90 promoted K48-linked ubiquitination of MITA and its proteasome-dependent degradation. Overexpression of RNF90 inhibited HSV-1- or cytosolic DNA-induced immune responses whereas RNF90 knockdown had the opposite effects. Moreover, RNF90-deficient bone marrow-derived dendritic cells (BMDCs), bone marrow-derived macrophages (BMMs) and mouse embryonic fibroblasts (MEFs) exhibited increased DNA virus- or cytosolic DNA-triggered signaling and RNF90 deficiency protected mice from DNA virus infection. Taken together, our findings suggested a novel function of RNF90 in innate immunity.

Indexed as

Immunity, InnateProteolysisAnimalsBone Marrow CellsDendritic CellsFibroblastsHerpesvirus 1, HumanMacrophagesMembrane ProteinsMiceMice, KnockoutSTING ProteinTripartite Motif ProteinsUbiquitinationUbiquitin-Protein LigasesMembrane ProteinsSting1 protein, mouseSTING ProteinTrim7 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID32126128
PMCPMC7069649
OpenAlexW3010305806

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.