Evidence map›Paper›PMID 34495699›Full record

ArticleJournal of virology2022

Innate Immune Evasion of Porcine Epidemic Diarrhea Virus through Degradation of the FBXW7 Protein via the Ubiquitin-Proteasome Pathway.

Mingwei Li, Yang Wu, Jianfei Chen, Hongyan Shi, Zhaoyanag Ji, Xin Zhang, Da Shi, Jianbo Liu, Jin Tian, Xiaobo Wang and 5 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  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

15 authors at 1 institution in 1 country.

Mingwei Li *State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Yang Wu *State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Jianfei ChenState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Hongyan ShiState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Zhaoyanag JiState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Xin ZhangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Da ShiState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Jianbo LiuState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Jin TianState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.ORCID 0000-0002-5202-7796
Xiaobo WangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Zhaorong ShiState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Hongling ZhangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Hao ZhangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Longjun GuoState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.
Li FengState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institutegrid.38587.31, Chinese Academy of Agricultural Sciences, Harbin, China.ORCID 0000-0003-4123-0892
Chinese Academy of Agricultural Sciences · CN

Funding

Central Public-interest Scientific Institution Basal Research Fund 1610302020001National Key Research and Development Program of China 2021YFD1801105National Natural Science Foundation of China (NSFC) 31872474Natural Science Foundation of Heilongjiang Province of China YQ2020C023
6 · The paper itself

Abstract

Porcine epidemic diarrhea virus (PEDV) causes a porcine disease associated with swine epidemic diarrhea. Different antagonistic strategies have been identified, and the mechanism by which PEDV infection impairs the production of interferon (IFN) and delays the activation of the IFN response to escape host innate immunity has been determined, but the pathogenic mechanisms of PEDV infection remain enigmatic. Our preliminary results revealed that endogenous F-box and WD repeat domain-containing 7 (FBXW7) protein, the substrate recognition component of the SCF-type E3 ubiquitin ligase, is downregulated in PEDV-infected Vero E6 cells, according to the results from an isobaric tags for relative and absolute quantification (iTRAQ) analysis. Overexpression of FBXW7 in target cells makes them more resistant to PEDV infection, whereas ablation of FBXW7 expression by small interfering RNA (siRNA) significantly promotes PEDV infection. In addition, FBXW7 was verified as an innate antiviral factor capable of enhancing the expression of RIG-I and TBK1, and it was found to induce interferon-stimulated genes (ISGs), which led to an elevated antiviral state of the host cells. Moreover, we revealed that PEDV nonstructural protein 2 (nsp2) interacts with FBXW7 and targets FBXW7 for degradation through the K48-linked ubiquitin-proteasome pathway. Consistent with the results proven

Indexed as

Immune EvasionImmunity, InnateAnimalsAntiviral AgentsChlorocebus aethiopsCoronavirus InfectionsF-Box-WD Repeat-Containing Protein 7Interferon Type IPorcine epidemic diarrhea virusProteasome Endopeptidase ComplexSignal TransductionSwineSwine DiseasesUbiquitinsVero CellsAntiviral AgentsF-Box-WD Repeat-Containing Protein 7Interferon Type IProteasome Endopeptidase ComplexUbiquitinscoronavirusF-box and WD repeat domain-containing 7 proteinPEDV

Identifiers

PMID34495699
PMCPMC8906424
OpenAlexW3198118333

What OpenQuestion holds

Textmetadata
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.