Evidence map›Paper›PMID 27227879›Full record

ArticlePloS one2016

Suppression of USP18 Potentiates the Anti-HBV Activity of Interferon Alpha in HepG2.2.15 Cells via JAK/STAT Signaling.

Lin Li, Qing-Song Lei, Shu-Jun Zhang, Ling-Na Kong, Bo Qin

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Role of STAT1 in the resistance of HBV to IFN-α.Experimental and therapeutic medicine · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Lin LiDepartment of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, P.R. China.
Qing-Song LeiDepartment of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, P.R. China.
Shu-Jun ZhangDepartment of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, P.R. China.
Ling-Na KongDepartment of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, P.R. China.
Bo QinDepartment of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, P.R. China.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-specific protease 18 (USP18, also known as UBP43) has both interferon stimulated gene 15 (ISG15) dependent and ISG15-independent functions. By silencing the expression of USP18 in HepG2.2.15 cells, we studied the effect of USP18 on the anti-HBV activity of IFN-F and demonstrated that knockdown of USP18 significantly Inhibited the HBV expression and increased the expression of ISGs. Levels of hepatitis B virus surface antigen (HBsAg), hepatitis B virus e antigen (HBeAg), HBV DNA and intracellular hepatitis B virus core antigen (HBcAg) were dramatically decreased with or without treatment of indicated dose of IFN-F. Suppression of USP18 activated the JAK/STAT signaling pathway as shown by the increased and prolonged expression of phosphorylated signal transducer and activator of transcription 1 (p-STAT1) in combination with enhanced expression of several interferon stimulated genes (ISGs). Our results indicated that USP18 modulates the anti-HBV activity of IFN-F via activation of the JAK/STAT signaling pathway in Hepg2.2.15 cells.

Indexed as

DNA, ViralEndopeptidasesGene Expression RegulationGene Expression Regulation, ViralHepatitis BHepatitis B e AntigensHepatitis B Surface AntigensHepatitis B virusHep G2 CellsHumansInterferon-alphaJanus KinasesSignal TransductionSTAT1 Transcription FactorUbiquitin ThiolesteraseDNA, ViralEndopeptidasesHepatitis B e AntigensHepatitis B Surface AntigensInterferon-alphaJanus KinasesSTAT1 protein, humanSTAT1 Transcription FactorUbiquitin ThiolesteraseUSP18 protein, human

Identifiers

PMID27227879
PMCPMC4882066
OpenAlexW2398936569

What OpenQuestion holds

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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.