Evidence map›Paper›PMID 19339353›Full record

ArticleJournal of virology2009

JNK and p38 mitogen-activated protein kinase pathways contribute to porcine circovirus type 2 infection.

Li Wei, Zhongwu Zhu, Jing Wang, Jue Liu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Tumor necrosis factor-α impairs cerebral blood flow in pregnant rats: role of vascular β-epithelial NaAmerican journal of physiology. Heart and circulatory physiology · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

4 authors at 2 institutions in 1 country.

Li WeiInstitute of Animal Husbandry and Veterinary Medicine, Beijing Municipal, Academy of Agriculture and Forestry Sciences, Haidian District, Beijing, People's Republic of China.
Zhongwu Zhu
Jing Wang
Jue Liu
Beijing Academy of Agricultural and Forestry Sciences · CNHunan Entry-Exit Inspection and Quarantine Bureau · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with a wide variety of viruses often perturbs host cell signaling pathways including the Jun NH(2)-terminal kinase/stress-activated kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38/MAPK), which are important components of cellular signal transduction pathways. The present study demonstrated for the first time that porcine circovirus type 2 (PCV2), which is the primary causative agent of an emerging swine disease, postweaning multisystemic wasting syndrome, can activate JNK1/2 and p38 MAPK pathways in PCV2-infected PK15 cells. However, PCV2 at an early stage of infection, as well as UV-irradiated PCV2, failed to activate these two MAPK families, which demonstrated that PCV2 replication was necessary for their activation. We further found that PCV2 activated the phosphorylation of JNK1/2 and p38 MAPK downstream targets c-Jun and ATF-2 with virus replication in the cultured cells. The roles of these kinases in PCV2 infection were further evaluated using specific inhibitors: the JNK inhibitor 1 for JNK1/2 and SB202190 for p38. Inhibition of JNK1/2 and p38 kinases by these specific inhibitors did result in significant reduction of PCV2 viral mRNA transcription and protein synthesis, viral progeny release, and blockage of PCV2-induced apoptotic caspase-3 activation in the infected cells. Taken together, these data suggest that JNK/SAPK and p38 MAPK pathways play important roles in the PCV2 replication and contribute to virus-mediated changes in host cells.

Indexed as

Activating Transcription Factor 2AnimalsCell LineCircovirusJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationPorcine Postweaning Multisystemic Wasting SyndromeProto-Oncogene Proteins c-junSignal TransductionSwineVirus ReplicationActivating Transcription Factor 2JNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-jun

Identifiers

PMID19339353
PMCPMC2687389
OpenAlexW1963982344

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.