Evidence map›Paper›PMID 16254323›Full record

ArticleJournal of virology2005

Stress-activated protein kinases are involved in coxsackievirus B3 viral progeny release.

Xiaoning Si, Honglin Luo, Andrew Morgan, Jingchun Zhang, Jerry Wong, Ji Yuan, Mitra Esfandiarei, Guang Gao, Caroline Cheung, Bruce M McManus

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.0field-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

45 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  19. Review
  20. Cleavage of Grb2-Associated Binding Protein 2 by Viral Proteinase 2A duringFrontiers in cellular and infection microbiology · 2017
    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

10 authors at 2 institutions in 1 country.

Xiaoning SiDepartment of Pathology and Laboratory Medicine, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia, Canada. hluo@mrl.ubc.ca
Honglin Luo
Andrew Morgan
Jingchun Zhang
Jerry Wong
Ji Yuan
Mitra Esfandiarei
Guang Gao
Caroline Cheung
Bruce M McManus
St. Paul's Hospital · CAUniversity of British Columbia · CA

Funding

CIHR 63854-1CIHR 64358-1
6 · The paper itself

Abstract

Stress-activated protein kinases (SAPKs), consisting of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), are activated upon various environmental stimuli, including viral infections. Cellular survival and death signaling events following coxsackievirus B3 (CVB3) infection have been studied in relationship to viral replication, but the role of SAPKs has not been scrutinized. In this study, we found that the phosphorylation of JNK1/2 and p38 MAPK was increased during active replication of CVB3 and that their phosphorylation was independent of CVB3-induced caspase activation or production of reactive oxygen species. The roles of these kinases in CVB3 infection were further evaluated using specific inhibitors: SP600125 for JNK1/2 and SB203580 for p38 MAPK. JNK1/2 inhibitors reduced CVB3-induced phosphorylation of activating transcription factor 2, and the p38 MAPK inhibitor reduced CVB3-induced phosphorylation of heat shock protein 27. Although inhibition of these kinases by specific inhibitors did not affect CVB3 viral protein synthesis, inhibition of p38 MAPK but not of JNK1/2 resulted in significant reduction of viral progeny release, suppression of CVB3-induced cell death, and blockage of CVB3-induced caspase-3 activation in infected cells. We conclude that SAPK pathways play critical roles in the life cycle of CVB3, particularly in viral progeny release.

Indexed as

Cell SurvivalEnterovirus B, HumanEnzyme ActivationHeLa CellsHumansKineticsMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9p38 Mitogen-Activated Protein KinasesPhosphorylationSignal TransductionViral ProteinsVirus ReplicationMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9p38 Mitogen-Activated Protein KinasesViral Proteins

Identifiers

PMID16254323
PMCPMC1280244
OpenAlexW2167621312

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.