Evidence map›Paper›PMID 11884562›Full record

ArticleJournal of virology2002

Coxsackievirus B3 replication is reduced by inhibition of the extracellular signal-regulated kinase (ERK) signaling pathway.

Honglin Luo, Bobby Yanagawa, Jingchun Zhang, Zongshu Luo, Mary Zhang, Mitra Esfandiarei, Christopher Carthy, Janet E Wilson, Decheng Yang, Bruce M McManus

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

93 citing papers in PubMed, 206 citations in OpenAlex.

  1. Article
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  5. Phosphorylation of enteroviral 2AJournal of medical virology · 2023
    Article
  6. Roles of inflammasomes in viral myocarditis.Frontiers in cellular and infection microbiology · 2023
    Review
  7. LncGBP9 knockdown alleviates myocardial inflammation and apoptosis in mice with acute viral myocarditis via suppressing NF-κB signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Advances in cell death mechanisms involved in viral myocarditis.Frontiers in cardiovascular medicine · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

33 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Honglin LuoDepartment of Pathology and Laboratory Medicine, McDonald Research Laboratories/The iCAPTURE Center, St. Paul's Hospital/Providence Health Care-University of British Columbia, Vancouver, British Columbia, Canada.
Bobby Yanagawa
Jingchun Zhang
Zongshu Luo
Mary Zhang
Mitra Esfandiarei
Christopher Carthy
Janet E Wilson
Decheng Yang
Bruce M McManus
St. Paul's Hospital · CAUniversity of British Columbia · CAProvidence Health Care · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coxsackievirus B3 (CVB3) is the most common human pathogen for viral myocarditis. We have previously shown that the signaling protein p21(ras) GTPase-activating protein (RasGAP) is cleaved and that mitogen-activated protein kinases (MAPKs) ERK1/2 are activated in the late phase of CVB3 infection. However, the role of intracellular signaling pathways in CVB3-mediated myocarditis and the relative advantages of such pathways to host or virus remain largely unclear. In this study we extended our prior studies by examining the interaction between CVB3 replication and intracellular signaling pathways in HeLa cells. We observed that CVB3 infection induced a biphasic activation of ERK1/2, early transient activation versus late sustained activation, which were regulated by different mechanisms. Infection by UV-irradiated, inactivated virus capable of receptor binding and endocytosis triggered early ERK1/2 activation, but was insufficient to trigger late ERK1/2 activation. By using a general caspase inhibitor (zVAD.fmk) we further demonstrated that late ERK1/2 activation was not a result of CVB3-mediated caspase cleavage. Treatment of cells with U0126, a selective inhibitor of MAPK kinase (MEK), significantly inhibited CVB3 progeny release and decreased virus protein production. Furthermore, inhibition of ERK1/2 activation circumvented CVB3-induced apoptosis and viral protease-mediated RasGAP cleavage. Taken together, these data suggest that ERK1/2 activation is important for CVB3 replication and contributes to virus-mediated changes in host cells. Our findings demonstrate coxsackievirus takeover of a particular host signaling mechanism and uncover a prospective approach to stymie virus spread and preserve myocardial integrity.

Indexed as

Amino Acid Chloromethyl KetonesApoptosisButadienesCaspase InhibitorsCysteine Proteinase InhibitorsEnterovirusEnzyme InhibitorsHeLa CellsHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNitrilesProvirusesras GTPase-Activating ProteinsAmino Acid Chloromethyl Ketonesbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneButadienesCaspase InhibitorsCysteine Proteinase InhibitorsEnzyme InhibitorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNitrilesras GTPase-Activating ProteinsU 0126Viral Proteins

Identifiers

PMID11884562
PMCPMC136021
OpenAlexW2169163045

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.