Evidence map›Paper›PMID 23015701›Full record

ArticleJournal of virology2012

Amplification of JNK signaling is necessary to complete the murine gammaherpesvirus 68 lytic replication cycle.

James A Stahl, Clinton R Paden, Shweta S Chavan, Veronica MacLeod, Ricky D Edmondson, Samuel H Speck, J Craig Forrest

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Deletion of Murine Gammaherpesvirus GeneJournal of virology · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

7 authors at 2 institutions in 1 country.

James A StahlDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Clinton R Paden
Shweta S Chavan
Veronica MacLeod
Ricky D Edmondson
Samuel H Speck
J Craig Forrest
University of Arkansas for Medical Sciences · USEmory University · US

Funding

Study of the Cell-specific Inflammasome Responses During Defense Against Gram-negative BacteriaP20GM103625 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI SMELTZER, MARK S · 2012 to 2021
$21.5M
Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
Function of the Gamma HV68 M2 AntigenR01AI058057 · NIAID · EMORY UNIVERSITY · PI SPECK, SAMUEL H · 2004 to 2016
$4.5M
Control of Gammaherpesvirus ReplicationR01CA052004 · NCI · WASHINGTON UNIVERSITY · PI SPECK, SAMUEL H · 1990 to 2013
$4.1M
NCATS NIH HHS UL1 TR000039NCATS NIH HHS UL1TR000039NCI NIH HHS R01 CA052004NCI NIH HHS R01CA052004NIAID NIH HHS R01 AI058057NIGMS NIH HHS P20 GM103625
6 · The paper itself

Abstract

Several studies have previously defined host-derived signaling events capable of driving lytic gammaherpesvirus replication or enhancing immediate-early viral gene expression. Yet signaling pathways that regulate later stages of the productive gammaherpesvirus replication cycle are still poorly defined. In this study, we utilized a mass spectrometric approach to identify c-Jun as an abundant cellular phosphoprotein present in late stages of lytic murine gammaherpesvirus 68 (MHV68) infection. Kinetically, c-Jun phosphorylation was enhanced as infection progressed, and this correlated with enhanced phosphorylation of the c-Jun amino-terminal kinases JNK1 and JNK2 and activation of AP-1 transcription. These events were dependent on progression beyond viral immediate-early gene expression, but not dependent on viral DNA replication. Both pharmacologic and dominant-negative blockade of JNK1/2 activity inhibited viral replication, and this correlated with inhibition of viral DNA synthesis and reduced viral gene expression. These data suggest a model in which MHV68 by necessity amplifies and usurps JNK/c-Jun signaling as infection progresses in order to facilitate late stages of the MHV68 lytic infection cycle.

Indexed as

Signal TransductionVirus ReplicationAmino Acid SequenceAnimalsGammaherpesvirinaeHumansMAP Kinase Kinase 4MiceMice, Inbred C57BLMolecular Sequence DataTandem Mass SpectrometryViral ProteinsMAP Kinase Kinase 4Viral Proteins

Identifiers

PMID23015701
PMCPMC3503053
OpenAlexW2003949540

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.