Evidence map›Paper›PMID 17151108›Full record

ArticleJournal of virology2007

Identification of differentially activated cell-signaling networks associated with pichinde virus pathogenesis by using systems kinomics.

Gavin C Bowick, Susan M Fennewald, Erin P Scott, Lihong Zhang, Barry L Elsom, Judith F Aronson, Heidi M Spratt, Bruce A Luxon, David G Gorenstein, Norbert K Herzog

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Junin Virus Activates p38 MAPK and HSP27 Upon Entry.Frontiers in cellular and infection microbiology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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 1 institution in 1 country.

Gavin C BowickDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Susan M Fennewald
Erin P Scott
Lihong Zhang
Barry L Elsom
Judith F Aronson
Heidi M Spratt
Bruce A Luxon
David G Gorenstein
Norbert K Herzog
The University of Texas Medical Branch at Galveston · US

Funding

WRCE Nonhuman Primate CoreU54AI057156 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WALKER, DAVID H · 2003 to 2013
$102.6M
Biodefense Proteomics CollaboratoryU01AI054827 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GORENSTEIN, DAVID G · 2003 to 2007
$6.1M
NHLBI PROTEOMICS INITIATIVEN01HV28184 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · 2007 to 2008
$5.6M
NHLBI PROTEOMICS INITIATIVE-N01HV28184N01HV028184 · HV · UNIV OF TEXAS MEDICAL BRANCH · PI KUROSKY, ALEXANDER NONE · 2002 to 2006
–
NHLBI NIH HHS N01 HV028184NHLBI NIH HHS N01 HV28184NIAID NIH HHS U01 AI054827NIAID NIH HHS U54 AI057156PHS HHS R01 A127744
6 · The paper itself

Abstract

Phosphorylation plays a key role in regulating many signaling pathways. Although studies investigating the phosphorylated forms of signaling pathways are now commonplace, global analysis of protein phosphorylation and kinase activity has lagged behind genomics and proteomics. We have used a kinomics approach to study the effect of virus infection on host cell signaling in infected guinea pigs. Delineating the host responses which lead to clearance of a pathogen requires the use of a matched, comparative model system. We have used two passage variants of the arenavirus Pichinde, used as a biosafety level 2 model of Lassa fever virus as it produces similar pathologies in guinea pigs and humans, to compare the host cell responses between infections which lead to either a mild, self-limiting infection or lethal disease. Using this model, we can begin to understand the differences in signaling events which give rise to these markedly different outcomes. By contextualizing these data using pathway analysis, we have identified key differences in cellular signaling matrices. By comparing these differentially involved networks, we have identified a number of key signaling "nodes" which show differential phosphorylations between mild and lethal infections. We believe that these nodes provide potential targets for the development of antiviral therapies by acting at the level of the host response rather than by directly targeting viral proteins.

Indexed as

Pichinde virusProteomicsSignal TransductionAnimalsArenaviridae InfectionsMiceMonocytesPhosphorylationProteinsTime FactorsProteins

Identifiers

PMID17151108
PMCPMC1797588
OpenAlexW2156671900

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.