Evidence map›Paper›PMID 19494016›Full record

ArticleJournal of virology2009

Activation of intracellular signaling pathways by the murine cytomegalovirus G protein-coupled receptor M33 occurs via PLC-{beta}/PKC-dependent and -independent mechanisms.

Joseph D Sherrill, Melissa P Stropes, Olivia D Schneider, Diana E Koch, Fabiola M Bittencourt, Jeanette L C Miller, William E Miller

Open access · greenAbstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Methods for Studying the Function of Cytomegalovirus GPCRs.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  8. Control of Cytokines in Latent Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

7 authors at 1 institution in 1 country.

Joseph D SherrillDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, OH 45267-0524, USA.
Melissa P Stropes
Olivia D Schneider
Diana E Koch
Fabiola M Bittencourt
Jeanette L C Miller
William E Miller
University of Cincinnati Medical Center · US

Funding

HCMV US28 Signal Transduction by Betaarrestin proteinsR01AI058159 · NIAID · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 2005 to 2009
$1.2M
NIAID NIH HHS AI058159NIAID NIH HHS R01 AI058159
6 · The paper itself

Abstract

The presence of numerous G protein-coupled receptor (GPCR) homologs within the herpesvirus genomes suggests an essential role for these genes in viral replication in the infected host. Such is the case for murine cytomegalovirus (MCMV), where deletion of the M33 GPCR or replacement of M33 with a signaling defective mutant has been shown to severely attenuate replication in vivo. In the present study we utilized a genetically altered version of M33 (termed R131A) in combination with pharmacological inhibitors to further characterize the mechanisms by which M33 activates downstream signaling pathways. This R131A mutant of M33 fails to support salivary gland replication in vivo and, as such, is an important tool that can be used to examine the signaling activities of M33. We show that M33 stimulates the transcription factor CREB via heterotrimeric G(q/11) proteins and not through promiscuous coupling of M33 to the G(s) pathway. Using inhibitors of signaling molecules downstream of G(q/11), we demonstrate that M33 stimulates CREB transcriptional activity in a phospholipase C-beta and protein kinase C (PKC)-dependent manner. Finally, utilizing wild-type and R131A versions of M33, we show that M33-mediated activation of other signaling nodes, including the mitogen-activated protein kinase family member p38alpha and transcription factor NF-kappaB, occurs in the absence of G(q/11) and PKC signaling. The results from the present study indicate that M33 utilizes multiple mechanisms to modulate intracellular signaling cascades and suggest that signaling through PLC-beta and PKC plays a central role in MCMV pathogenesis in vivo.

Indexed as

Signal TransductionAnimalsCell LineFemaleHerpesviridae InfectionsHumansMiceMice, Inbred BALB CMuromegalovirusPhospholipase C betaProtein Kinase CReceptors, G-Protein-CoupledSalivary GlandsViral ProteinsVirus ReplicationPhospholipase C betaProtein Kinase CReceptors, G-Protein-CoupledViral Proteins

Identifiers

PMID19494016
PMCPMC2715766
OpenAlexW2129994873

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.