Evidence map›Paper›PMID 27497185›Full record

ArticleVirology2016

The HCMV US28 vGPCR induces potent Gαq/PLC-β signaling in monocytes leading to increased adhesion to endothelial cells.

Shu-En Wu, William E Miller

Open access · greenAbstract read
In one paragraph

Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Methods for Studying the Function of Cytomegalovirus GPCRs.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Human cytomegalovirus G protein-coupled receptor US28 promotes latency by attenuating c-fos.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Review
  18. Review
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Shu-En WuDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0524, USA.
William E MillerDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0524, USA. Electronic address: william.miller@uc.edu.
Sabin Vaccine Institute · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
HCMV US28 Signal Transduction by Betaarrestin proteinsR01AI058159 · NIAID · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 2005 to 2009
$1.2M
The Role of US28 During HCMV LatencyR21AI119415 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI O'CONNOR, CHRISTINE M · 2015 to 2016
$457k
Mechanisms of vGPCR mediated Cytomegalovirus Growth in the Salivary GlandR56AI121028 · NIAID · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 2016 to 2016
$395k
Role of Cytomegalovirus GPCRs in Pathogenesis in VivoR56AI095442 · NIAID · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 2012 to 2012
$306k
NCATS NIH HHS UL1 TR001425NIAID NIH HHS R01 AI058159NIAID NIH HHS R21 AI119415NIAID NIH HHS R56 AI095442NIAID NIH HHS R56 AI121028
6 · The paper itself

Abstract

US28 transcripts have been detected in primary monocytes and in THP-1 monocytes infected with HCMV but US28 protein expression has not yet been demonstrated in these cell types. Moreover, the mechanism(s) by which US28 signals and contributes to viral pathogenesis in monocytes remains unclear. Here, we show that US28 protein is robustly expressed in HCMV infected THP-1 monocytes and that US28 can trigger Gαq dependent signaling in THP-1 cells infected with HCMV and in THP-1 cells stably expressing US28. US28 signaling in these cells is dependent on G-protein coupling, but independent of chemokine binding. Importantly, we demonstrate that this US28 signaling is functionally important as it stimulates the adhesion of monocytes to an endothelial monolayer. Our studies, which demonstrate that US28-driven Gαq signaling has profound effects on monocyte biology, suggest that US28 driven phenotypic changes in HCMV infected monocytes may play important roles in HCMV dissemination and/or pathogenesis.

Indexed as

Signal TransductionCell AdhesionCell LineCells, CulturedCytomegalovirusCytomegalovirus InfectionsEndothelial CellsGTP-Binding Protein alpha Subunits, Gq-G11HumansMonocytesPhospholipase C betaReceptors, ChemokineViral ProteinsGTP-Binding Protein alpha Subunits, Gq-G11Phospholipase C betaReceptors, ChemokineUS28 receptor, CytomegalovirusViral ProteinsCytomegalovirusEndothelial adhesionGαqHCMVLatencyLytic replicationMacrophagesMonocytesUS28vGPCR

Identifiers

PMID27497185
PMCPMC5026607
OpenAlexW2506860390

What OpenQuestion holds

Textmetadata
LicenceTDM
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.