Evidence map›Paper›PMID 19594424›Full record

ReviewInfectious disorders drug targets2009

Human Cytomegalovirus US28: a functionally selective chemokine binding receptor.

Jennifer Vomaske, J A Nelson, Daniel N Streblow

Abstract readReview
In one paragraph

Review in Infectious disorders drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Cytomegalovirus disrupts Lamin A/C to control microtubule-mediated nuclear movement and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  5. Review
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  9. Review
  10. Review
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  14. HCMV latency: what regulates the regulators?Medical microbiology and immunology · 2019
    Review
  15. Review
  16. Article
  17. Article
  18. Review
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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

3 authors at 1 institution.

Jennifer VomaskeDepartment of Molecular Microbiology and Immunology and The Vaccine and Gene Therapy Institute, Oregon Health and Sciences University, Portland, OR 97201, USA.
J A Nelson
Daniel N Streblow
Vaccine and Gene Therapy Institute

Funding

CHEMOKINE RECEPTORS IN VASCULAR DISEASER01HL065754 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI NELSON, JAY A · 2000 to 2007
$2.7M
Cellular Basis of CMV Accelerated VasculopathyR01HL071695 · NHLBI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI NELSON, JAY A · 2002 to 2005
$1.5M
NHLBI NIH HHS HL65754NHLBI NIH HHS HL71695NHLBI NIH HHS R01 HL065754NHLBI NIH HHS R01 HL071695
6 · The paper itself

Abstract

Chemokines are small cytokines that are part of a large family of molecules that bind to G-protein coupled receptors, which, as a family, are the most widely targeted group of molecules in the treatment of disease. Chemokines are critical for recruiting and activating the cells of the immune system during inflammation especially during viral infections. However, a number of viruses including the large herpes virus human cytomegalovirus (HCMV) encode mechanisms to impede the effects of chemokines or has gained the ability to use these molecules to its own advantage. The Human Cytomegalovirus (HCMV)-encoded chemokine receptor US28 is the best characterized of the four unique chemokine receptor-like molecules found in the HCMV genome. US28 has been studied as an important virulence factor for HCMV-mediated vascular disease and, more recently, in models of HCMV-associated malignancy. US28 is a rare multi-chemokine family binding receptor with the ability to bind ligands from two distinct chemokine classes. Ligand binding to US28 activates cell-type and ligand-specific signaling pathways leading to cellular migration, which is an important example of receptor functional selectivity. Additionally, US28 has been demonstrated to constitutively activate phospholipase C (PLC) and NF-kB signaling pathways. Understanding the structure/function relationships between US28, its ligands and intracellular signaling molecules will provide essential clues for effective pharmacological targeting of this multifunctional chemokine receptor.

Indexed as

Binding SitesChemokinesCytomegalovirusDrug DesignHumansLigandsNF-kappa BProtein BindingReceptors, ChemokineSignal TransductionStructure-Activity RelationshipType C PhospholipasesViral ProteinsChemokinesLigandsNF-kappa BReceptors, ChemokineType C PhospholipasesUS28 receptor, CytomegalovirusViral Proteins

Identifiers

PMID19594424
PMCPMC3496389
OpenAlexW2120183643

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.