Evidence map›Paper›PMID 18054964›Full record

ReviewLife sciences2008

Desensitization of herpesvirus-encoded G protein-coupled receptors.

Joseph D Sherrill, William E Miller

Open access · greenAbstract readReview
In one paragraph

Review in Life sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Joseph D SherrillDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0524, USA.
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 R01 AI 058159NIAID NIH HHS R01 AI058159
6 · The paper itself

Abstract

Members of the herpesvirus family, including human cytomegalovirus (HCMV) and Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8), encode G protein-coupled receptor (GPCR) homologs, which strongly activate classical G protein signal transduction networks within the cell. In animal models of herpesvirus infection, the viral GPCRs appear to play physiologically important roles by enabling viral replication within tropic tissues and by promoting reactivation from latency. While a number of studies have defined intracellular signaling pathways activated by herpesviral GPCRs, it remains unclear if their physiological function is subjected to the process of desensitization as observed for cellular GPCRs. G protein-coupled receptor kinases (GRK) and arrestin proteins have been recently implicated in regulating viral GPCR signaling; however, the role that these desensitization proteins play in viral GPCR function in vivo remains unknown. Here, we review what is currently known regarding viral GPCR desensitization and discuss potential biological ramifications of viral GPCR regulation by the host cell desensitization machinery.

Indexed as

AnimalsCytomegalovirusDisease Models, AnimalDown-RegulationHerpesvirus 8, HumanHumansReceptors, ChemokineSignal TransductionViral ProteinsG protein-coupled receptor, Human herpesvirus 8Receptors, ChemokineUL33 protein, human cytomegalovirusUS28 receptor, CytomegalovirusViral Proteins

Identifiers

PMID18054964
PMCPMC2239238
OpenAlexW1975180353

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.