Evidence map›Paper›PMID 19640558›Full record

ArticleVirology2009

Kaposi sarcoma-associated herpes virus (KSHV) G protein-coupled receptor (vGPCR) activates the ORF50 lytic switch promoter: a potential positive feedback loop for sustained ORF50 gene expression.

Virginie Bottero, Neelam Sharma-Walia, Nagaraj Kerur, Arun George Paul, Sathish Sadagopan, Mark Cannon, Bala Chandran

Abstract read
In one paragraph

Article in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  11. Hijacking GPCRs by viral pathogens and tumor.Biochemical pharmacology · 2016
    Review
  12. The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Kaposi's sarcoma-associated herpesvirus interacts with EphrinA2 receptor to amplify signaling essential for productive infection.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  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

7 authors at 2 institutions in 1 country.

Virginie BotteroH. M. Bligh Cancer Research Laboratories, Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA.
Neelam Sharma-Walia
Nagaraj Kerur
Arun George Paul
Sathish Sadagopan
Mark Cannon
Bala Chandran
Rosalind Franklin University of Medicine and Science · USUniversity of Minnesota · US

Funding

ANTIGENS OF KAPOSIS SARCOMA ASSOCIATED HERPESVIRUSR01CA075911 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHANDRAN, BALA · 1998 to 2012
$3.5M
Early events of in vitro KSHV infectionR01CA168472 · NCI · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI SHARMA-WALIA, NEELAM · 2012 to 2016
$1.6M
Biology of HHV-8 interactions with host cellsR01CA099925 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHANDRAN, BALA · 2004 to 2007
$1.2M
NCI NIH HHS CA 099925NCI NIH HHS R01 CA075911NCI NIH HHS R01 CA099925NCI NIH HHS R01 CA168472
6 · The paper itself

Abstract

KSHV vGPCR, a lytic cycle associated protein, induces several signaling pathways leading to the activation of various transcription factors and consequently the expression of cellular and viral genes. Though the role of vGPCR in KSHV tumorigenicity has been well studied, its function related to the viral life cycle is poorly understood. Reduction in vGPCR by RNA interference also resulted in the reduction in KSHV lytic switch ORF50 gene and protein expression. Induction of vGPCR by doxycycline in BC3.14 cells also resulted in more KSHV production. When this was explored, induction of the ORF50 promoter by vGPCR expression was observed. Further examination of the molecular mechanisms by which vGPCR regulates the ORF50 promoter, using various ORF50 promoter constructs, revealed that induction of ORF50 promoter by vGPCR did not involve AP1 but was dependent on Sp1 and Sp3 transcription factors. vGPCR signaling led to an increase in Sp1 and Sp3 DNA binding activity and a decrease in histone deacetylase (HDAC) activity. These activities were pertussis toxin independent, did not involve Rho and Rac-GTPases and involved the heterotrimeric G protein subunits Galpha12 and Galphaq. Studies using pharmacologic inhibitors and dominant-negative proteins identified phospholipase C, the novel protein kinase C (novel PKC) family and protein kinase D (PKD) as part of the signaling initiated by vGPCR leading to ORF50 promoter activation. Taken together, this study suggests a role for vGPCR in the sustained expression of ORF50 which could lead to a continued activation of lytic cycle genes and ultimately to successful viral progeny formation.

Indexed as

Base SequenceBinding SitesCell LineDoxycyclineFeedback, PhysiologicalGene ExpressionGenes, ViralHerpesvirus 8, HumanHumansImmediate-Early ProteinsModels, BiologicalMutationPromoter Regions, GeneticReceptors, Chemokinerho GTP-Binding ProteinsRNA, MessengerDoxycyclineG protein-coupled receptor, Human herpesvirus 8Immediate-Early ProteinsReceptors, Chemokinerho GTP-Binding ProteinsRNA, MessengerRNA, Small InterferingRNA, ViralRta protein, Human herpesvirus 8Sp1 Transcription FactorTrans-Activators

Identifiers

PMID19640558
PMCPMC2747482
OpenAlexW1999910275

What OpenQuestion holds

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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.