Evidence map›Paper›PMID 20451233›Full record

ArticleVirology2010

Extracellular Hsp90 serves as a co-factor for MAPK activation and latent viral gene expression during de novo infection by KSHV.

Zhiqiang Qin, Michael DeFee, Jennifer S Isaacs, Chris Parsons

Abstract read
In one paragraph

Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. KSHV Genome Replication and Maintenance.Frontiers in microbiology · 2016
    Review
  8. Article
  9. Article
  10. Article
  11. Immunogenic HSV-mediated oncolysis shapes the antitumor immune response and contributes to therapeutic efficacy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Article
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  13. Article
  14. Article
  15. Article
  16. Article
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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

4 authors at 1 institution in 1 country.

Zhiqiang QinDepartment of Medicine, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Michael DeFee
Jennifer S Isaacs
Chris Parsons
Medical University of South Carolina · US

Funding

THE ROLE OF THE RNA BINDING PROTEIN LA IN ORAL TUMOR BIOLOGYP20RR017696 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KIRKWOOD, KEITH L · 2002 to 2011
$20.7M
T-COHR: Training in Craniofacial and Oral Health ResearchT32DE017551 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YAO, HAI · 2006 to 2025
$10.3M
An Animal Model for Kaposi's SarcomaK08CA103858 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI PARSONS, CHRISTOPHER H · 2004 to 2009
$715k
The role of cell surface heat shock protein 90 in KSHV pathogenesisF30DE020203 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DEFEE, MICHAEL ROBERT · 2009 to 2013
$217k
NCI NIH HHS K08-1CA103858NCI NIH HHS K08 CA103858NCRR NIH HHS P20 RR017696NIDCR NIH HHS 5T32DE017551-03NIDCR NIH HHS F30 DE020203NIDCR NIH HHS T32 DE017551
6 · The paper itself

Abstract

The Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma (KS), an important cause of morbidity and mortality in immunocompromised patients. KSHV interaction with the cell membrane triggers activation of specific intracellular signal transduction pathways to facilitate virus entry, nuclear trafficking, and ultimately viral oncogene expression. Extracellular heat shock protein 90 localizes to the cell surface (csHsp90) and facilitates signal transduction in cancer cell lines, but whether csHsp90 assists in the coordination of KSHV gene expression through these or other mechanisms is unknown. Using a recently characterized non-permeable inhibitor specifically targeting csHsp90 and Hsp90-specific antibodies, we show that csHsp90 inhibition suppresses KSHV gene expression during de novo infection, and that this effect is mediated largely through the inhibition of mitogen-activated protein kinase (MAPK) activation by KSHV. Moreover, we show that targeting csHsp90 reduces constitutive MAPK expression and the release of infectious viral particles by patient-derived, KSHV-infected primary effusion lymphoma cells. These data suggest that csHsp90 serves as an important co-factor for KSHV-initiated MAPK activation and provide proof-of-concept for the potential benefit of targeting csHsp90 for the treatment or prevention of KSHV-associated illnesses.

Indexed as

Gene Expression Regulation, ViralHost-Pathogen InteractionsHerpesvirus 8, HumanHSP90 Heat-Shock ProteinsHumansLymphocytesLymphomaMitogen-Activated Protein KinasesSarcoma, KaposiHSP90 Heat-Shock ProteinsMitogen-Activated Protein Kinases

Identifiers

PMID20451233
PMCPMC3202419
OpenAlexW2037720741

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.