Evidence map›Paper›PMID 15078930›Full record

ArticleJournal of virology2004

Activation of the NF-kappaB pathway in human cytomegalovirus-infected cells is necessary for efficient transactivation of the major immediate-early promoter.

Ian B DeMeritt, Liesl E Milford, Andrew D Yurochko

Abstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 144 citations in OpenAlex.

  1. Review
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  10. Article
  11. Human cytomegalovirus and neonatal infection.Current research in microbial sciences · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Deletion of the non-adjacent genesFrontiers in immunology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

31 more citing papers are in PubMed but not listed here.

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 in 1 country.

Ian B DeMerittDepartment of Microbiology and Immunology and Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932, USA.
Liesl E Milford
Andrew D Yurochko
Louisiana State University Health Sciences Center Shreveport · US

Funding

RECRUITMENT YEAR FOR PI#5P20RR018724 · NCRR · LOUISIANA STATE UNIV HSC SHREVEPORT · PI O'CALLAGHAN, DENNIS JOHN · 2003 to 2011
$16.1M
Analysis of HCMV Infection of Monocytes and MacrophagesR01AI056077 · NIAID · LOUISIANA STATE UNIV HSC SHREVEPORT · PI YUROCHKO, ANDREW D · 2004 to 2020
$4.7M
NCRR NIH HHS 1-P20-RR018724-01NCRR NIH HHS P20 RR018724NIAID NIH HHS R01 AI056077
6 · The paper itself

Abstract

We previously demonstrated that human cytomegalovirus (HCMV) infection induced the activation of the cellular transcription factor NF-kappaB. Here, we investigate the mechanism for the HCMV-induced NF-kappaB activation and the role that the induced NF-kappaB plays in transactivation of the major immediate-early promoter (MIEP) and production of immediate-early (IE) proteins. Using a dominant-negative inhibitor of NF-kappaB, the IkappaB-superrepressor, we demonstrated that active NF-kappaB is critical for transactivation of the HCMV MIEP. Investigation of the mechanisms of NF-kappaB activation following HCMV infection showed a rapid and sustained decrease in the inhibitors of NF-kappaB, IkappaBalpha and IkappaBbeta. Because the IkappaB kinases (IKKs) regulate the degradation of the IkappaBs, virus-mediated changes in the IKKs were examined next. Using dominant-negative forms of the IKKs, we showed significant decreases in transactivation of the MIEP in the presence of these mutants. In addition, protein levels of members of the IKK complex and IKK kinase activity were upregulated throughout the time course of infection. Lastly, the role NF-kappaB plays in HCMV IE mRNA and protein production during infection was examined. Using aspirin and MG-132, we demonstrated that production of IE protein and mRNA was significantly decreased and delayed in infected cells treated with these drugs. Together, the results of these studies suggest that virus-mediated NF-kappaB activation, through the dysregulation of the IKK complex, plays a primary role in the initiation of the HCMV gene cascade in fibroblasts and may provide new targets for therapeutic intervention.

Indexed as

Transcriptional ActivationCells, CulturedCytomegalovirusCytomegalovirus InfectionsDown-RegulationFibroblastsGene Expression Regulation, ViralHumansI-kappa B KinaseI-kappa B ProteinsImmediate-Early ProteinsNF-kappa BNF-KappaB Inhibitor alphaPromoter Regions, GeneticProtein Serine-Threonine KinasesCHUK protein, humanI kappa B beta proteinI-kappa B KinaseI-kappa B ProteinsIKBKB protein, humanIKBKE protein, humanImmediate-Early ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID15078930
PMCPMC387686
OpenAlexW2112033054

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.