Evidence map›Paper›PMID 18474555›Full record

ArticleThe Journal of general virology2008

DNA-binding transcription factor NF-1A negatively regulates JC virus multiplication.

Veerasamy Ravichandran, Eugene O Major

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. [Progress on pathogenesis of progressive multifocal leukoence-phalopathy].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    Review
  6. Article
  7. Article
  8. Clonal immortalized human glial cell lines support varying levels of JC virus infection due to differences in cellular gene expression.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Molecular regulation of JC virus tropism: insights into potential therapeutic targets for progressive multifocal leukoencephalopathy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  16. Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Veerasamy RavichandranLaboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Eugene O MajorLaboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
National Institute of Neurological Disorders and Stroke · US

Funding

Molecular Pathogenesis Of JC Virus & Progressive Multifocal LeukoencephalopathyZIANS001983 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI NATH, AVINDRA · 2009 to 2015
$6.6M
MOLECULAR PATHOGENESIS OF JC VIRUS &PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHYZ01NS001983 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI MAJOR, EUGENE O. · 1985 to 2008
$3.7M
Intramural NIH HHS Z01 NS001983
6 · The paper itself

Abstract

JC virus (JCV) DNA replication occurs in the nuclei of infected cells. The level of JCV genome expression depends on nucleotide sequences in the viral regulatory region and their interaction with host-cell nuclear transcription factors. Our previous studies showed a higher level of NF-1X in JCV-permissive cells compared with the other members of the NF-1 family, NF-1A, B and C, which suggests that NF-1X plays a positive role in JCV multiplication. It remained unclear whether a reduction in the level of NF-1A, which is expressed abundantly in JCV-non-permissive cell types, leads to an increase in JCV multiplication. In this study, we show that downregulation of NF-1A expression in JCV-non-susceptible progenitor and HeLa cells results in a reversion to susceptibility for JCV multiplication. These data demonstrate that a higher level of NF-1A protein in JCV-non-permissive cell types, compared with the level of NF-1X, may be acting as a negative regulator at the JCV promoter to control JCV multiplication.

Indexed as

Cell NucleusCells, CulturedDown-RegulationFetusHeLa CellsHumansJC VirusNFI Transcription FactorsPolyomavirus InfectionsStem CellsTelencephalonTumor Virus InfectionsVirus ReplicationNFI Transcription Factors

Identifiers

PMID18474555
PMCPMC2701216
OpenAlexW2143141686

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.