Evidence map›Paper›PMID 19360424›Full record

ArticleActa neuropathologica2009

Hypoxia inducible factor-1 alpha activation of the JCV promoter: role in the pathogenesis of progressive multifocal leukoencephalopathy.

Sergio Piña-Oviedo, Kamel Khalili, Luis Del Valle

Abstract read
In one paragraph

Article in Acta neuropathologica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Impact of Hypoxia over Human Viral Infections and Key Cellular Processes.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
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  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  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
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.

Sergio Piña-OviedoDepartment of Neuroscience, Center for Neurovirology and Neuropathology Core, Temple University School of Medicine, 1900 N. 12th Street, Philadelphia, PA 19122, USA.
Kamel Khalili
Luis Del Valle
Temple University · US

Funding

TRANSCRIPTION OF HIV-1 PROMOTER IN CENTRAL NERVOUS SYSTEM DERIVED CELLSP01NS030916 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI KHALILI, KAMEL · 1993 to 2009
$10.6M
Involvement of Survivin in the Development of PMLR01NS055644 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI DEL VALLE, LUIS · 2007 to 2011
$1.5M
NINDS NIH HHS P01 NS030916NINDS NIH HHS R01 NS055644
6 · The paper itself

Abstract

Activation of viral promoter transcription is a crucial event in the life cycle of several viruses. Hypoxia inducible factor-1 alpha (HIF-1alpha) is an inducible transcription factor whose activity is dependent on environmental conditions, most notably oxygen levels and cellular stress. HIF-1alpha has been implicated in the pathogenesis of several viruses, including HIV-1, HHV-8 and RSV. Under hypoxic conditions or oxidative stress, HIF-1alpha becomes stable and translocates to the nucleus, where it modulates gene transcription. The objective of the present study was to investigate a possible role for HIF-1alpha in the activation of JCV. Glial cell cultures infected with JCV demonstrated a significant increase in the levels of HIF-1alpha, in where it is located to the nucleus. Immunohistochemical studies corroborated upregulation of HIF-1alpha in JCV infected oligodendrocytes and astrocytes in clinical samples of PML compared with normal glial cells from the same samples in which HIF-1alpha expression is weak. CAT assays performed in co-transfected glial cells demonstrated activation of the JCV early promoter in the presence of HIF-1alpha. This activation was potentiated in the presence of Smad3 and Smad4. Finally, chromatin immunoprecipitation assays demonstrated the binding of HIF-1alpha to the JCV control region. These results suggest a role for HIF-1alpha in the activation of JCV; understanding of this pathway may lead to the development of more effective therapies for PML, thus far an incurable disease.

Indexed as

AdultAgedCells, CulturedChromatin ImmunoprecipitationFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitImmunohistochemistryJC VirusLeukoencephalopathy, Progressive MultifocalMaleMiddle AgedOligodendrogliaTranscriptional ActivationHIF1A protein, humanHypoxia-Inducible Factor 1, alpha Subunit

Identifiers

PMID19360424
PMCPMC2856344
OpenAlexW2061227669

What OpenQuestion holds

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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.