Evidence map›Paper›PMID 15452225›Full record

ArticleJournal of virology2004

Identification of differentially expressed genes in scrapie-infected mouse brains by using global gene expression technology.

Wei Xiang, Otto Windl, Gerda Wünsch, Martin Dugas, Alexander Kohlmann, Nicola Dierkes, Ingo M Westner, Hans A Kretzschmar

Open access · greenAbstract readComparative Study
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 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Mechanisms of prion-induced toxicity.Cell and tissue research · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Goats naturally devoid of PrPVeterinary research · 2020
    Article
  20. RNA editing alterations define manifestation of prion diseases.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

20 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

8 authors at 3 institutions in 3 countries.

Wei XiangInstitute of Neuropathology, Department of Internal Medicine III, Ludwig-Maximilians-University Munich, Feodor-Lynen-Strasse 23, D-81377 Munich, Germany.
Otto Windl
Gerda Wünsch
Martin Dugas
Alexander Kohlmann
Nicola Dierkes
Ingo M Westner
Hans A Kretzschmar
Institute of Neuroimmunology of the Slovak Academy of Sciences · SKLudwig-Maximilians-Universität München · DEZimmer Biomet (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of prion diseases, a class of transmissible fatal neurodegenerative diseases in humans and animals, is still unclear. The aim of this study was to identify the differentially regulated genes that correlate with the development of prion diseases for a better understanding of their pathological mechanisms. We employed Affymetrix Mouse Expression Arrays 430A containing >22,000 transcripts and compared the global gene expression profiles from brains of mice who were intracerebrally inoculated with scrapie strains ME7 and RML with those from brains of uninfected and mock-infected mice. The microarray data were analyzed by Significance Analysis of Microarrays, revealing 121 genes whose expression increased at least twofold in both ME7- and RML-infected mouse brains, with an estimated false discovery rate of < or =5%. These genes encode proteins involved in proteolysis, protease inhibition, cell growth and maintenance, the immune response, signal transduction, cell adhesion, and molecular metabolism. The time course of expression generally showed up-regulation of these genes from 120 days postinoculation (dpi) for ME7-inoculated mouse brains and from 90 dpi for RML-inoculated mouse brains. The onset of elevated expression correlated temporally with the onset of PrP(Sc) accumulation and the activation of glia, which may have contributed to neuronal cell death. Among the differentially regulated genes reported in the present study, the emergence of genes for several cathepsins and S100 calcium binding proteins was conspicuous. These and other genes reported here may represent novel potential diagnostic and therapeutic targets for prion disease.

Indexed as

Gene Expression ProfilingAnimalsBrainCathepsinsGene Expression RegulationMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisProteinsPrPSc ProteinsS100 ProteinsScrapieUp-RegulationCathepsinsProteinsPrPSc ProteinsS100 Proteins

Identifiers

PMID15452225
PMCPMC521804
OpenAlexW1985384585

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.