Evidence map›Paper›PMID 19308092›Full record

ArticleMolecular systems biology2009

A systems approach to prion disease.

Daehee Hwang, Inyoul Y Lee, Hyuntae Yoo, Nils Gehlenborg, Ji-Hoon Cho, Brianne Petritis, David Baxter, Rose Pitstick, Rebecca Young, Doug Spicer and 5 more

Abstract read
In one paragraph

Article in Molecular systems biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed
–field-weighted citation impact
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

157 citing papers in PubMed.

  1. Article
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  4. What Is QSP and Why Does It Exist?: A Brief History.Handbook of experimental pharmacology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Prion disease modelled in Drosophila.Cell and tissue research · 2023
    Review
  12. Mechanisms of prion-induced toxicity.Cell and tissue research · 2023
    Review
  13. Review
  14. Article
  15. A single-cell map of antisense oligonucleotide activity in the brain.bioRxiv : the preprint server for biology · 2023
    Article
  16. Beta-endoproteolysis of the cellular prion protein by dipeptidyl peptidase-4 and fibroblast activation protein.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Daehee HwangInstitute for Systems Biology, Seattle, WA 98103, USA.
Inyoul Y Lee
Hyuntae Yoo
Nils Gehlenborg
Ji-Hoon Cho
Brianne Petritis
David Baxter
Rose Pitstick
Rebecca Young
Doug Spicer
Nathan D Price
John G Hohmann
Stephen J Dearmond
George A Carlson
Leroy E Hood

Funding

Quantitative Systems BiologyP50GM076547 · NIGMS · INSTITUTE FOR SYSTEMS BIOLOGY · PI BALIGA, NITIN S · 2006 to 2016
$30.6M
TRANSGENETICS OF CHIMERIC PROTEINS IN PRION REPLICATION &DISEASEP01NS041997 · NINDS · MC LAUGHLIN RESEARCH INSTITUTE · PI DEARMOND, STEPHEN J. · 2001 to 2011
$15.0M
NIGMS NIH HHS GM076547NIGMS NIH HHS P50 GM076547NINDS NIH HHS NS41997NINDS NIH HHS P01 NS041997
6 · The paper itself

Abstract

Prions cause transmissible neurodegenerative diseases and replicate by conformational conversion of normal benign forms of prion protein (PrP(C)) to disease-causing PrP(Sc) isoforms. A systems approach to disease postulates that disease arises from perturbation of biological networks in the relevant organ. We tracked global gene expression in the brains of eight distinct mouse strain-prion strain combinations throughout the progression of the disease to capture the effects of prion strain, host genetics, and PrP concentration on disease incubation time. Subtractive analyses exploiting various aspects of prion biology and infection identified a core of 333 differentially expressed genes (DEGs) that appeared central to prion disease. DEGs were mapped into functional pathways and networks reflecting defined neuropathological events and PrP(Sc) replication and accumulation, enabling the identification of novel modules and modules that may be involved in genetic effects on incubation time and in prion strain specificity. Our systems analysis provides a comprehensive basis for developing models for prion replication and disease, and suggests some possible therapeutic approaches.

Indexed as

AnimalsAstrocytesGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHumansMiceMice, TransgenicMicrogliaOligonucleotide Array Sequence AnalysisPrion DiseasesPrPSc ProteinsSystems BiologyTime FactorsPrPSc Proteins

Identifiers

PMID19308092
PMCPMC2671916

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.