Evidence map›Paper›PMID 7912827›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1994

Structure and polymorphism of the mouse prion protein gene.

D Westaway, C Cooper, S Turner, M Da Costa, G A Carlson, S B Prusiner

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Mutability of prions.EMBO reports · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Identification of multiple quantitative trait loci linked to prion disease incubation period in mice.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  20. 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

6 authors at 2 institutions in 1 country.

D WestawayDepartment of Neurology, University of California, San Francisco 94143.
C Cooper
S Turner
M Da Costa
G A Carlson
S B Prusiner
University of California, San Francisco · USMcLaughlin Research Institute · US

Funding

VIRAL DEGENERATIVE DEMENTING DISEASE IN AGING (SUPP)P01AG002132 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SALI, ANDREJ · 1985 to 2024
$51.7M
TRANSGENIC STUDIES OF SCRAPIE "STRAINS" AND CNS DEGENERATION BY MUTANT PRP GENESP50NS014069 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI DE ARMOND, STEPHEN J. · 1994 to 2002
$4.2M
PURIFICATION AND MOLECULAR STRUCTURE OF THE SCRAPIE AGENTP01NS014069 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PRUSINER, STANLEY B · 1985 to 1993
–
TRANSMISSIBLE AND GENETIC NEURODENGENERATIVE DISEASESP01NS022786 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CARLSON, GEORGE A. · 1985 to 1999
–
NIA NIH HHS AG02132NINDS NIH HHS NS14069NINDS NIH HHS NS22786
6 · The paper itself

Abstract

Missense mutations in the prion protein (PrP) gene, overexpression of the cellular isoform of PrP (PrPC), and infection with prions containing the scrapie isoform of PrP (PrPSc) all cause neurodegenerative disease. To understand better the physiology and expression of PrPC, we retrieved mouse PrP gene (Prn-p) yeast artificial chromosome (YAC), cosmid, phage, and cDNA clones. Physical mapping positions Prn-p approximately 300 kb from ecotropic virus integration site number 4 (Evi-4), compatible with failure to detect recombination between Prn-p and Evi-4 in genetic crosses. The Prn-pa allele encompasses three exons, with exons 1 and 2 encoding the mRNA 5' untranslated region. Exon 2 has no equivalent in the Syrian hamster and human PrP genes. The Prn-pb gene shares this intron/exon structure but harbors an approximately 6-kb deletion within intron 2. While the Prn-pb open reading frame encodes two amino acid substitutions linked to prolonged scrapie incubation periods, a deletion of intron 2 sequences also characterizes inbred strains such as RIII/S and MOLF/Ei with shorter incubation periods, making a relationship between intron 2 size and scrapie pathogenesis unlikely. The promoter regions of a and b Prn-p alleles include consensus Sp1 and AP-1 sites, as well as other conserved motifs which may represent binding sites for as yet unidentified transcription factors.

Indexed as

Polymorphism, GeneticPromoter Regions, GeneticAnimalsBase SequenceBrainCloning, MolecularCricetinaeDNADNA, ComplementaryDNA PrimersDNA Transposable ElementsExonsHumansIntronsMesocricetusMiceDNADNA, ComplementaryDNA PrimersDNA Transposable ElementsPrionsPrPSc Proteins

Identifiers

PMID7912827
PMCPMC44213
OpenAlexW2019032600

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.