Evidence map›Paper›PMID 26155834›Full record

ArticleScientific reports2015

Involvement of PrP(C) in kainate-induced excitotoxicity in several mouse strains.

Patricia Carulla, Franc Llorens, Andreu Matamoros-Angles, Patricia Aguilar-Calvo, Juan Carlos Espinosa, Rosalina Gavín, Isidre Ferrer, Giuseppe Legname, Juan Maria Torres, José A del Río

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Prion Protein: The Molecule of Many Forms and Faces.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. PrPFrontiers in molecular neuroscience · 2021
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Cerebellar compartmentation of prion pathogenesis.Brain pathology (Zurich, Switzerland) · 2018
    Article
  16. Article
  17. Sisyphus in Neverland.Journal of Alzheimer's disease : JAD · 2018
    Article
  18. Article
  19. Review
  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

10 authors at 5 institutions in 2 countries.

Patricia Carulla1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Franc Llorens1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain [4] German Center for Neurodegenerative Diseases (DZNE), Robert-Koch Str. 40, 37075, Göttingen, Germany.
Andreu Matamoros-Angles1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Patricia Aguilar-CalvoCentro de Investigación en Sanidad Animal (CISA-INIA), Valdeolmos, Madrid, Spain.
Juan Carlos EspinosaCentro de Investigación en Sanidad Animal (CISA-INIA), Valdeolmos, Madrid, Spain.
Rosalina Gavín1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Isidre Ferrer1] Institut de Neuropatologia, IDIBELL-Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain [2] Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Giuseppe LegnameLaboratory of Prion Biology, Department of Neuroscience, Scuola Internazionale Superiore di Studi Avanzati (SISSA), Trieste, Italy.
Juan Maria TorresCentro de Investigación en Sanidad Animal (CISA-INIA), Valdeolmos, Madrid, Spain.
José A del Río1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Centro de Investigación en Sanidad AnimalInstitute for Bioengineering of Catalonia · ESUniversitat de Barcelona · ESBellvitge University Hospital · ESScuola Internazionale Superiore di Studi Avanzati · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular prion protein (PrP(C)) has been associated with a plethora of cellular functions ranging from cell cycle to neuroprotection. Mice lacking PrP(C) show an increased susceptibility to epileptic seizures; the protein, then, is neuroprotective. However, lack of experimental reproducibility has led to considering the possibility that other factors besides PrP(C) deletion, such as the genetic background of mice or the presence of so-called "Prnp flanking genes", might contribute to the reported susceptibility. Here, we performed a comparative analysis of seizure-susceptibility using characterized Prnp(+/+) and Prnp(0/0) mice of B6129, B6.129, 129/Ola or FVB/N genetic backgrounds. Our study indicates that PrP(C) plays a role in neuroprotection in KA-treated cells and mice. For this function, PrP(C) should contain the aa32-93 region and needs to be linked to the membrane. In addition, some unidentified "Prnp-flanking genes" play a role parallel to PrP(C) in the KA-mediated responses in B6129 and B6.129 Prnp(0/0) mice.

Indexed as

AnimalsBiomarkersCell DeathCell LineCytokinesDisease Models, AnimalGene ExpressionGenetic Predisposition to DiseaseGliosisHippocampusInflammation MediatorsKainic AcidMiceMice, KnockoutPrPC ProteinsSeizuresBiomarkersCytokinesInflammation MediatorsKainic AcidPrPC Proteins

Identifiers

PMID26155834
PMCPMC4648388
OpenAlexW1036700737

What OpenQuestion holds

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Registered trials

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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.