Evidence map›Paper›PMID 28851967›Full record

ArticleScientific reports2017

Generation of a new infectious recombinant prion: a model to understand Gerstmann-Sträussler-Scheinker syndrome.

Saioa R Elezgarai, Natalia Fernández-Borges, Hasier Eraña, Alejandro M Sevillano, Jorge M Charco, Chafik Harrathi, Paula Saá, David Gil, Qingzhong Kong, Jesús R Requena and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  10. Detection of amyloid fibrils in Parkinson's disease using plasmonic chirality.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Journal of virology · 2017
    Article
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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

12 authors at 6 institutions in 3 countries.

Saioa R ElezgaraiCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.
Natalia Fernández-BorgesCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.
Hasier ErañaCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.
Alejandro M SevillanoCIMUS Biomedical Research Institute, University of Santiago de Compostela-IDIS, Santiago de Compostela, Spain.
Jorge M CharcoCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.ORCID 0000-0003-3476-1855
Chafik HarrathiCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.
Paula SaáAmerican Red Cross, Gaithersburg, MD, USA.ORCID 0000-0001-6077-4532
David GilCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain.
Qingzhong KongDepartment of Pathology, Case Western Reserve University, Cleveland, OH, 44106, USA.ORCID 0000-0003-0298-5264
Jesús R RequenaCIMUS Biomedical Research Institute, University of Santiago de Compostela-IDIS, Santiago de Compostela, Spain.
Olivier AndréolettiEcole Nationale du Veterinaire, Service de Pathologie du Bétail, Toulouse, 31076, France.
Joaquín CastillaCIC bioGUNE, Parque tecnológico de Bizkaia, Derio, 48160, Bizkaia, Spain. castilla@joaquincastilla.com.ORCID 0000-0002-2216-1361
CIC bioGUNE · ESUniversidade de Santiago de Compostela · ESAmerican Red Cross · USCase Western Reserve University · USÉcole Nationale Vétérinaire de Toulouse · FRIkerbasque · ES

Funding

Cervid to human prion transmissionR01NS088604 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI KONG, QINGZHONG · 2015 to 2018
$1.4M
NINDS NIH HHS R01 NS088604
6 · The paper itself

Abstract

Human transmissible spongiform encephalopathies (TSEs) or prion diseases are a group of fatal neurodegenerative disorders that include Kuru, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome (GSS), and fatal familial insomnia. GSS is a genetically determined TSE caused by a range of mutations within the prion protein (PrP) gene. Several animal models, based on the expression of PrPs carrying mutations analogous to human heritable prion diseases, support that mutations might predispose PrP to spontaneously misfold. An adapted Protein Misfolding Cyclic Amplification methodology based on the use of human recombinant PrP (recPMCA) generated different self-propagating misfolded proteins spontaneously. These were characterized biochemically and structurally, and the one partially sharing some of the GSS PrP

Indexed as

Recombination, GeneticAmino Acid SubstitutionAnimalsDisease Models, AnimalEvolution, MolecularGerstmann-Straussler-Scheinker DiseaseHumansMiceMice, TransgenicMutationPrion ProteinsProtein AggregatesProtein Aggregation, PathologicalProtein ConformationProtein FoldingSelection, GeneticPrion ProteinsProtein Aggregates

Identifiers

PMID28851967
PMCPMC5575253
OpenAlexW2750223280

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.