Evidence map›Paper›PMID 34065232›Full record

ArticleInternational journal of molecular sciences2021

Tau Exon 10 Inclusion by PrP

Laia Lidón, Laura Llaó-Hierro, Mario Nuvolone, Adriano Aguzzi, Jesús Ávila, Isidro Ferrer, José Antonio Del Río, Rosalina Gavín

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. 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

8 authors at 3 institutions in 3 countries.

Laia LidónMolecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Scientific Park of Barcelona, The Barcelona Institute for Science and Technology (BIST), 08028 Barcelona, Spain.ORCID 0000-0002-2083-3515
Laura Llaó-HierroMolecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Scientific Park of Barcelona, The Barcelona Institute for Science and Technology (BIST), 08028 Barcelona, Spain.
Mario NuvoloneAmyloidosis Research and Treatment Center, Foundation IRCCS Policlinico San Matteo, Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy.
Adriano AguzziInstitute of Neuropathology, University Hospital of Zurich, 8091 Zurich, Switzerland.
Jesús ÁvilaNetwork Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, 28031 Madrid, Spain.ORCID 0000-0002-6288-0571
Isidro FerrerNetwork Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, 28031 Madrid, Spain.ORCID 0000-0001-9888-8754
José Antonio Del RíoMolecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Scientific Park of Barcelona, The Barcelona Institute for Science and Technology (BIST), 08028 Barcelona, Spain.ORCID 0000-0002-5214-4909
Rosalina GavínMolecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Scientific Park of Barcelona, The Barcelona Institute for Science and Technology (BIST), 08028 Barcelona, Spain.ORCID 0000-0003-1982-2162
Instituto de Salud Carlos III · ESUniversity Hospital of Zurich · CHUniversity of Pavia · IT

Funding

CERCA Programme, the Spanish Ministry of Education and Professional Formation FPU15/02705CIBERNED CMED2018-2Commission for Universities and Research of the Department of Innovation, Universities, and Enterprise of the Generalitat de Catalunya SGR2017-648"la Caixa" Foundation (ID 100010434) LCF/PR/HR19/52160007María de Maeztu Unit of Excellence (Institute of Neurosciences, University of Barcelona) MDM-2017-0729Spanish Ministry of Science, Innovation and Universities RTI2018-099773-B-I00
6 · The paper itself

Abstract

Tau protein is largely responsible for tauopathies, including Alzheimer's disease (AD), where it accumulates in the brain as insoluble aggregates. Tau mRNA is regulated by alternative splicing, and inclusion or exclusion of exon 10 gives rise to the 3R and 4R isoforms respectively, whose balance is physiologically regulated. In this sense, one of the several factors that regulate alternative splicing of tau is GSK3β, whose activity is inhibited by the cellular prion protein (PrP

Indexed as

AdultAgedAged, 80 and overAlternative SplicingAlzheimer DiseaseAnimalsBrainDisease Models, AnimalDown-RegulationExonsFemaleGlycogen Synthase Kinase 3 betaHumansInclusion BodiesMaleMiceGlycogen Synthase Kinase 3 betaPrionsProtein IsoformsRNA, Messengertau Proteinsalternative splicingAlzheimer’s diseasecellular prion proteinGSK3βmicrotubule-associated protein tautauopathies

Identifiers

PMID34065232
PMCPMC8161268
OpenAlexW3163675851

What Socratic 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 Socratic graph.