Evidence map›Paper›PMID 34518368›Full record

ArticleeNeuro

Isoform-Specific Reduction of the Basic Helix-Loop-Helix Transcription Factor TCF4 Levels in Huntington's Disease.

Kaja Nurm, Mari Sepp, Carla Castany-Pladevall, Jordi Creus-Muncunill, Jürgen Tuvikene, Alex Sirp, Hanna Vihma, Derek J Blake, Esther Perez-Navarro, Tõnis Timmusk

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

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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 3 institutions in 3 countries.

Kaja NurmDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia.
Mari SeppDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia.ORCID 0000-0003-1733-8385
Carla Castany-PladevallDepartament de Biomedicina, Facultat de Medicina i Ciències de la Salut, Institut de Neurociències, Universitat de Barcelona, Barcelona, Catalonia 08036, Spain.
Jordi Creus-MuncunillDepartament de Biomedicina, Facultat de Medicina i Ciències de la Salut, Institut de Neurociències, Universitat de Barcelona, Barcelona, Catalonia 08036, Spain.
Jürgen TuvikeneDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia.ORCID 0000-0002-9665-760X
Alex SirpDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia.
Hanna VihmaDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia.
Derek J BlakeDivision of Psychological Medicine and Clinical Neurosciences, MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff CF24 4HQ, United Kingdom.ORCID 0000-0002-5005-4731
Esther Perez-NavarroDepartament de Biomedicina, Facultat de Medicina i Ciències de la Salut, Institut de Neurociències, Universitat de Barcelona, Barcelona, Catalonia 08036, Spain.
Tõnis TimmuskDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn 12618, Estonia tonis.timmusk@taltech.ee.
Tallinn University of Technology · EEBiomedical Research Networking Center on Neurodegenerative Diseases · ESCardiff University · GB

Funding

Medical Research Council MR/L010305/1
6 · The paper itself

Abstract

Huntington's disease (HD) is an inherited neurodegenerative disorder with onset of characteristic motor symptoms at midlife, preceded by subtle cognitive and behavioral disturbances. Transcriptional dysregulation emerges early in the disease course and is considered central to HD pathogenesis. Using wild-type (wt) and HD knock-in mouse striatal cell lines we observed a HD genotype-dependent reduction in the protein levels of transcription factor 4 (TCF4), a member of the basic helix-loop-helix (bHLH) family with critical roles in brain development and function. We characterized mouse

Indexed as

Huntington DiseaseAdultAnimalsDisease Models, AnimalHippocampusHumansMaleMiceMice, TransgenicNeuronsProtein IsoformsTranscription Factor 4Protein IsoformsTCF4 protein, humanTranscription Factor 4basic helix-loop-helix transcription factorHuntington’s diseaseneurodegenerative diseaseTCF4transcriptional regulation

Identifiers

PMID34518368
PMCPMC8519306
OpenAlexW3201117512

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.