Evidence map›Paper›PMID 27988204›Full record

ArticleCellular signalling2017

SMAD transcription factors are altered in cell models of HD and regulate HTT expression.

K R Bowles, T Stone, P Holmans, N D Allen, S B Dunnett, L Jones

Open access · hybridAbstract read
In one paragraph

Article in Cellular signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. NEDD4L induces mitochondrial dysfunction and neurodegeneration by promoting LIPT2 degradation in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

6 authors at 1 institution in 1 country.

K R BowlesThe MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff CF24 4HQ, UK. Electronic address: kathryn.bowles@mssm.edu.
T StoneThe MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff CF24 4HQ, UK. Electronic address: stonetc@cardiff.ac.uk.
P HolmansThe MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff CF24 4HQ, UK. Electronic address: holmanspa@cardiff.ac.uk.
N D AllenCardiff School of Biosciences, The Sir Martin Evans Building, Museum Avenue, Cardiff CF10 3AX, UK. Electronic address: allennd@cardiff.ac.uk.
S B DunnettThe Brain Repair Group, School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, UK. Electronic address: dunnettsb@Cardiff.ac.uk.
L JonesThe MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University School of Medicine, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff CF24 4HQ, UK. Electronic address: jonesl1@cardiff.ac.uk.
Cardiff University · GB

Funding

Medical Research Council MR/L023784/1Medical Research Council MR/L023784/2Wellcome TrustWellcome Trust 089640/Z/09/Z
6 · The paper itself

Abstract

Transcriptional dysregulation is observable in multiple animal and cell models of Huntington's disease, as well as in human blood and post-mortem caudate. This contributes to HD pathogenesis, although the exact mechanism by which this occurs is unknown. We therefore utilised a dynamic model in order to determine the differential effect of growth factor stimulation on gene expression, to highlight potential alterations in kinase signalling pathways that may be in part responsible for the transcriptional dysregulation observed in HD, and which may reveal new therapeutic targets. We demonstrate that cells expressing mutant huntingtin have a dysregulated transcriptional response to epidermal growth factor stimulation, and identify the transforming growth factor-beta pathway as a novel signalling pathway of interest that may regulate the expression of the Huntingtin (HTT) gene itself. The dysregulation of HTT expression may contribute to the altered transcriptional phenotype observed in HD.

Indexed as

Gene Expression RegulationModels, BiologicalAnimalsCluster AnalysisGene Expression ProfilingHumansHuntingtin ProteinHuntington DiseaseInduced Pluripotent Stem CellsMiceMolecular Sequence AnnotationMutationNeural Stem CellsPhosphorylationPromoter Regions, GeneticSignal TransductionHuntingtin ProteinSmad ProteinsTransforming Growth Factor betaEGFHuntington's DiseaseKinase signallingSMADTGF-betaTranscription

Identifiers

PMID27988204
PMCPMC5310119
OpenAlexW2567634772

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.