Evidence map›Paper›PMID 27689884›Full record

ArticleJournal of psychiatry & neuroscience : JPN2017

Knockdown of the schizophrenia susceptibility gene

Matthew J Hill, Richard Killick, Katherinne Navarrete, Aleksandra Maruszak, Gemma M McLaughlin, Brenda P Williams, Nicholas J Bray

Open access · bronzeAbstract read
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Psychiatric Genomics 2025: State of the Art and the Path Forward.The Psychiatric clinics of North America · 2025
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  9. Review
  10. Review
  11. Article
  12. Daughterless, theDisease models & mechanisms · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Genetic association and functional characterization of MCPH1 gene variation in bipolar disorder and schizophrenia.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. Recent Advances in the Genetics of Schizophrenia.Molecular neuropsychiatry · 2018
    Review
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

7 authors at 2 institutions in 1 country.

Matthew J HillFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Richard KillickFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Katherinne NavarreteFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Aleksandra MaruszakFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Gemma M McLaughlinFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Brenda P WilliamsFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
Nicholas J BrayFrom the Department of Basic and Clinical Neuroscience, King's College London, London, UK (Hill, Killick, Maruszak, McLaughlin, Williams, Bray); the MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK (Navarrete); Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK (Hill); and the MRC Centre for Neuropsychiatric Genetics & Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK (Bray).
King's College London · GBCardiff University · GB

Funding

Medical Research Council G0802166Medical Research Council MR/L010305/1
6 · The paper itself

Abstract

backgroundCommon variants in the

methodsTo explore molecular and cellular mechanisms by which TCF4 perturbation could interfere with human cortical development, we experimentally reduced the endogenous expression of TCF4 in a neural progenitor cell line derived from the developing human cerebral cortex using RNA interference. Effects on genome-wide gene expression were assessed by microarray, followed by Gene Ontology and pathway analysis of differentially expressed genes. We tested for genetic association between the set of differentially expressed genes and schizophrenia using genome-wide association study data from the Psychiatric Genomics Consortium and competitive gene set analysis (MAGMA). Effects on cell proliferation were assessed using high content imaging.

resultsGenes that were differentially expressed following TCF4 knockdown were highly enriched for involvement in the cell cycle. There was a nonsignificant trend for genetic association between the differentially expressed gene set and schizophrenia. Consistent with the gene expression data, TCF4 knockdown was associated with reduced proliferation of cortical progenitor cells in vitro. LIMITATIONS: A detailed mechanistic explanation of how TCF4 knockdown alters human neural progenitor cell proliferation is not provided by this study.

conclusionOur data indicate effects of TCF4 perturbation on human cortical progenitor cell proliferation, a process that could contribute to cognitive deficits in individuals with Pitt-Hopkins syndrome and risk for schizophrenia.

Indexed as

Cell LineCell ProliferationCerebral CortexGene Expression Regulation, DevelopmentalGene OntologyGenetic Association StudiesGenetic Predisposition to DiseaseHumansMicroarray AnalysisNeural Stem CellsRNA InterferenceSchizophreniaTranscription Factor 4TCF4 protein, humanTranscription Factor 4

Identifiers

PMID27689884
PMCPMC5403663
OpenAlexW2532246947

What OpenQuestion holds

Textmetadata
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.