ArticleMolecular psychiatry2023
Psychiatric risk gene Transcription Factor 4 (TCF4) regulates the density and connectivity of distinct inhibitory interneuron subtypes.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Molecular and neural circuit mechanisms of parvalbumin (PV) neurons in depression: Insights and advances.iScience · 2026Review
- Transcription Factors in the Pathogenesis of Schizophrenia.Life (Basel, Switzerland) · 2026Review
- Article
- Selective enrichment of TCF4 in GABAergic neurons during postnatal primate development.Frontiers in neuroanatomy · 2026Article
- Distinct molecular patterns in R6/2 HD mouse brain: Insights from spatiotemporal transcriptomics.Neuron · 2025Article
- Tcf4 Deficiency causes recurrent seizures in mice.Progress in neurobiology · 2025Article
- Review
- Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons.Nature communications · 2025Article
- Fast-spiking parvalbumin-positive interneurons: new perspectives of treatment and future challenges in dementia.Molecular psychiatry · 2025Review
- Transcription factor 4 expression in the developing non-human primate brain: a comparative analysis with the mouse brain.Frontiers in neuroanatomy · 2024Article
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10 authors at 3 institutions in 1 country.
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Abstract
Transcription factor 4 (TCF4) is a basic helix-loop-helix transcription factor that is implicated in a variety of psychiatric disorders including autism spectrum disorder (ASD), major depression, and schizophrenia. Autosomal dominant mutations in TCF4 are causal for a specific ASD called Pitt-Hopkins Syndrome (PTHS). However, our understanding of etiological and pathophysiological mechanisms downstream of TCF4 mutations is incomplete. Single cell sequencing indicates TCF4 is highly expressed in GABAergic interneurons (INs). Here, we performed cell-type specific expression analysis (CSEA) and cellular deconvolution (CD) on bulk RNA sequencing data from 5 different PTHS mouse models. Using CSEA we observed differentially expressed genes (DEGs) were enriched in parvalbumin expressing (PV+) INs and CD predicted a reduction in the PV+ INs population. Therefore, we investigated the role of TCF4 in regulating the development and function of INs in the Tcf4
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