ArticleNeuron2019
Recapitulation and Reversal of Schizophrenia-Related Phenotypes in Setd1a-Deficient Mice.
Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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Who cites it
71 citing papers in PubMed, 136 citations in OpenAlex.
- Establishment of a Common Marmoset Lineage Carrying a Frameshift Mutation in SETD1A, a Schizophrenia Risk Gene.Journal of neurochemistry · 2026Article
- Altered thalamo-prefrontal synchrony dynamics during spatial working memory task performance in a SETD1A loss-of-function mouse model of schizophrenia predisposition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Article
- Identification of autoantibodies against L1CAM in patients with schizophrenia.Brain, behavior, & immunity - health · 2026Article
- Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026Review
- Clinical, cellular, and genomic consequences of a population-enrichedResearch square · 2026Article
- Loss of function of the chromatin remodeling geneProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Setd1a Loss-of-function Disrupts Epigenetic Regulation of Ribosomal Genes via Altered DNA Methylation.Schizophrenia bulletin · 2026Article
- Reducing methylation of histone 3.3 lysine 4 in the medial ganglionic eminence and hypothalamus recapitulates neurodevelopmental disorder phenotypes.Nature communications · 2026Article
- Disorganized Inhibitory Dynamics in Hippocampal area CA1 of 22q11.2 Deletion Mutant Mice.bioRxiv : the preprint server for biology · 2026Article
- Altered thalamo-prefrontal synchrony dynamics during spatial working memory task performance in a SETD1A loss-of-function mouse model of schizophrenia predisposition.bioRxiv : the preprint server for biology · 2026Article
- Dendritic compartment-specific spine formation in layer 5 neurons underlies cortical circuit maturation during adolescence.Science advances · 2026Article
- Review
- SETD1A regulates psychiatric gene networks involved in genomic stability and synaptic function in rare and sporadic schizophrenia.Nature communications · 2025Article
- Mutations of schizophrenia risk gene SETD1A dysregulate synaptic function in human neurons.Molecular psychiatry · 2025Article
- A postnatal molecular switch drives activity-dependent maturation of parvalbumin interneurons.Cell · 2025Article
- Autoantibodies and Inflammation in Schizophrenia.Psychiatry and clinical neurosciences · 2025Review
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 2025Review
- Synaptic Deficits in Adnp-Mutant Mice Are Ameliorated by Histone Demethylase LSD1 Inhibition.Autism research : official journal of the International Society for Autism Research · 2025Article
- Recapitulation and reversal of neuropsychiatric phenotypes in a mouse model of human endogenous retrovirus type W expression.Molecular psychiatry · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
SETD1A, a lysine-methyltransferase, is a key schizophrenia susceptibility gene. Mice carrying a heterozygous loss-of-function mutation of the orthologous gene exhibit alterations in axonal branching and cortical synaptic dynamics accompanied by working memory deficits. We show that Setd1a binds both promoters and enhancers with a striking overlap between Setd1a and Mef2 on enhancers. Setd1a targets are highly expressed in pyramidal neurons and display a complex pattern of transcriptional up- and downregulations shaped by presumed opposing functions of Setd1a on promoters and Mef2-bound enhancers. Notably, evolutionarily conserved Setd1a targets are associated with neuropsychiatric genetic risk burden. Reinstating Setd1a expression in adulthood rescues cognitive deficits. Finally, we identify LSD1 as a major counteracting demethylase for Setd1a and show that its pharmacological antagonism results in a full rescue of the behavioral and morphological deficits in Setd1a-deficient mice. Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.
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Registered trials
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.