ArticleProceedings of the National Academy of Sciences of the United States of America2016
Reversal of dendritic phenotypes in 16p11.2 microduplication mouse model neurons by pharmacological targeting of a network hub.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Review
- Functional impact of genetic background on variable expressivity in neurodevelopmental disorders.Nature communications · 2026Article
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- Mapping spatially organized molecular and genetic signatures of schizophrenia across multiple scales in human prefrontal cortex.bioRxiv : the preprint server for biology · 2026Article
- Article
- βIV spectrin abundancy, cellular distribution and sensitivity to AKT/GSK3 regulation in schizophrenia.Molecular psychiatry · 2025Article
- Circulating Blood-Based Proteins in Psychopathology and Cognition: A Mendelian Randomization Study.JAMA psychiatry · 2025Article
- Nucleus Accumbens Proteome Disbalance in an Adolescent Mouse Model of Schizophrenia and Nicotine Misuse Comorbidity.Biomedicines · 2025Article
- Neurological Insights into 16p11.2- And 22q11.2-Related Disorders: A Mini-Review.Current genomics · 2025Review
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- Large-Scale Mendelian Randomization Study Reveals Circulating Blood-based Proteomic Biomarkers for Psychopathology and Cognitive Task Performance.medRxiv : the preprint server for health sciences · 2024Article
- Mechanisms of copy number variants in neuropsychiatric disorders: From genes to therapeutics.Current opinion in neurobiology · 2023Review
- Multiple genes in a single GWAS risk locus synergistically mediate aberrant synaptic development and function in human neurons.Cell genomics · 2023Article
- Lithium rescues dendritic abnormalities in Ank3 deficiency models through the synergic effects of GSK3β and cyclic AMP signaling pathways.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- The molecular pathology of schizophrenia: an overview of existing knowledge and new directions for future research.Molecular psychiatry · 2023Review
- TAOK2 rescues autism-linked developmental deficits in a 16p11.2 microdeletion mouse model.Molecular psychiatry · 2022Article
- Tissue- and cell-type-specific molecular and functional signatures of 16p11.2 reciprocal genomic disorder across mouse brain and human neuronal models.American journal of human genetics · 2022Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The architecture of dendritic arbors contributes to neuronal connectivity in the brain. Conversely, abnormalities in dendrites have been reported in multiple mental disorders and are thought to contribute to pathogenesis. Rare copy number variations (CNVs) are genetic alterations that are associated with a wide range of mental disorders and are highly penetrant. The 16p11.2 microduplication is one of the CNVs most strongly associated with schizophrenia and autism, spanning multiple genes possibly involved in synaptic neurotransmission. However, disease-relevant cellular phenotypes of 16p11.2 microduplication and the driver gene(s) remain to be identified. We found increased dendritic arborization in isolated cortical pyramidal neurons from a mouse model of 16p11.2 duplication (dp/+). Network analysis identified MAPK3, which encodes ERK1 MAP kinase, as the most topologically important hub in protein-protein interaction networks within the 16p11.2 region and broader gene networks of schizophrenia-associated CNVs. Pharmacological targeting of ERK reversed dendritic alterations associated with dp/+ neurons, outlining a strategy for the analysis and reversal of cellular phenotypes in CNV-related psychiatric disorders.
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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.