ArticleNPJ schizophrenia2017
Patient-derived hiPSC neurons with heterozygous CNTNAP2 deletions display altered neuronal gene expression and network activity.
Article in NPJ schizophrenia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Loss of function of the chromatin remodeling geneProceedings of the National Academy of Sciences of the United States of America · 2026Article
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Human stem cell-based models to study synaptic dysfunction and cognition in schizophrenia: A narrative review.Schizophrenia research · 2024Review
- nlr-1/CNTNAP regulates dopamine circuit structure and foraging behaviors in C. elegans.Communications biology · 2024Article
- Article
- A Missense Pathogenic Variant in a Conserved Region ofMolecular syndromology · 2023Article
- Current advancements of modelling schizophrenia using patient-derived induced pluripotent stem cells.Acta neuropathologica communications · 2022Review
- Transcription-associated DNA DSBs activate p53 during hiPSC-based neurogenesis.Scientific reports · 2022Article
- Sex-Specific Cannabidiol- and Iloperidone-Induced Neuronal Activity Changes in an In Vitro MAM Model System of Schizophrenia.International journal of molecular sciences · 2021Article
- Is pseudoexfoliation glaucoma a neurodegenerative disorder?Journal of biosciences · 2021Review
- Investigation of de novo mutations in a schizophrenia case-parent trio by induced pluripotent stem cell-based in vitro disease modeling: convergence of schizophrenia- and autism-related cellular phenotypes.Stem cell research & therapy · 2020Article
- Exploring the mechanisms underlying excitation/inhibition imbalance in human iPSC-derived models of ASD.Molecular autism · 2020Review
- CRISPR-based functional evaluation of schizophrenia risk variants.Schizophrenia research · 2020Article
- Intronic Variant inFrontiers in pediatrics · 2020Article
- Investigation of Schizophrenia with Human Induced Pluripotent Stem Cells.Advances in neurobiology · 2020Review
- Imaging Flow Cytometry Quantifies Neural Genome Dynamics.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2019Article
- Cross-species models of attention-deficit/hyperactivity disorder and autism spectrum disorder: lessons from CNTNAP2, ADGRL3, and PARK2.Psychiatric genetics · 2019Review
- New considerations for hiPSC-based models of neuropsychiatric disorders.Molecular psychiatry · 2019Review
- Robust Generation of Person-Specific, Synchronously Active Neuronal Networks Using Purely Isogenic Human iPSC-3D Neural Aggregate Cultures.Frontiers in neuroscience · 2019Article
- An integrated biomanufacturing platform for the large-scale expansion and neuronal differentiation of human pluripotent stem cell-derived neural progenitor cells.Acta biomaterialia · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variants in CNTNAP2, a member of the neurexin family of genes that function as cell adhesion molecules, have been associated with multiple neuropsychiatric conditions such as schizophrenia, autism spectrum disorder and intellectual disability; animal studies indicate a role for CNTNAP2 in axon guidance, dendritic arborization and synaptogenesis. We previously reprogrammed fibroblasts from a family trio consisting of two carriers of heterozygous intragenic CNTNAP2 deletions into human induced pluripotent stem cells (hiPSCs) and described decreased migration in the neural progenitor cells (NPCs) differentiated from the affected CNTNAP2 carrier in this trio. Here, we report the effect of this heterozygous intragenic deletion in CNTNAP2 on global gene expression and neuronal activity in the same cohort. Our findings suggest that heterozygous CNTNAP2 deletions affect genes involved in neuronal development and neuronal activity; however, these data reflect only one family trio and therefore more deletion carriers, with a variety of genetic backgrounds, will be needed to understand the molecular mechanisms underlying CNTNAP2 deletions.
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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.