Back to search

Article

Cross-Platform Validation of Neurotransmitter Release Impairments in Schizophrenia Patient-Derived <i>NRXN1</i> -Mutant Neurons

2020-11-03

Abstract excerpt

<h4>ABSTRACT</h4> Heterozygous NRXN1 deletions constitute the most prevalent currently known single-gene mutation predisposing to schizophrenia. Previous studies showed that engineered heterozygous NRXN1 deletions impaired neurotransmitter release in human neurons, suggesting a synaptic pathophysiological mechanism. Utilizing this observation for drug discovery, however, requires confidence in its robustness an...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
5f80f45b-95d0-5cfe-bbae-9d858d659306
DOI
10.1101/2020.11.03.366617
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
Cross-Platform Validation of Neurotransmitter Release Impairments in Schizophrenia Patient-Derived <i>NRXN1</i> -Mutant NeuronsDOI 10.1101/2020.11.03.366617
Cross-platform validation of neurotransmitter release impairments in schizophrenia patient-derived NRXN1-mutant neurons.Semantic proximity
Human Neuropsychiatric Disease Modeling using Conditional Deletion Reveals Synaptic Transmission Defects Caused by Heterozygous Mutations in NRXN1.Semantic proximity
Distinct Synaptic Mechanisms Drive <i>NRXN1</i> Variant-Mediated Pathogenesis in iPSC-Derived Neuronal Models of Autism and SchizophreniaSemantic proximity
Assessing the impact of mono- and bi-allelic deletions in <i>NRXN1</i> on synaptic functionSemantic proximity
<i>SCN1A</i> -deficient hiPSC-derived excitatory neuronal networks display mutation-specific phenotypesSemantic proximity
Distinctive <i>in vitro</i> phenotypes in iPSC-derived neurons from patients with gain- and loss-of-function <i>SCN2A</i> developmental and epileptic encephalopathySemantic proximity
Unraveling Mechanisms of Patient-Specific NRXN1 Mutations in Neuropsychiatric Diseases Using Human Induced Pluripotent Stem Cells.Semantic proximity
<i>CNTN5</i> <sup>−/+</sup> or <i>EHMT2</i> <sup>−/+</sup> iPSC-Derived Neurons from Individuals with Autism Develop Hyperactive Neuronal NetworksSemantic proximity
Schizophrenia-associated <i>NRXN1</i> deletions induce developmental-timing- and cell-type-specific vulnerabilities in human brain organoidsSemantic proximity
Enlisting hESCs to Interrogate Genetic Variants Associated with Neuropsychiatric Disorders.Semantic proximity
GABAergic neuron dysregulation in a human neurodevelopmental model for major psychiatric disordersSemantic proximity
Cellular phenotypes associated with NRXN1 mutations in autism : an iPSC studySemantic proximity
Select a neighboring publication to make it the new centre.