ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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55 citing papers in PubMed, 106 citations in OpenAlex.
- Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion.Molecular psychiatry · 2026Article
- An exploratory fetal MRI study examining the impact of 22q11.2 microdeletion syndrome on early brain growth.Journal of neurodevelopmental disorders · 2025Article
- Dysregulation of myelination-related genes in schizophrenia.Journal of neurochemistry · 2024Review
- NgR1 binding to reovirus reveals an unusual bivalent interaction and a new viral attachment protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Synaptic Plasticity Dysfunctions in the Pathophysiology of 22q11 Deletion Syndrome: Is There a Role for Astrocytes?International journal of molecular sciences · 2022Review
- Opposing white matter microstructure abnormalities in 22q11.2 deletion and duplication carriers.Translational psychiatry · 2021Article
- The CNS/PNS Extracellular Matrix Provides Instructive Guidance Cues to Neural Cells and Neuroregulatory Proteins in Neural Development and Repair.International journal of molecular sciences · 2021Review
- Nogo-A aggravates oxidative damage in oligodendrocytes.Neural regeneration research · 2021Article
- Identifying neurodevelopmental anomalies of white matter microstructure associated with high risk for psychosis in 22q11.2DS.Translational psychiatry · 2020Article
- That's a Wrap! Molecular Drivers Governing Neuronal Nogo Receptor-Dependent Myelin Plasticity and Integrity.Frontiers in cellular neuroscience · 2020Review
- Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Oxytocin pathway gene networks in the human brain.Nature communications · 2019Article
- The nociceptin receptor inhibits axonal regeneration and recovery from spinal cord injury.Science signaling · 2018Article
- The rs696880 Polymorphism in the Nogo-A Receptor Gene (Frontiers in aging neuroscience · 2018Article
- A novel rare variant R292H in RTN4R affects growth cone formation and possibly contributes to schizophrenia susceptibility.Translational psychiatry · 2017Article
- Emerging genotype-phenotype relationships in patients with large NF1 deletions.Human genetics · 2017Review
- Nogo-A Antibodies for Progressive Multiple Sclerosis.CNS drugs · 2017Review
- Spatiotemporal and Long Lasting Modulation of 11 Key Nogo Signaling Genes in Response to Strong Neuroexcitation.Frontiers in molecular neuroscience · 2017Article
- Erasure of fear memories is prevented by Nogo Receptor 1 in adulthood.Molecular psychiatry · 2016Article
- A fast and powerful W-test for pairwise epistasis testing.Nucleic acids research · 2016Article
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19 authors at 3 institutions in 3 countries.
Funding
Abstract
In schizophrenia, genetic predisposition has been linked to chromosome 22q11 and myelin-specific genes are misexpressed in schizophrenia. Nogo-66 receptor 1 (NGR or RTN4R) has been considered to be a 22q11 candidate gene for schizophrenia susceptibility because it encodes an axonal protein that mediates myelin inhibition of axonal sprouting. Confirming previous studies, we found that variation at the NGR locus is associated with schizophrenia in a Caucasian case-control analysis, and this association is not attributed to population stratification. Within a limited set of schizophrenia-derived DNA samples, we identified several rare NGR nonconservative coding sequence variants. Neuronal cultures demonstrate that four different schizophrenia-derived NgR1 variants fail to transduce myelin signals into axon inhibition, and function as dominant negatives to disrupt endogenous NgR1. This provides the first evidence that certain disease-derived human NgR1 variants are dysfunctional proteins in vitro. Mice lacking NgR1 protein exhibit reduced working memory function, consistent with a potential endophenotype of schizophrenia. For a restricted subset of individuals diagnosed with schizophrenia, the expression of dysfunctional NGR variants may contribute to increased disease risk.
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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.