ArticlePloS one2007
Nogo Receptor 1 (RTN4R) as a candidate gene for schizophrenia: analysis using human and mouse genetic approaches.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 77 citations in OpenAlex.
- PICK1 links KIBRA and AMPA receptor subunit GluA2 in coiled-coil-driven supramolecular complexes.The Journal of biological chemistry · 2025Article
- Genomic and Reverse Translational Analysis Discloses a Role for Small GTPase RhoA Signaling in the Pathogenesis of Schizophrenia: Rho-Kinase as a Novel Drug Target.International journal of molecular sciences · 2023Review
- 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
- The 22q11.2 region regulates presynaptic gene-products linked to schizophrenia.Nature communications · 2022Article
- 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
- Molecular genetics of 22q11.2 deletion syndrome.American journal of medical genetics. Part A · 2018Review
- 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
- A fast and powerful W-test for pairwise epistasis testing.Nucleic acids research · 2016Article
- Identification of genetic variants of LGI1 and RTN4R (NgR1) linked to schizophrenia that are defective in NgR1-LGI1 signaling.Molecular genetics & genomic medicine · 2016Article
- Article
- Genetic variants in Nogo receptor signaling pathways may be associated with early life adversity in schizophrenia susceptibility.BBA clinical · 2015Article
- Nogo-A-deficient Transgenic Rats Show Deficits in Higher Cognitive Functions, Decreased Anxiety, and Altered Circadian Activity Patterns.Frontiers in behavioral neuroscience · 2014Article
- Copy number variation at 22q11.2: from rare variants to common mechanisms of developmental neuropsychiatric disorders.Molecular psychiatry · 2013Review
- Article
- N-Methyl-d-Aspartate Receptor - Nitric Oxide Synthase Pathway in the Cortex of Nogo-A-Deficient Rats in Relation to Brain Laterality and Schizophrenia.Frontiers in behavioral neuroscience · 2013Article
- An environmental analysis of genes associated with schizophrenia: hypoxia and vascular factors as interacting elements in the neurodevelopmental model.Molecular psychiatry · 2012Review
- Avoiding mouse traps in schizophrenia genetics: lessons and promises from current and emerging mouse models.Neuroscience · 2012Review
- Molecular mechanisms in 22q11 deletion syndrome.Schizophrenia bulletin · 2011Review
- Contribution of nonprimate animal models in understanding the etiology of schizophrenia.Journal of psychiatry & neuroscience : JPN · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundNOGO Receptor 1 (RTN4R) regulates axonal growth, as well as axon regeneration after injury. The gene maps to the 22q11.2 schizophrenia susceptibility locus and is thus a strong functional and positional candidate gene. METHODOLOGY/PRINCIPAL
findingsWe evaluate evidence for genetic association between common RTN4R polymorphisms and schizophrenia in a large family sample of Afrikaner origin and screen the exonic sequence of RTN4R for rare variants in an independent sample from the U.S. We also employ animal model studies to assay a panel of schizophrenia-related behavioral tasks in an Rtn4r-deficient mouse model. We found weak sex-specific evidence for association between common RTN4R polymorphisms and schizophrenia in the Afrikaner patients. In the U.S. sample, we identified two novel non-conservative RTN4R coding variants in two patients with schizophrenia that were absent in 600 control chromosomes. In our complementary mouse model studies, we identified a haploinsufficient effect of Rtn4r on locomotor activity, but normal performance in schizophrenia-related behavioral tasks. We also provide evidence that Rtn4r deficiency can modulate the long-term behavioral effects of transient postnatal N-methyl-D-aspartate (NMDA) receptor hypofunction.
conclusionsOur results do not support a major role of RTN4R in susceptibility to schizophrenia or the cognitive and behavioral deficits observed in individuals with 22q11 microdeletions. However, they suggest that RTN4R may modulate the genetic risk or clinical expression of schizophrenia in a subset of patients and identify additional studies that will be necessary to clarify the role of RTN4R in psychiatric phenotypes. In addition, our results raise interesting issues about evaluating the significance of rare genetic variants in disease and their role in causation.
Indexed as
Identifiers
What OpenQuestion holds
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.