ArticleEBioMedicine2019
Identification of the primate-specific gene BTN3A2 as an additional schizophrenia risk gene in the MHC loci.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
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- Integrative multi-omics data from early development to identify the genes and cell types underlying attention-deficit/hyperactivity disorder.BMC psychiatry · 2025Article
- Atlas of Proteomic signatures of brain structure and its links to brain disorders.Nature communications · 2025Article
- Genetic Links Between Subcortical Brain Morphometry and Suicide Attempt Risk in Children and Adults.Human brain mapping · 2025Article
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- Identification of novel therapeutic targets for chronic kidney disease and kidney function by integrating multi-omics proteome with transcriptome.Genome medicine · 2024Article
- Asian-European differentiation of schizophrenia-associated genes driven by admixture and natural selection.iScience · 2024Article
- Significance of an altered lncRNA landscape in schizophrenia and cognition: clues from a case-control association study.European archives of psychiatry and clinical neuroscience · 2023Article
- Comprehensive and integrative analyses identify TYW5 as a schizophrenia risk gene.BMC medicine · 2022Article
- Genetics of common cerebral small vessel disease.Nature reviews. Neurology · 2022Review
- Joint-Tissue Integrative Analysis Identified Hundreds of Schizophrenia Risk Genes.Molecular neurobiology · 2022Article
- Brain age estimation at tract group level and its association with daily life measures, cardiac risk factors and genetic variants.Scientific reports · 2021Article
- Mendelian randomization integrating GWAS and eQTL data revealed genes pleiotropically associated with major depressive disorder.Translational psychiatry · 2021Article
- Low expression of BTN3A3 indicates poor prognosis and promotes cell proliferation, migration and invasion in non-small cell lung cancer.Annals of translational medicine · 2021Article
- SZDB2.0: an updated comprehensive resource for schizophrenia research.Human genetics · 2020Article
- Identification of a functional human-unique 351-bp Alu insertion polymorphism associated with major depressive disorder in the 1p31.1 GWAS risk loci.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Genome-wide association study of MRI markers of cerebral small vessel disease in 42,310 participants.Nature communications · 2020Article
- Further confirmation of netrin 1 receptor (DCC) as a depression risk gene via integrations of multi-omics data.Translational psychiatry · 2020Article
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Authors and funding
13 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundSchizophrenia is a complex mental disorder resulting in poor life quality and high social and economic burden. Despite the fact that genome-wide association studies (GWASs) have successfully identified a number of risk loci for schizophrenia, identifying the causal genes at the risk loci and elucidating their roles in disease pathogenesis remain major challenges.
methodsThe summary data-based Mendelian randomization analysis (SMR) was used to integrate a large-scale GWAS of schizophrenia with brain expression quantitative trait loci (eQTL) data and brain methylation expression quantitative trait loci (meQTL) data, to identify novel risk gene(s) for schizophrenia. We then analyzed the mRNA expression and methylation statuses of the gene hit BTN3A2 during the early brain development. Electrophysiological analyses of CA1 pyramidal neurons were performed to evaluate the excitatory and inhibitory synaptic activity after overexpression of BTN3A2 in rat hippocampal slices. Cell surface binding assay was used to test the interaction of BTN3A2 and neurexins.
findingsWe identified BTN3A2 as a potential risk gene for schizophrenia. The mRNA expression and methylation data showed that BTN3A2 expression in human brain is highest post-natally. Further electrophysiological analyses of rat hippocampal slices showed that BTN3A2 overexpression specifically suppressed the excitatory synaptic activity onto CA1 pyramidal neurons, most likely through its interaction with the presynaptic adhesion molecule neurexins.
interpretationIncreased expression of BTN3A2 might confer risk for schizophrenia by altering excitatory synaptic function. Our result constitutes a paradigm for distilling risk gene using an integrative analysis and functional characterization in the post-GWAS era. FUND: This study was supported by the Strategic Priority Research Program (B) of the Chinese Academy of Sciences (XDB02020003 to Y-GY), the National Natural Science Foundation of China (31730037 to Y-GY), and the Bureau of Frontier Sciences and Education, Chinese Academy of Sciences (QYZDJ-SSW-SMC005 to Y-GY).
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