ArticleHuman molecular genetics2015
Transcriptome outlier analysis implicates schizophrenia susceptibility genes and enriches putatively functional rare genetic variants.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Evolution is in the details: Regulatory differences in modern human and Neanderthal.Computational and structural biotechnology journal · 2025Article
- Lack of Helios During Neural Development Induces Adult Schizophrenia-Like Behaviors Associated With Aberrant Levels of the TRIF-Recruiter Protein WDFY1.Frontiers in cellular neuroscience · 2020Article
- The TMEM106B FTLD-protective variant, rs1990621, is also associated with increased neuronal proportion.Acta neuropathologica · 2020Article
- Dopamine perturbation of gene co-expression networks reveals differential response in schizophrenia for translational machinery.Translational psychiatry · 2018Article
- Transcriptomic signatures of schizophrenia revealed by dopamine perturbation in an ex vivo model.Translational psychiatry · 2018Article
- Transcriptome sequencing study implicates immune-related genes differentially expressed in schizophrenia: new data and a meta-analysis.Translational psychiatry · 2017Article
- SZGR 2.0: a one-stop shop of schizophrenia candidate genes.Nucleic acids research · 2017Article
- Non-Coding Loss-of-Function Variation in Human Genomes.Human heredity · 2016Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
We searched a gene expression dataset comprised of 634 schizophrenia (SZ) cases and 713 controls for expression outliers (i.e., extreme tails of the distribution of transcript expression values) with SZ cases overrepresented compared with controls. These outlier genes were enriched for brain expression and for genes known to be associated with neurodevelopmental disorders. SZ cases showed higher outlier burden (i.e., total outlier events per subject) than controls for genes within copy number variants (CNVs) associated with SZ or neurodevelopmental disorders. Outlier genes were enriched for CNVs and for rare putative regulatory variants, but this only explained a small proportion of the outlier subjects, highlighting the underlying presence of additional genetic and potentially, epigenetic mechanisms.
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