ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2021
Schizophrenia risk alleles often affect the expression of many genes and each gene may have a different effect on the risk: A mediation analysis.
Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 0 citations in OpenAlex.
- Identification of Schizophrenia-Risk Regulatory Variant rs1399178 in the Non-coding Region With Its Impact on NRF1 Binding.CNS neuroscience & therapeutics · 2025Article
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- How Variation in Risk Allele Output and Gene Interactions Shape the Genetic Architecture of Schizophrenia.Genes · 2022Article
- Inherited L1 Retrotransposon Insertions Associated With Risk for Schizophrenia and Bipolar Disorder.Schizophrenia bulletin open · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Variants identified by genome-wide association studies (GWAS) are often expression quantitative trait loci (eQTLs), suggesting they are proxies or are themselves regulatory. Across many data sets, analyses show that variants often affect multiple genes. Lacking data on many tissue types, developmental time points, and homogeneous cell types, the extent of this one-to-many relationship is underestimated. This raises questions on whether a disease eQTL target gene explains the genetic association or is a bystander and puts into question the direction of expression effect of on the risk, since the many variants-regulated genes may have opposing effects, imperfectly balancing each other. We used two brain gene expression data sets (CommonMind and BrainSeq) for mediation analysis of schizophrenia-associated variants. We confirm that eQTL target genes often mediate risk but the direction in which expression affects risk is often different from that in which the risk allele changes expression. Of 38 mediator genes significant in both data sets 33 showed consistent mediation direction (Chi
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