ArticleAmerican journal of human genetics2018
Landscape of Conditional eQTL in Dorsolateral Prefrontal Cortex and Co-localization with Schizophrenia GWAS.
Article in American journal of human genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 7 of them syntheses that pooled it.
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Who cites it
94 citing papers in PubMed, 7 syntheses or guidelines pooled it.
- Integrating cell-type-specific gene expression and genome-wide associations identifies risk genes for schizophrenia.Molecular psychiatry · 2026Pooled it
- Cross-population GWAS and proteomics improve risk prediction and reveal mechanisms in atrial fibrillation.Nature communications · 2025Pooled it
- Adipose tissue eQTL meta-analysis highlights the contribution of allelic heterogeneity to gene expression regulation and cardiometabolic traits.Nature genetics · 2025Pooled it
- Depression pathophysiology, risk prediction of recurrence and comorbid psychiatric disorders using genome-wide analyses.Nature medicine · 2023Pooled it
- Population-scale analysis of common and rare genetic variation associated with hearing loss in adults.Communications biology · 2022Pooled it
- Multi-ancestry eQTL meta-analysis of human brain identifies candidate causal variants for brain-related traits.Nature genetics · 2022Pooled it
- Pleiotropic Meta-Analysis of Cognition, Education, and Schizophrenia Differentiates Roles of Early Neurodevelopmental and Adult Synaptic Pathways.American journal of human genetics · 2019Pooled it
- Dynamic neuro-immune regulation of psychiatric risk loci in human neurons.Nature communications · 2026Article
- Article
- Higher eQTL power reveals signals that boost GWAS colocalization.American journal of human genetics · 2026Article
- Multimodal bioinformatic analyses of genome-scale expression beyond gene-centric differential expression.Briefings in bioinformatics · 2026Review
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- Exploring Endoplasmic Reticulum Stress in Gestational Diabetes Mellitus: MultiOmics Insights Through Mendelian Randomization.International journal of women's health · 2026Article
- Multi-omics identifies a T2DM-associated immune-regulatory network modulated by electroacupuncture.Frontiers in endocrinology · 2026Article
- A novel DCSTAMP antagonist impedes preosteoclast fusion via modulation of RAP1B-RAC1-mediated cytoskeletal remodeling.Experimental & molecular medicine · 2025Article
- The role of circadian rhythm-related genes in type 2 diabetes from a multi-omics perspective.Journal of global health · 2025Article
- Higher eQTL power reveals signals that boost GWAS colocalization.bioRxiv : the preprint server for biology · 2025Article
- Genetic effects on chromatin accessibility uncover mechanisms of liver gene regulation and quantitative traits.Genome research · 2025Article
- Investigating the potential of oxidative stress-related gene as predictive markers in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Psychiatric Genomics 2025: State of the Art and the Path Forward.The Psychiatric clinics of North America · 2025Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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22 authors.
Funding
Abstract
Causal genes and variants within genome-wide association study (GWAS) loci can be identified by integrating GWAS statistics with expression quantitative trait loci (eQTL) and determining which variants underlie both GWAS and eQTL signals. Most analyses, however, consider only the marginal eQTL signal, rather than dissect this signal into multiple conditionally independent signals for each gene. Here we show that analyzing conditional eQTL signatures, which could be important under specific cellular or temporal contexts, leads to improved fine mapping of GWAS associations. Using genotypes and gene expression levels from post-mortem human brain samples (n = 467) reported by the CommonMind Consortium (CMC), we find that conditional eQTL are widespread; 63% of genes with primary eQTL also have conditional eQTL. In addition, genomic features associated with conditional eQTL are consistent with context-specific (e.g., tissue-, cell type-, or developmental time point-specific) regulation of gene expression. Integrating the 2014 Psychiatric Genomics Consortium schizophrenia (SCZ) GWAS and CMC primary and conditional eQTL data reveals 40 loci with strong evidence for co-localization (posterior probability > 0.8), including six loci with co-localization of conditional eQTL. Our co-localization analyses support previously reported genes, identify novel genes associated with schizophrenia risk, and provide specific hypotheses for their functional follow-up.
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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.