ArticleCell genomics2025
Multiomic QTL mapping reveals phenotypic complexity of GWAS loci and prioritizes putative causal variants.
Article in Cell genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Article
- Post-genome-wide association study variant-to-function challenges in asthma research.The Journal of allergy and clinical immunology · 2026Review
- Genome-wide association analyses highlight the neuronal contribution to multiple sclerosis susceptibility.Nature genetics · 2026Article
- Comparing machine learning methods predicting transcriptome from epigenome with applications to association studies.Genome biology · 2026Article
- FastGxC: Fast and powerful context-specific eQTL mapping in bulk and single-cell data.Cell genomics · 2026Article
- Predicting gene-specific regulation with transcriptomic and epigenetic single-cell data.Bioinformatics (Oxford, England) · 2026Article
- Regulatory risk loci link disrupted androgen response to the pathophysiology of polycystic ovary syndrome.Journal of the Endocrine Society · 2026Article
- Mapping functional non-coding variation in individual human genomes through haplotyping, multiomics, and deep learning.Nature communications · 2026Article
- A meta-analysis of chromatin-associated loci provides insights into mechanistic interpretations of trait heritability.bioRxiv : the preprint server for biology · 2026Article
- Expanded chromatin accessibility mapping explains genetic variation associated with complex traits in liver.American journal of human genetics · 2026Article
- Farm animal evolution demonstrates hidden molecular basis of human traits.bioRxiv : the preprint server for biology · 2026Article
- Leveraging low-cost short-read sequencing: revolutionizing complex trait genetics.Molecular biology and evolution · 2026Article
- PRISM-xQTL: Pleiotropic Relationships Integrated with System-level Multiomic QTL analysis for causal genes and molecular mediators in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Bridging the variant-to-function gap in type 2 diabetes: advances and challenges.Diabetologia · 2026Review
- Integrating multi-omic QTLs and predictive models reveals regulatory architectures at immune related GWAS loci in CD4+ T cells.medRxiv : the preprint server for health sciences · 2026Article
- Impact of disease-associated chromatin accessibility QTLs across immune cell types and contexts.Cell genomics · 2026Article
- Harnessing iPSC technology for population-level human disease/traits modeling -where are we?Frontiers in cell and developmental biology · 2026Review
- Article
- Pharmacoepigenomics in Personalized Medicine: A Hypothesis-Generating Approach to Introduce CpG-PGx SNPs as New Candidates for a Systematic Insight into Genomic-Epigenomic-Phenomic-Pharmacogenomics (G-E-Ph-PGx) Axis.Journal of personalized medicine · 2025Article
- Circulating chromatin reveals the effects of disease-associated variants on gene regulation.bioRxiv : the preprint server for biology · 2025Article
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Abstract
Most GWAS loci are presumed to affect gene regulation; however, only ∼43% colocalize with expression quantitative trait loci (eQTLs). To address this colocalization gap, we map eQTLs, chromatin accessibility QTLs (caQTLs), and histone acetylation QTLs (haQTLs) using molecular samples from three early developmental-like tissues. Through colocalization, we annotate 10.4% (n = 540) of GWAS loci in 15 traits by QTL phenotype, temporal specificity, and complexity. We show that integration of chromatin QTLs results in a 2.3-fold higher annotation rate of GWAS loci because they capture distal GWAS loci missed by eQTLs, and that 5.4% (n = 13) of GWAS colocalizing eQTLs are early developmental specific. Finally, we utilize the iPSCORE multiomic QTLs to prioritize putative causal variants overlapping transcription factor motifs to elucidate the potential genetic underpinnings of 296 GWAS-QTL colocalizations.
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