ArticleNature communications2025
Gene expression QTL mapping in stimulated iPSC-derived macrophages provides insights into common complex diseases.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Article
- Harnessing iPSC technology for population-level human disease/traits modeling -where are we?Frontiers in cell and developmental biology · 2026Review
- Psoriasis risk allele function in activated Th1/17 cells with "memory" to antigen exposure.PloS one · 2026Article
- Splicing QTL mapping in stimulated macrophages associates low-usage splice junctions with immune-mediated disease risk.Nature communications · 2025Article
- Oxygen-induced stress reveals context-specific gene regulatory effects in human brain organoids.Genome research · 2025Article
- Cell-type-resolved genetic regulatory variation shapes inflammatory bowel disease risk.medRxiv : the preprint server for health sciences · 2025Article
- Stimulating Wnt signaling reveals context-dependent genetic effects on gene regulation in primary human neural progenitors.Nature neuroscience · 2024Article
- Adaptation in human immune cells residing in tissues at the frontline of infections.Nature communications · 2024Article
- Fine-mapping and molecular characterisation of primary sclerosing cholangitis genetic risk loci.Nature communications · 2024Article
- Oxygen-induced stress reveals context-specific gene regulatory effects in human brain organoids.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Many disease-associated variants are thought to be regulatory but are not present in existing catalogues of expression quantitative trait loci (eQTL). We hypothesise that these variants may regulate expression in specific biological contexts, such as stimulated immune cells. Here, we used human iPSC-derived macrophages to map eQTLs across 24 cellular conditions. We found that 76% of eQTLs detected in at least one stimulated condition were also found in naive cells. The percentage of response eQTLs (reQTLs) varied widely across conditions (3.7% - 28.4%), with reQTLs specific to a single condition being rare (1.11%). Despite their relative rarity, reQTLs were overrepresented among disease-colocalizing eQTLs. We nominated an additional 21.7% of disease effector genes at GWAS loci via colocalization of reQTLs, with 38.6% of these not found in the Genotype-Tissue Expression (GTEx) catalogue. Our study highlights the diversity of genetic effects on expression and demonstrates how condition-specific regulatory variation can enhance our understanding of common disease risk alleles.
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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.