ArticleeLife2025
Chromatin accessibility variation provides insights into missing regulation underlying immune-mediated diseases.
Article in eLife, 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
- Comparing machine learning methods predicting transcriptome from epigenome with applications to association studies.Genome biology · 2026Article
- Predicting gene-specific regulation with transcriptomic and epigenetic single-cell data.Bioinformatics (Oxford, England) · 2026Article
- A meta-analysis of chromatin-associated loci provides insights into mechanistic interpretations of trait heritability.bioRxiv : the preprint server for biology · 2026Article
- Integrating multi-omics and multi-context QTL data with GWAS reveals the genetic architecture of complex traits and improves the discovery of risk genes.medRxiv : the preprint server for health sciences · 2026Article
- 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
- Circulating chromatin reveals the effects of disease-associated variants on gene regulation.bioRxiv : the preprint server for biology · 2025Article
- Genetic integration with cell-specific nucleosome positioning resolves causal relationships underlying chromatin accessibility profiles.bioRxiv : the preprint server for biology · 2025Article
- The identification of blood-derived response eQTLs reveals complex effects of regulatory variants on inflammatory and infectious disease risk.PLoS genetics · 2025Article
- Genotype inference from aggregated chromatin accessibility data reveals genetic regulatory mechanisms.Genome biology · 2025Article
- Genotype inference from aggregated chromatin accessibility data reveals genetic regulatory mechanisms.bioRxiv : the preprint server for biology · 2024Article
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Abstract
Most genetic loci associated with complex traits and diseases through genome-wide association studies (GWAS) are noncoding, suggesting that the causal variants likely have gene regulatory effects. However, only a small number of loci have been linked to expression quantitative trait loci (eQTLs) detected currently. To better understand the potential reasons for many trait-associated loci lacking eQTL colocalization, we investigated whether chromatin accessibility QTLs (caQTLs) in lymphoblastoid cell lines (LCLs) explain immune-mediated disease associations that eQTLs in LCLs did not. The power to detect caQTLs was greater than that of eQTLs and was less affected by the distance from the transcription start site of the associated gene. Meta-analyzing LCL eQTL data to increase the sample size to over a thousand led to additional loci with eQTL colocalization, demonstrating that insufficient statistical power is still likely to be a factor. Moreover, further eQTL colocalization loci were uncovered by surveying eQTLs of other immune cell types. Altogether, insufficient power and context specificity of eQTLs both contribute to the 'missing regulation'.
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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 Socratic graph.