Struan F.A. Grant

This study identifies DPYD's role in sleep regulation through glial lipid metabolism and myelination across species, linking genetic variants to oligodendrocyte-specific control.

This study identifies cell type-specific eQTLs in the human pancreas using single-cell RNA-seq data and deconvoluted bulk RNA-seq data, revealing new genetic signals and associations with metabolic disease.

The paper introduces GAVURD, a system to identify putative pathogenic non-coding variants in unresolved rare disease patients using trio whole genome sequencing and TAD data, and identifies six potentially causal variants in ten probands.

This study maps POAG risk variants to candidate effector genes in ocular cell types, identifying ARHGEF12 as a potential target.

The paper identifies MEIS1 as a gene involved in sleep abnormalities and cerebellar development using cross-species variant-to-function analyses in zebrafish.

The paper identifies EGR2 as a conserved sleep regulator by analyzing sub-threshold genetic signals across sleep-related traits in multiple species.

The paper identifies cell-type-specific genes regulating sleep by mapping GWAS variants to effector genes in human and Drosophila models, revealing ruby/AP3B2 as a conserved glial regulator.

This study analyzes chromatin accessibility QTLs (caQTLs) to better understand how genetic variants influence trait heritability through regulatory mechanisms.

The paper identifies beat-Ia/CADM2 as a gene involved in hypersomnia by showing its role in sleep regulation across species and demonstrates potential therapeutic targets.

This study identifies 14 genome-wide significant loci for obstructive sleep apnea, including three independent of BMI, and highlights genetic pathways involving obesity, neurological, and craniofacial factors.

The paper identifies EGFR as a potential therapeutic target in Alzheimer's disease by linking a risk variant to increased EGFR expression in brain cell types through genomic analysis and CRISPRi validation.

The paper integrates GWAS data with a CRISPRi screen in osteoblasts to identify genes affecting bone mineral density and reveals pleiotropy across non-bone tissues.

The paper uses in vitro hematopoiesis systems to analyze gene expression and chromatin organization during HPC formation, identifying genetic impacts on blood traits and disease.

The paper identifies 693 SNPs associated with transcription factor binding in liver ATAC-seq data by analyzing footprint quantitative trait loci (fpQTLs).

This study identifies 91 risk loci for gallstone disease through a trans-ancestry GWAS, including 37 novel loci, and links them to metabolic and liver-related traits.

The paper introduces a framework for time-varying GWAS to identify age-varying genetic effects on BMI across childhood, finding 28 genome-wide significant variants, including a novel one in DAOA.

The paper identifies candidate causal variants and genes at melanoma risk loci using capture-HiC and integrates multi-omics data to prioritize cis-regulatory interactions.

This study identifies a genome-wide association for neonatal jaundice, revealing distinct genetic pathways compared to adult bilirubin metabolism.

The paper maps GWAS variants associated with late-onset Alzheimer's disease to functional effects in microglial cells, identifying RTFDC1 as a novel effector gene at the CASS4 locus.

This paper identifies shared and unique chromatin accessibility and 3D interactions of SUD loci, implicating non-neural cell types like pancreatic β-cells and showing a causal link between T2D and AUD.

Population-stratified GWAS of 2,068 traits in 635,969 Million Veteran Program participants, 29% genetically non-European, yields 98,485 associations and 57,601 fine-mapped signals with largely shared cross-population architecture.

The paper identifies rs7132908 as a causal variant in the chr12q13 obesity locus, showing it affects FAIM2 expression and neurodevelopment through cis-regulatory mechanisms.

This paper introduces PhenoPLIER, a method that maps gene-trait and drug associations into gene modules to reveal disease mechanisms and drug targets.

This study identifies rs3752495 as the causal variant at the insomnia WDR90 GWAS locus that influences PIG-Q expression through a regulatory mechanism.

This study identifies genetic loci associated with gestational duration and preterm delivery, showing maternal and fetal genetic effects and antagonistic pleiotropy with birth weight.

The paper identifies GPI-anchor biosynthesis as a conserved regulator of sleep through variant-to-gene mapping and cross-species genetic screening in humans and model organisms.

The paper identifies conserved genes at insomnia GWAS loci using zebrafish CRISPR screens and chromatin interaction data, finding that MEIS1 and SKIV2L mutations produce insomnia-like behaviors.

This study conducts a trans-ancestry GWAS using chronic ALT elevation as a proxy for NAFLD, identifies 77 significant loci, and validates 17 SNPs with histology and imaging data, revealing genetic links to metabolic and inflammatory traits.

The paper uses 3D chromatin maps to identify cell-type-specific regulatory architecture of type 2 diabetes risk by analyzing pancreatic cell types.

The paper maps cis-regulatory elements in human ESC-derived hypothalamic neurons and links them to GWAS loci for complex traits, identifying candidate genes and regulatory elements involved in hypothalamic development.