Kimberly Lorenz

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 identifies eQTLs and eGenes in tonsil-derived immune cells from children, linking them to childhood atopic diseases and expanding known genetic contributors.

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.

This study integrates multi-omics data to identify genetic variants and molecular mechanisms associated with type 2 diabetes and highlights potential drug targets.

This study uses Mendelian randomization to assess the causal effect of height on cardiovascular diseases, finding that established risk factors largely explain the association, with minimal residual effect.

This study identifies 1,289 genetic signals for type 2 diabetes in 2.5 million individuals, revealing distinct clusters linked to vascular complications and highlighting ancestry-specific genetic risk factors.

ColocQuiaL performs colocalization analysis between GWAS and eQTL/sQTL data to identify candidate causal genes for GWAS signals.

The paper develops TSABL predictors to identify causal variants in GWAS loci by leveraging trait-specific regulatory features and genomic annotations.

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.

Multi-ethnic type 2 diabetes (T2D) meta-analysis of 228,499 cases and 1,178,783 controls finds 318 previously unreported loci, 804 expression-colocalized genes, and 13 SNP-by-T2D vascular-outcome interactions.

This study identifies TPM1 as a causal gene for hematopoietic traits using genome-wide association data and CRISPR/Cas9 knockout in iPSCs, showing enhanced in vitro hematopoiesis.