Casey E. Romanoski

This study identifies inflammation-induced alternative splicing in human endothelial cells and links it to cardiovascular disease risk through genetic mechanisms.

The paper identifies a CAD risk SNP rs880890 in an endothelial enhancer that reduces CALCRL expression by impairing HSF binding under shear stress.

This study profiles human aortic endothelial cells in vitro and atherosclerotic lesions ex vivo, revealing heterogeneous subtypes and their responses to perturbations.

The paper identifies functional non-coding SNPs in human endothelial cells that influence vascular traits by affecting transcriptional regulation and chromatin states.

The paper systematically analyzes naturally occurring insertions and deletions (InDels) to assess their impact on transcription factor spacing and identifies tolerant and sensitive TF pairs.

The paper uses RNA-seq to compare transcriptional profiles of neurons infected with Toxoplasma gondii, bystander neurons, and controls, finding immune cell transcripts enriched in infected neurons.

This study identifies a genetic variant at 1p32.2 that regulates endothelial responses to hemodynamics by modulating an enhancer region in vascular endothelium.

MARGE identifies collaborative transcription factor pairs by integrating genetic variation with epigenetic data to interpret non-coding genetic variation.