Chong Yon Park

The paper uses Perturb-seq in mice to identify genes that promote collateral artery formation by comparing gene expression between guinea pigs and mice.

The paper identifies causal genetic mechanisms at CAD GWAS loci using CRISPR screens and chromatin analysis, revealing enhancer-gene links and ancestry/sex-specific risk factors.

This study shows dioxin exposure accelerates atherosclerosis by promoting inflammatory smooth muscle cell phenotypes and oxidative stress, with AHR in SMC providing protective effects.

This study identifies novel causal genes for NAFLD using a combination of GWAS, genetic colocalization, and CRISPRi functional screens.

CROP-Seq uses CRISPRi and scRNA-Seq to screen gene targets in adipocytes, identifying gene knock-down effects and novel regulators of adipogenesis and metabolic disease.

The paper identifies environmental modulators of genetic risk factors for complex traits by integrating perturbation data with GWAS.

The paper uses DeGAs to identify genetic components across 2,138 phenotypes in the UK Biobank, revealing novel adipocyte biology through variant and gene contributions to obesity-related traits.