Dennis C. Ko

This study shows that mitochondrial copper deficiency drives MASLD by causing ferroptosis, senescence, and fibrosis, and that restoring copper homeostasis can alleviate disease.

The paper identifies sex-biased genes and eQTL across the human genome, showing their association with autoimmune diseases and sex differences in gene regulation.

This study identifies cathepsin Z as a susceptibility factor for tuberculosis severity in both mice and humans, showing its role in disease outcomes through genetic and cellular analyses.

The paper identifies FCRL3 as a receptor for Yersinia pestis using a genome-wide association study and shows a variant in FCRL3 is linked to both plague susceptibility and hepatitis C risk.

The paper identifies shared genetic variants between critically ill COVID-19 and idiopathic pulmonary fibrosis by integrating GWAS with context-specific eQTLs and transcriptomics.

This study identifies DDX39B as a regulator of FOXP3 RNA splicing, which influences T regulatory cell fate and immune tolerance, linking it to multiple sclerosis risk.

The paper identifies genetic variation in MCOLN2 that limits Salmonella Typhi replication via magnesium deprivation in human cells.

The paper identifies a nonsynonymous ERAP1 variant associated with increased susceptibility to influenza virus using scHi-HOST, a single-cell method for genetic susceptibility testing.

The paper connects genetic architecture of human diseases with molecular phenotypes to uncover mechanisms of COVID-19 susceptibility.

The paper identifies 70 gene-level associations with 26 infectious disease traits using transcriptome-wide association studies and explores their molecular basis and implications for host-pathogen interactions.

The paper links genetic variation to pathogen-induced cellular traits and disease by integrating GWAS data with clinical and experimental validation.