Cornelius Y. Taabazuing

This study shows human CASP4 and CASP5 form SMOCs in response to LPS structures that evade TLR4 and Casp11, revealing their distinct roles in sensing bacterial LPS and implications for sepsis therapy.

DIPTAR converts protein degradation into a selectable phenotype to enable functional studies of degradation pathways and host-pathogen interactions.

This study shows that distributed clonal deletion checkpoints prevent autoimmune disease by restricting autoreactive B cell diversification and persistence.

This study identifies CASP4/5 as activators of CASP3/7 and GSDME in human macrophages, showing that CASP3 restricts Salmonella replication through apoptosis.

The paper develops a new peptide-based inhibitor targeting caspase-8 and reveals shared specificities between inflammatory and apoptotic caspases.