David J. Sherman

This paper identifies PNPLA3-I148M as a neomorphic variant that impairs ApoB secretion and lipid metabolism, contributing to fatty liver disease.

This study investigates the cellular effects of the PNPLA3-I148M variant, revealing its role in altering lipid droplet-Golgi dynamics and inducing proteomic and transcriptomic changes associated with liver disease.

The paper quantifies MHC Class I peptide origins under UPS perturbation, revealing 30% of peptides are UPS-independent and 10% proteasome-independent, with implications for immune activation.