Marcus Conrad

The paper identifies oxidized phospholipids that impair lysosomal membrane repair and promote ferroptosis across multiple cell types and conditions.

Genetic deletion or pharmacological inhibition of ferroptosis suppressor protein 1 (FSP1) induces lipid peroxidation and restricts lung adenocarcinoma growth in vivo, establishing FSP1 as a therapeutic vulnerability.

This study identifies riboflavin as a modulator of ferroptosis sensitivity by supporting FSP1 stability and antioxidant recycling, with implications for therapeutic targeting.

The paper introduces a machine learning model that learns spatial preference maps for drug-receptor interactions to guide drug discovery.

This study investigates whether ACSL4 deletion in liver cells prevents MASLD progression in mice but finds no significant differences compared to wild-type mice.

This study shows that ferroptosis and apoptosis can intersect, and BH3-mimetics can either enhance or suppress cell death depending on context.

The paper shows PRDX6 influences ferroptosis sensitivity by managing cellular selenium levels, which affects GPX4 function.

This study shows that aging increases ferroptotic vulnerability in round spermatids, leading to a Y-chromosome skew in sperm, which can be modulated by vitamin E.

This study shows that ferrous-glutathione coupling promotes ferroptosis and frailty in C. elegans, and blocking ferroptosis extends lifespan and healthspan.