Stephen W. G. Tait

This paper identifies a metabolic vulnerability in leptomeningeal ALL cells due to thiol scarcity in CSF, making them susceptible to ferroptosis through disruption of selenocysteine biosynthesis and GPX4 activity.

The paper shows that Apaf1 forms transient foci during apoptosis, which correspond to the apoptosome and regulate apoptosis progression.

This study shows that mitochondrial outer membrane permeabilization triggers ubiquitin-dependent NF-κB inflammation by recruiting NEMO to ubiquitylated mitochondria.