Michał Turek

This study identifies critical residues in the BAG2 domain using C. elegans UNC-23, showing limited predictive power of current methods and distinct stabilizing interactions across species.

This study shows that loss of mitochondrial glutathione reductase and thioredoxin reductase in C. elegans causes growth, fertility, and muscle defects, activates a constitutive UPRmt, and alters mitochondrial morphology.

This study shows that C. elegans distinguishes pathogen proximity through compound types, activating EV-dependent physiological responses tailored to immediate or anticipated threats.

The paper shows that mitochondrial protein import defects lead to cytosolic aggregation of proteins, disrupting homeostasis and contributing to neurodegenerative disease mechanisms.

The paper identifies wake-active neurons that depolarize sleep-active neurons to initiate sleep in C. elegans by coordinating locomotion circuits during lethargus.