Joost C. M. Holthuis

This study uses lysosomal proteomics and knockdowns to analyze the cargo spectra of GARP and EARP complexes, revealing their distinct roles in protein trafficking and their links to neurodegenerative disorders.

This study identifies VPS13C/PARK23 as a key protein involved in lysosomal repair by facilitating lipid transfer and membrane remodeling in response to damage.

This study shows ceramides disrupt VDAC-HKI complex assembly by modulating VDAC tilt and membrane thinning, revealing a mechanism for ceramide-induced apoptosis.

This study shows MTMR14 is recruited to damaged lysosomes to remodel lipids, reduce mTORC1 signaling, and support proteostasis during lysosomal injury.

This study challenges models of ceramide-induced apoptosis by showing ceramides cannot form channels or substitute for cardiolipin in Bax pore formation.

The paper develops an in vitro assay to study HKI-VDAC1 complex assembly and shows the critical role of a bilayer-facing glutamate in pH-sensitive binding.

This study shows that TMEM16F-mediated lipid scrambling drives the formation and release of apoptotic-like vesicles without affecting cytosolic calcium or the cytoskeleton.

This study identifies a charged glutamate on VDAC1 and VDAC2 that interacts with HKI's N-terminal helix, revealing structural and mechanistic insights into their complex formation.

This study introduces light-sensitive sphingosines (caSphs) that allow reversible control of sphingolipid biosynthesis through photo-isomerization, enabling precise manipulation of lipid production in living cells.

The paper systematically analyzes the sphingomyelin synthase family in C. elegans, identifying three SM synthases and one CPE synthase with distinct subcellular distributions.