Abdou Rachid Thiam

The paper identifies cholesterol esterification as a mechanism that creates switch-like regulation of the INSIG/SCAP/SREBP2 pathway through ER membrane phase transitions.

This study shows that Seipin regulates tripartite ER-mitochondria-lipid droplet contact sites, which are critical for adipocyte lipid storage and metabolic flexibility.

This study uses molecular dynamics simulations and theoretical models to analyze the shape and budding propensity of lipid droplets, finding that their shape resembles a spherical cap and is influenced by membrane properties.

This study shows lipid droplets are the site of VLCFA activation by Fat1, with Fat1 targeting LDs via an amphipathic helix and using a hydrophobic cavity to access substrates.

The paper shows that the CE/TG ratio determines lipid droplet size and phase behavior, influencing their function and disease relevance.

This paper identifies DDHD2 as a neutral lipid lipase and transacylase that remodels triglyceride acyl chains by transferring acyl groups between lipids.

This study identifies ORP5 as a key regulator of phosphatidic acid partitioning between triacylglycerol and cardiolipin synthesis at MAM-LD junctions, showing its role in balancing lipid metabolism and mitochondrial health.

The paper identifies steric repulsion as a mechanism regulating ER-to-LD protein movement, showing high-affinity proteins exclude lower-affinity ones during adipocyte differentiation.

This study shows that seipin regulates CAV1 trafficking and organelle interactions by controlling lipid metabolism and membrane order, impacting cellular homeostasis and metabolic disorders.

This study shows ceramide links TNF-α stress to membrane remodeling and lipid metabolism, altering vesicle trafficking and intracellular function.

This paper introduces ControLD, a method to control lipid droplet dynamics by sequestering and releasing them via engineered condensates, showing that isolation impairs their remobilization during metabolic needs.

This study shows α-Synuclein binds lipid droplets, senses cholesteryl-ester, regulates organelle size and abundance, and links its dysfunction to neurodegenerative diseases.