Sterol kinetics and cell-based assays reveal a heretofore unknown step in cholesterol trafficking through the endolysosomal compartment, involving a direct functional interaction between NPC2 and lysosbisphosphatidic acid.

Cholesterol exhibits transient interaction with A2AR and regulates receptor conformational equilibria through indirect membrane effects.

GRAMD1 proteins sense a transient expansion of the accessible pool of plasma membrane cholesterol and facilitate its transport to the endoplasmic reticulum at ER-PM contact sites.

The glucose-sensing transcription factor MondoA regulates zebrafish epiboly via cholesterol biosynthesis genes including the human disease gene Nsdhl, revealing an unknown role for metabolic glucose signalling in vertebrate development.

A post-lysosomal cholesterol transport inhibitor reveals how the endoplasmic reticulum membrane regulates total cellular cholesterol by constantly monitoring a critical pool of cholesterol in the plasma membrane.

A phase transition of TIR-1/SARM1 induced by either pathogen or non-pathogen stress potentiates its intrinsic NADase activity, which activates the p38 PMK-1 signaling cascade to induce protective immune defenses in Caenorhabditis elegans intestinal epithelial cells.

Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Inactivation of SURF4 leads to impaired secretion of PCSK9 and apolipoproteins resulting in low plasma cholesterol without detrimental consequences to the liver.

Atomistic simulations reveal how lipids can allosterically modulate membrane receptors.

A nanomolar inhibitor of cholesterol transport out of endosomes/lysosomes can be crosslinked to the “sterol-sensing domain” of NPC1, which implicates this domain in the transmembrane transport of cholesterol.