作者: Carlos Enrich , Carles Rentero , Thomas Grewal , Clare E. Futter , Emily R. Eden
关键词: Phenotype 、 Chemistry 、 Endoplasmic reticulum 、 Cell biology 、 Mutant 、 Endocytic cycle 、 Cholesterol 、 Organelle 、 Endosome 、 NPC1
摘要: Delivery of low-density lipoprotein-derived cholesterol to the endoplasmic reticulum (ER) is essential for homeostasis, yet mechanism this transport has largely remained elusive. Two recent reports shed some light on process, uncovering a role Niemann Pick type-C1 protein (NPC1) in formation membrane contact sites (MCS) between late endosomes (LE)/lysosomes (Lys) and ER. Both studies identified loss MCS cells lacking functional NPC1, where accumulates endocytic organelles. Remarkably, taking different approaches, both have made striking observation that expansion LE/Lys-ER can rescue accumulation phenotype NPC1 mutant or deficient cells. In cases, was shown be transported ER, demonstrating importance ER-LE/Lys direct