... that cholesterol plays a crucial role in the regulation of insulin-stimulated mTORC1 signaling. The rapid progression of insulin-induced mTORC1 signaling declines in sterol-depleted cells and restores in cholesterol-repleted cells. In insulin-stimulated cells, cholesterol promotes recruitment of mTORC1 onto...

...Amber Shaheen; Claire L. Richter Gorey; Adam Sghaier; Jeffrey S. Dason ABSTRACT Changes in cholesterol content of neuronal membranes occur during development and brain aging. Little is known about whether synaptic activity regulates cholesterol levels in neuronal membranes and whether these changes...

... at FAs with imaging and biochemical approaches. Using the cholesterol-specific probe D4 with total internal reflection fluorescence microscopy and super-resolution microscopy, we show an enrichment of cholesterol at FAs simultaneously with FA assembly. Furthermore, we establish a method to isolate...

... Gerstbauer; Edward H. Hinchcliffe; Kevin T. Vaughan ABSTRACT The pathological accumulation of cholesterol is a signature feature of Niemann–Pick type C (NPC) disease, in which excessive lipid levels induce Purkinje cell death in the cerebellum. NPC1 encodes a lysosomal cholesterol-binding protein...

... uncertain. The cystic fibrosis transmembrane conductance regulator (CFTR), which is mutated in cystic fibrosis (CF), forms clusters that are cholesterol dependent and become incorporated into long-lived platforms during hormonal stimulation. We report here that clustering does not involve known tethering...

...-expressing human cells impairs proteolytic Shh release from its lipidated terminal peptides, a process called ectodomain shedding. We also show that cholesterol export from Disp-deficient cells is reduced, that these cells contain increased cholesterol amounts in the plasma membrane, and that Shh shedding...

... for caveolar morphogenesis, presumably through the shaping of the caveolar neck. Caveolar membranes contain abundant cholesterol. However, the role of cholesterol in PACSIN2-mediated membrane deformation remains unclear. Here, we show that the binding of PACSIN2 to the membrane can be negatively regulated...

... and results in mistargeting of LBR to the ER. LBR possesses a modular structure and corresponding bifunctionality, acting in heterochromatin organization via its N-terminus and in cholesterol biosynthesis via its sterol-reductase C-terminal domain. We show that TMEM147 physically interacts with LBR...

... of osteoclast-like cells (OCLs). LDLR/LOX-1 dKO and LDLR sKO preosteoclasts exhibited decreased uptake of LDL. The cell surface cholesterol levels of both LDLR/LOX-1 dKO and LDLR sKO osteoclasts were lower than the levels of wild-type OCLs. Additionally, the amount of phosphatidylethanolamine (PE) on the cell...

... roles of caveolins in a variety of cellular contexts including liver, brain, lymphocytes, cilia and cancer cells, as well as consider insights from invertebrate systems. Non-caveolar caveolins can determine the intracellular fluxes of active lipids, including cholesterol and sphingolipids. Accordingly...

... that atherosclerotic plaque macrophages contact agLDL and form an extracellular digestive compartment similar to that observed in vitro . During macrophage catabolism of agLDL in vitro , levels of free cholesterol in the agLDL are increased. HDL can extract free cholesterol directly from this agLDL and inhibit...

... organizing system (MICOS) complexes, and to a lesser extent in OPA1. Moreover, muscles lacking ATAD3 showed altered cholesterol metabolism, accumulation of mitochondrial DNA (mtDNA) replication intermediates, progressive mtDNA depletion and deletions. Unexpectedly, decreases in the levels of some OXPHOS...

... degeneration. The signalling platform is dependent on cholesterol released from cholesterol esters by cholesterol ester hydrolases (CEHs). The activation of cPLA 2 requires cholesterol released from cholesterol esters by cholesterol ester hydrolases (CEHs), enzymes dependent upon platelet activating factor...

...Ewan West; Craig Osborne; Clive Bate ABSTRACT Cholesterol is required for the formation and function of some signalling platforms. In synaptosomes, amyloid-β (Aβ) oligomers, the causative agent in Alzheimer's disease, bind to cellular prion proteins (PrP C ) resulting in increased cholesterol...

...Ji Hyun Kim; Ashutosh Singh; Maurizio Del Poeta; Deborah A. Brown; Erwin London ABSTRACT Ordered lipid domains (rafts) in plasma membranes have been hypothesized to participate in endocytosis based on inhibition of endocytosis by removal or sequestration of cholesterol. To more carefully...

... of endosomal Rab7 inhibited, and lowering membrane cholesterol levels favored STxB–saporin translocation. Interestingly, experiments with reducible and non-reducible linker-arm–STxB conjugates led to the conclusion that after translocation, STxB remains associated with the cytosolic membrane leaflet...

...Masashi Maekawa; Gregory D. Fairn ABSTRACT Cholesterol is an essential component of metazoan cellular membranes and it helps to maintain the structural integrity and fluidity of the plasma membrane. Here, we developed a cholesterol biosensor, termed D4H, based on the fourth domain of Clostridium...

... (SNAP) receptor (SNARE) proteins, which are key players in vesicle transport at the cell surface and intracellular compartments, but is also tightly modulated by cholesterol. Cholesterol-sensitive SNAREs at the cell surface are relatively well characterized, but it is less well understood how altered...

... and the endosomal system. ER–endosome contacts intensify when endosomes mature, and the ER participates in endosomal processes, such as the termination of surface receptor signaling, multi-vesicular body formation, and transport and fusion events. Cholesterol and Ca 2+ are transferred between the ER and endosomes...

.... , Gilbert   D. , Meinhof   T. , Wirkner   U. , Erfle   H. , Muckenthaler   M. , Pepperkok   R.   ( 2009 ). Identification of cholesterol-regulating genes by targeted RNAi screening.   Cell Metab.   10 , 63 – 75 . 10.1016/j.cmet.2009.05.009 Beisiegel   U. , Schneider   W. J...