PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22551668-0	2012	Cholesterol-depletion corrects APP and BACE1 misstrafficking in NPC1-deficient cells.	Cholesterol	0-11	beta-secretase 1	Homo sapiens	39-44	
22551668-2	2012	We previously reported that cholesterol accumulation in NPC-cells leads to cholesterol-dependent increased APP processing by beta-secretase (BACE1) and decreased APP expression at the cell surface (Malnar et al.	Cholesterol	28-39	beta-secretase 1	Homo sapiens	141-146	
22551668-2	2012	We previously reported that cholesterol accumulation in NPC-cells leads to cholesterol-dependent increased APP processing by beta-secretase (BACE1) and decreased APP expression at the cell surface (Malnar et al.	Cholesterol	75-86	beta-secretase 1	Homo sapiens	141-146	
22551668-5	2012	We hypothesized that increased formation of APP-CTFs and Abeta in NPC disease is due to cholesterol-mediated altered endocytic trafficking of APP and/or BACE1.	Cholesterol	88-99	beta-secretase 1	Homo sapiens	153-158	
22551668-7	2012	Moreover, we observed that NPC cells show cholesterol dependent sequestration and colocalization of APP and BACE1 within enlarged early/recycling endosomes which can lead to increased beta-secretase processing of APP.	Cholesterol	42-53	beta-secretase 1	Homo sapiens	108-113	
22551668-9	2012	Our findings suggest that increased cholesterol levels, such as in NPC disease and sporadic AD, may be the upstream effector that drives amyloidogenic APP processing characteristic for Alzheimer"s disease by altering endocytic trafficking of APP and BACE1.	Cholesterol	36-47	beta-secretase 1	Homo sapiens	250-255