Title : Cholesterol-depletion corrects APP and BACE1 misstrafficking in NPC1-deficient cells.

Pub. Date : 2012 Aug

PMID : 22551668






6 Functional Relationships(s)
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Protein Name
Organism
1 Cholesterol-depletion corrects APP and BACE1 misstrafficking in NPC1-deficient cells. Cholesterol beta-secretase 1 Homo sapiens
2 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 beta-secretase 1 Homo sapiens
3 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 beta-secretase 1 Homo sapiens
4 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 beta-secretase 1 Homo sapiens
5 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 beta-secretase 1 Homo sapiens
6 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 beta-secretase 1 Homo sapiens