[HTML][HTML] Dissection of the endogenous cellular pathways of PCSK9-induced low density lipoprotein receptor degradation: evidence for an intracellular route
Elevated levels of plasma low density lipoprotein (LDL)-cholesterol, leading to familial
hypercholesterolemia, are enhanced by mutations in at least three major genes, the LDL
receptor (LDLR), its ligand apolipoprotein B, and the proprotein convertase PCSK9. Single
point mutations in PCSK9 are associated with either hyper-or hypocholesterolemia.
Accordingly, PCSK9 is an attractive target for treatment of dyslipidemia. PCSK9 binds the
epidermal growth factor domain A (EGF-A) of the LDLR and directs it to endosomes …
hypercholesterolemia, are enhanced by mutations in at least three major genes, the LDL
receptor (LDLR), its ligand apolipoprotein B, and the proprotein convertase PCSK9. Single
point mutations in PCSK9 are associated with either hyper-or hypocholesterolemia.
Accordingly, PCSK9 is an attractive target for treatment of dyslipidemia. PCSK9 binds the
epidermal growth factor domain A (EGF-A) of the LDLR and directs it to endosomes …