Abstract
Aim: Plasma low density lipoprotein (LDL) cholesterol is a major risk factor for developing cardiovascular disease. The therapeutic inefficacy of the current lipid lowering medications in a significantly large group of patients necessitate the search for new cholesterol-lowering treatments. We hypothesise that proteolysis of the human LDLR regulates cellular LDL uptake and hence plasma LDL-cholesterol.
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