T he identification of PCSK9 in 2003 1 has resulted in sub- stantial revision to previous knowledge regarding cholesterol homeostasis, provided new insights into low-density lipoprotein (LDL) metabolism and LDL receptor (LDLR) function, and presented a new compelling therapeutic target to reduce LDL cholesterol (LDL-C).PCSK9 is a serine protease expressed predominantly in the liver, intestine, and kidney and regulates plasma LDL-C levels by binding to the epidermal growth factor A of the LDLR, targeting it for degradation rather than for recycling to the cell surface.
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Stein et al. (2013) studied this question.
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