Adenoviral-mediated expression of Pcsk9 in mice results in a low-density lipoprotein receptor knockout phenotype.

By K. Maxwell, J. Breslow. Proceedings of the National Academy of Sciences of the United States of America, 2004

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Molecular biology of PCSK9: its role in LDL metabolism. (2007, background): “does not increase plasma cholesterol levels [19,20,23], the combined data indicate that, if PCSK9 does alter ApoB secretion, it is likely to be a secondary event related to the reduction in LDLRs.”
Molecular characterization of loss-of-function mutations in PCSK9 and identification of a compound heterozygote. (2006, background): “High-level expression of wild-type PCSK9 (PCSK9WT) in the liver of mice results in a pronounced reduction in hepatic low-density lipoprotein receptor (LDLR) protein (but not mRNA).(10,11) Since hepatic LDLR-mediated endocytosis is the major route of LDL clearance,(12) the mice expressing high levels”
Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9 (2005, background): “These mutations are probably gain-of-function mutations, as overexpression of PCSK9 in the liver of mice produces hypercholesterolemi”