Open AccessGenetic Variation at the Proprotein Convertase Subtilisin/Kexin Type 5 Gene Modulates High-Density Lipoprotein Cholesterol Levels
Author(s) -
Iulia Iatan,
Zari Dastani,
Ron Do,
Daphna WeissglasVolkov,
Isabelle L. Ruel,
Jenny C. Lee,
Adriana HuertasVázquez,
MarjaRiitta Taskinen,
Annik Prat,
Nabil G. Seidah,
Päivi Pajukanta,
James C. Engert,
Jacques Genest
Publication year - 2009
Publication title -
circulation cardiovascular genetics
Language(s) - English
Resource type - Journals
eISSN - 1942-325X
pISSN - 1942-3268
DOI - 10.1161/circgenetics.109.877811
Subject(s) - kexin , single nucleotide polymorphism , high density lipoprotein , hepatic lipase , medicine , biology , endocrinology , pcsk9 , lipoprotein lipase , proprotein convertase , cholesterylester transfer protein , lipoprotein , cholesterol , genetics , gene , genotype , ldl receptor , adipose tissue
A low level of plasma high-density lipoprotein cholesterol (HDL-C) is a risk factor for cardiovascular disease. HDL particles are modulated by a variety of lipases, including endothelial lipase, a phospholipase present on vascular endothelial cells. The proprotein convertase subtilisin/kexin type 5 (PCSK5) gene product is known to directly inactivate endothelial lipase and indirectly cleave and activate angiopoetin-like protein 3, a natural inhibitor of endothelial lipase. We therefore investigated the effect of human PCSK5 genetic variants on plasma HDL-C levels.
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