PCSK9 is a crucial player in the regulation of plasma cholesterol homeostasis. It binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.
Immunogen Region
31-691 (end)
Tag
C-terminal His-Avi-tag
Description
Rat proprotein convertase subtilisin/kexin type 9 (PCSK9), also known as FH3, HCHOLA3, and PC9, GenBank Accession No. NM_199253, a.a. 31-691(end), with C-terminal His-Avi-tag, MW=76 kDa (calculated), expressed in a HEK293 cell expression system.
Formulation
40 mM Tris-HCl pH 8.0, 110 mM NaCl, 2.2 mM KCl, 0.04% Tween20, and 20% glycerol.
Species
Rat
Application
Useful for studying protein binding and screening small molecules for drug discovery.