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.
Clonality
Monoclonal (human)
Description
Neutralizing recombinant human antibody (IgG1) recognizing the LDLR binding region of human PCSK9.
assay conditions: 3.8 ng/ul biotinylated PCSK9 was incubated with various concentrations of Anti-PCSK9 for 1 hr in a 50 ul reaction mix. Mixture was incubated on LDLR coated plate for 2 hr. Streptavidin labeled HRP was added and incubated for 1 hr. Finally, HRP chemiluminescent substrates were added and luminescence was read.
Formulation
40 mM Tris-HCl, pH 8.0, 110 mM NaCl, 2.2 mM KCl, and 20% glycerol.