PCSK9, His-Avi-Tag (Rat) Recombinant

Catalog #
71220-1
$260 *
Size: 20 µg
Qty
*US Pricing only. For international pricing, please contact your local distributor.
Purchase
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.

Synonyms
FH3, HCHOLA3, PC9, NARC1, Neural Apoptosis Regulated Convertase 1
Product Info
Storage and Usage
Citations
Species
Rat
Host Species/Expression System
HEK293 cells
Purity

≥67%

Formulation
40 mM Tris-HCl pH 8.0, 110 mM NaCl, 2.2 mM KCl, 0.04% Tween20, and 20% glycerol.
MW
76 kDa
Amino Acids
31-691 (end)
Genbank #
NM_199253
Tag(s)
C-terminal His-Avi-tag
Background
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.
References
1. Abifadel, M., et al., Nat Genet. 2003 Jun,34(2):154-6.
2. Abifadel, M., et al., Hum Mutat. 2009 Apr,30(4):520-9.