PCSK9, His-tag Recombinant
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Catalog #
71204
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$305
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Description
Recombinant human PCSK9 (proprotein convertase subtilisin/kexin type 9), encompassing amino acids 31-692 (end), containing pro-PCSK9 sequence (31-152). This construct contains a C-terminal His-tag (6xHis). The recombinant protein was affinity purified.
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Synonyms
proprotein convertase subtilisin/kexin type 9, PCSK-9, FH3, Proprotein convertase 9, Subtilisin/kexin-like protease PC9, PC9, FHCL3, NARC1, LDLCQ1, Neural apoptosis-regulated convertase 1, NARC-1, HCHOLA3, PSEC0052
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Product Data Gallery
Product Info
Storage and Usage
Citations
Species
Human
Construct
PCSK9(31-692(end)-His)
Host Species/Expression System
HEK293 cells
Purity
≥90%
Format
Aqueous buffer solution
Formulation
8 mM Phosphate, pH 7.4, 110 mM NaCl, 2.2 mM KCl, and 20% glycerol
MW
Pro: 14 kDa; Mature: 58 kDa + glycans
Amino Acids
31–692(end)
Glycosylation
This protein runs at higher MW by SDS-PAGE due to glycosylation.
Genbank #
NM_174936
UniProt #
Q8NBP7
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.