PCSK9, C-terminal His-Avi-Tag, Biotin-Labeled Recombinant

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Catalog #
71304
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Description

Recombinant human PCSK9 (proprotein convertase subtilisin/kexin type 9), encompassing amino acids 31-692(end). This construct contains the proprotein PCSK9 at the N-terminal encompassing amino acids 31-152. At the C-terminal this construct contains a His-tag (6xHis) followed by an Avi-tag. The recombinant protein was enzymatically biotinylated using the Avi-Tag™ and affinity purified.

Synonyms
Proprotein convertase subtilisin/kexin type 9, Neural apoptosis-regulated convertase 1, NARC-1, Proprotein convertase 9, PC9, Subtilisin/kexin-like protease PC9, PSEC0052
Product Info
Storage and Usage
Citations
Species
Human
Construct
PCSK9 (31-692(end)-His-Avi)-(Biotin)
Host Species/Expression System
HEK293
Purity

≥90%

Format
Aqueous buffer solution
Formulation
8 mM Phosphate, pH 7.4, 110 mM NaCl, 2.2 mM KCl, and 20% glycerol.
MW
74 kDa
Amino Acids
31-692(end)
Aggregation
<10%
Genbank #
NM_174936
UniProt #
Q8NBP7
Tag(s)
C-terminal His, Avi Tags
Label

This protein is enzymatically biotinylated using Avi-Tag™ technology. Biotinylation confirmed to be ≥90%.

For more information on enzymatic biotinylation, please see our Tech Note

Background
PCSK9 (PCSK9 Biotin-Labeled) 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.