>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its binding ability in a functional ELISA. When Recombinant Mouse LDLR (Catalog # 2255-LD) is coated at 2 µg/mL, Recombinant Mouse Proprotein Convertase 9/PCSK9 (Catalog # 9258-SE) binds with an ED50 = 25-150 ng/mL.
Mouse myeloma cell line, NS0-derived Ser156-Gln694 with a C-terminal 10-His tag; Gln35-Gln155
Recombinant Mouse Proprotein Convertase 9/ PCSK9 Binds toRecombinant Mouse LDL R in an ELISA Binding Assay. When Recombinant Mouse LDL R Recombinant Mouse LDL R (Catalog # 2255-LD) is coated at 2 µg/mL, Recombinant Mouse Proprotein Convertase 9/PCSK9 (Catalog # 9258-SE) binds with an ED50 = 25-150 ng/mL.
Background: Proprotein Convertase 9/PCSK9
PCSK9 (proprotein convertase subtilisin kexin 9), also known as NARC-1, is a member of the proteinase K subfamily of subtilisin-related serine endoproteases. It is highly expressed in the liver, intestine, and kidney and plays an important role in regulating LDL R expression and circulating cholesterol levels (1). PCSK9 is synthesized as precursor protein that is autocatalytically cleaved in the endoplasmic reticulum to generate a 14 kDa prodomain and a 60 kDa catalytic domain (2). Within the secretion pathway, the prodomain remains associated with and functions as a chaperone for the catalytic domain. Mouse PCSK9 shares 78% and 93% amino acid identity with human and rat PCSK9, respectively. PCSK9 plays a key role in the regulation of cholesterol metabolism by binding to hepatic LDL R, LRP-1, VLDL R, and Apolipoprotein E R2 and promoting their lysosomal degradation instead of recycling to the plasma membrane (3-8). It can also regulate cholesterol and triglyceride handling in the intestine and adipose tissue (9-11). The ability of PCSK9 to regulate LDL R expression is inhibited by its binding to LDL particles or Annexin A2 or by additional proteolytic cleavage (12-17).
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