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Recombinant Macaca nemestrina PCSK9 (C-6His)

For research use only. Not intended for any clinical use.

Cat. No. :   RP00212 Tag :   C-6His

Expressed Region :   Gln31-Gln152&Ser153-Gln692 Expression System :   Human Cell

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Product Information

Gene Information

Cat. No. RP00212
Description The Recombinant Macaca nemestrina PCSK9 (C-6His) is produced in our Human Cell expression system. The amino acid region expressed is Gln31-Gln152&Ser153-Gln692 with a 6His tag at the C terminus.
Species Macaca nemestrina
Tag C-6His
Mol Weight 14&59 KDa
Conjugate Unconjugated
Format Liquid
Expressed Region Gln31-Gln152&Ser153-Gln692
Expression System Human Cell
Formulation Supplied as a 0.2 μm filtered solution of 20mM PB, 150mM NaCl, 0.1M Arg, 0.1M Glu, 20% glycerol, 0.01% tween20, 5% Trehalose, pH 6.0.
Purity >95% as determined by SDS-PAGE.
>90% as determined by SEC-MALS.
Endotoxin Level < 1 EU/µg of protein by LAL method
Storage Upon receipt, this product is stable for up to 6 months at temperatures below -70°C. Once reconstituted, the product is stable for up to 1 week at 4°C and up to 3 months at -20°C. Please avoid repeated freeze-thaw cycles.
Shipping The product is shipped with ice packs. Upon receipt, store it immediately at the temperature recommended below.
Target Gene PCSK9
Synonyms Proprotein Convertase Subtilisin/Kexin Type 9; Proprotein Convertase 9; PC9; Subtilisin/Kexin-Like Protease PC9; PCSK9
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This gene encodes a member of the subtilisin-like proprotein convertase family, which includes proteases that process protein and peptide precursors trafficking through regulated or constitutive branches of the secretory pathway. The encoded protein undergoes an autocatalytic processing event with its prosegment in the ER and is constitutively secreted as an inactive protease into the extracellular matrix and trans-Golgi network. It is expressed in liver, intestine and kidney tissues and escorts specific receptors for lysosomal degradation. It plays a role in cholesterol and fatty acid metabolism. Mutations in this gene have been associated with autosomal dominant familial hypercholesterolemia. Alternative splicing results in multiple transcript variants.

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