Recombinant Mouse Pcsk9 Protein(His tag) (MH0238PL)

Cat.No.

MH0238PL

Synonyms

PCSK9; NARC-1; FH3; PC9; Narc1

Accession

Pcsk9

Predicted N Terminal

Gln 35

Form

Lyophilized from sterile 15mM Tris, 90mM NaCl, 50% Glycerol, pH 7.5, 5 % trehalose and 5 % mannitol.

Bio-activity

Measured by its binding ability in a functional ELISA . Immobilized mouse PCSK9 at 10 μg/ml (100 μl/well) can bind biotinylated recombinant human LDLR. The EC50 of biotinylated human LDLR is 0.12 μg/ml.

Molecular Mass

Recombinant Mouse PCSK9 consists of 671 amino acids and has a calculated molecular mass of 72.6 kDa. As a result of proteolysis and glycosylation, Recombinant protein migRates as doublet with apparent molecular mass of approximately 19 & 65 kDa, cprresponding to the prodomain and the mature form of PCSK9 respectively in SDS-PAGE under reducing conditions.

Endotoxin

< 1.0 EU per 1 microgram of protein (determined by LAL method).

Purity

> 95 % by SDS-PAGE.

Storage

In lyophilized state for 1 year (4°C); After reconstitution under sterile conditions for 3 months (-70°C). Avoid repeated freeze/thaw cycles.

Reconstitution

Reconstitute in sterile distilled water to a concentration of 0.1-1.0 mg/mL.

Warning

For research use only!

Background

Crucial player in the regulation of plasma cholesterol homeostasis. 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 in intracellular acidic compartments. 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.

Tag

His

Species

Mouse

Source

HEK293

Background

Crucial player in the regulation of plasma cholesterol homeostasis. 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 in intracellular acidic compartments. 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.