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Cat. Number
069568526340744
Chemical Name
PCSK9 Monoclonal Antibody (Clone 15A6)
References
Synonyms
  • Proprotein Convertase Subtilisin Kexin 9
  • NARC-1
Formulation 500 µg of IgG1 lyophilized
Stability 1 year
Storage -20°C
Shipping Wet ice in continental US; may vary elsewhere
Specificity
Human recombinant PCSK9 +

Background Reading

Maxwell, K.N., and Breslow, J.L. Proprotein convertase subtilisin kexin 9: The third locus implicated in autosomal dominant hypercholesterolemia. Curr Opin Lipidol 16 167-172 (2005).

Abifadel, M., Varret, M., Rabès, J., et al. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nat Genet 34(2) 154-156 (2003).

Maxwell, K.N., Fisher, E.A., and Breslow, J.L. Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment. Proc Natl Acad Sci USA 102(6) 2069-2074 (2005).

Lagace, T.A., Curtis, D.E., Garuti, R., et al. Secreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic mice. J Clin Invest 116(11) 2995-3005 (2006).

Seidah, N.G., Benjannet, S., Wickham, L., et al. The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): Liver regeneration and neuronal differentiation. Proc Natl Acad Sci USA 100(3) 928-933 (2003).

Maxwell, K.N., and Breslow, J.L. Adenoviral-mediated expression of Pcsk9 in mice results in a low-density lipoprotein receptor knockout phenotype. Proc Natl Acad Sci USA 101(18) 7100-7105 (2004).

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Description

Antigen: purified human recombinant PCSK9 · Clone designation: 15A6 · Host: mouse · Isotype: IgG1 · Application(s): PCSK9 ligand blotting (nondenaturing conditions) and WB · Proprotein convertase subtilisin kexin 9 (PCSK9) is a member of the subtilisin serine protease family with an important role in lipoprotein metabolism.1 Gain-of-function mutations in the PCSK9 gene are associated with autosomal dominant hypercholesterolemia which is characterized by an increase in low-density lipoprotein (LDL) cholesterol levels.2 PCSK9 overexpression in wild-type mice doubles the plasma total cholesterol, possibly through accelerated LDL receptor degredation.3,1 PCSK9 mRNA is detected in various tissues such as liver, kidney, lung, spleen, jejunum, ileum, colon, and muscle with the highest expression in the liver.4 Human PCSK9 precursor is 692 amino acids in length with an estimated molecular weight of 74 kDa. This proprotein is self-cleaved to form a mature protein at around 63 kDa in the Golgi body.5

1 Maxwell, K.N., Fisher, E.A., and Breslow, J.L. Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment. Proc Natl Acad Sci USA 102(6) 2069-2074 (2005).

2 Abifadel, M., Varret, M., Rabès, J., et al. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nat Genet 34(2) 154-156 (2003).

3 Maxwell, K.N., and Breslow, J.L. Adenoviral-mediated expression of Pcsk9 in mice results in a low-density lipoprotein receptor knockout phenotype. Proc Natl Acad Sci USA 101(18) 7100-7105 (2004).

4 Seidah, N.G., Benjannet, S., Wickham, L., et al. The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): Liver regeneration and neuronal differentiation. Proc Natl Acad Sci USA 100(3) 928-933 (2003).

5 Maxwell, K.N., and Breslow, J.L. Proprotein convertase subtilisin kexin 9: The third locus implicated in autosomal dominant hypercholesterolemia. Curr Opin Lipidol 16 167-172 (2005).

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