PCSK9 (human) Monoclonal Antibody (Clone 15A6)

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.^1,3 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 Cayman’s PCSK9 (human) Monoclonal Antibody (Clone 15A6) can be used for immunofluorescence (IF) and Western blot (WB) applications. The antibody recognizes PCSK9 at 78 kDa from human samples.

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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.P., 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(2), 167-172 (2005).