Product Pathways - Metabolism
PCSK9 (D7U6L) Rabbit mAb #85813
|85813S||100 µl ( 10 western blots )||￥3,100.00 现货查询||购买询价|
|85813||carrier free & custom formulation / quantity||email request|
|W||1:1000||Human,||Endogenous||65, 80||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation,
Specificity / Sensitivity
PCSK9 (D7U6L) Rabbit mAb recognizes endogenous levels of total PCSK9 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln190 of human PCSK9 protein.
Western blot analysis of extracts from T84 cells, untreated (-) or treated with Brefeldin A #9972 (100 ng/ml, 16 hrs; +), using PCSK9 (D7U6L) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).
The proprotein convertases (PCs) are enzymes that activate precursor proteins through proteolytic cleavage within the secretory pathway. PCs comprise several enzymes that are basic amino acid-specific proteinases (furin, PC1/3, PC2, PC4, PACE4, PC5/6, and PC7), as well as nonbasic amino acid convertases (S1P and PC9) (1). PCs have a common structure that includes an N-terminal signal peptide for secretory pathway targeting; a pro-domain that is thought to act as an intramolecular chaperone; a catalytic domain containing the active site; a P-domain that contributes to the overall folding of the enzyme by regulating stability, calcium-, and pH-dependence; and a C-terminal domain that interacts with the membrane (2). PCs act in a tissue- and substrate-specific fashion to generate an array of bioactive peptides and proteins from precursors, both in the brain and the periphery (3).
Mutations in the PCSK9 gene (encoding proprotein converts subtilisin/kexin type 9, PC9) have been found to cause autosomal-dominant hypercholesterolemia. PCSK9 was therefore demonstrated to be a key factor involved in lipoprotein metabolism (4). PCSK9 acts as a chaperone protein that binds the LDL receptor (LDLR) at the cell membrane and induces LDLR lysosomal degradation rather than recycling (5). PCSK9 inhibition has since been a new therapeutic strategy for the treatment of hypercholesterolemia (6).
- Scamuffa, N. et al. (2006) FASEB J 20, 1954-63.
- Fugère, M. and Day, R. (2005) Trends Pharmacol Sci 26, 294-301.
- Seidah, N.G. and Chrétien, M. (1999) Brain Res 848, 45-62.
- Abifadel, M. et al. (2003) Nat Genet 34, 154-6.
- Cariou, B. et al. (2011) Atherosclerosis 216, 258-65.
- Cohen, J.C. et al. (2006) N Engl J Med 354, 1264-72.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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