Cell Signaling Technology

Product Pathways - Metabolism

PCSK9 (D7U6L) Rabbit mAb #85813

No. Size Price
85813S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
85813 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 65, 80 Rabbit IgG
IP 1:50

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 Blotting

Western Blotting

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).

IP

IP

Immunoprecipitation of PCSK9 from T84 cell extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is PCSK9 (D7U6L) Rabbit mAb. Western blot analysis was performed using PCSK9 (D7U6L) Rabbit mAb.

Background

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).

  1. Scamuffa, N. et al. (2006) FASEB J 20, 1954-63.
  2. Fugère, M. and Day, R. (2005) Trends Pharmacol Sci 26, 294-301.
  3. Seidah, N.G. and Chrétien, M. (1999) Brain Res 848, 45-62.
  4. Abifadel, M. et al. (2003) Nat Genet 34, 154-6.
  5. Cariou, B. et al. (2011) Atherosclerosis 216, 258-65.
  6. Cohen, J.C. et al. (2006) N Engl J Med 354, 1264-72.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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