More info
Assay Range | 156 - 10,000 pg/mL |
Sensitivity | 10.0 pg/mL |
Size | 96T |
Storage | Store at 2 - 8ºC. Keep reconstituted standard and detection Ab at -20 ºC |
Assay Principle | Sandwich ELISA |
Sample volume | 100 µL final volume, dilution factor varies on samples. |
Detection Method | Chromogenic |
Kit Components
1. Recombinant Mouse PCSK9 standard: 2 vials.
2. One 96-well plate precoated with anti- Mouse PCSK9 Ab
3. Sample diluent buffer: 12 mL - 1
4. Detection antibody: 130 µL, dilution 1:100.
5. Streptavidin-HRP: 130 µL, dilution 1:100
6. Antibody diluent buffer: 12 mL x1
7. Streptavidin-HRP diluent buffer: 12 mL x1
8. TMB developing agent: 10 mL x1
9. Stop solution: 10 mL x1.
10. Washing solution (20x): 25 mL x1.
Background
Proprotein convertase subtilisin kexin 9 (PCSK9), also known as neural apoptosis-regulated convertase 1 (NARC-1), proprotein convertase 9 (PC9), subtilisin/kexin-like protease PC9, is a member of the proteinase K subfamily of subtilisin-related serine endoprotease family. The full-length mouse PCSK9 is a 694 amino acid (aa) precursor protein composed of a signal peptide, a prodomain, and a catalytic domain. Initially synthesized as a soluble 74 kDa precursor protein, PCSK9 is subjected to autocatalytic intramolecular cleavage in the endoplasmic reticulum to generate a 14 kDa prodomain and a 60 kDa catalytic domain. During secretion, a portion of active PCSK9 may undergo additional N-terminal proteolysis by furin or proprotein convertase 5/6A, creating an inactive 53 kDa form. This cleavage site is conserved between mouse and human or rat PCSK9, which share 78% or 93% amino acid sequence identity, respectively. PCSK9 plays a major role in cholesterol homeostasis. It binds to the epidermal growth factor-like repeat A (EGF-A) domain of the low-density lipoprotein receptor (LDLR) to induce LDLR degradation. Reduced LDLR levels result in decreased metabolism of LDL-C, which could lead to hypercholesterolemia. It is showed that, in PCSK9 knock-out mice, the number of LDL R in hepatocytes is increased, whereas overexpression of PCSK9 causes reduction of the amount of LDL R protein in the liver. In humans, genetic analyses have shown that individuals who have nonsense or loss-of-function mutations in the PCSK9 gene have significantly lower plasma LDL cholesterol levels, indicating that PCSK9 plays a key role in reducing the hepatic LDL R levels. Serum PCSK9 concentrations have been found to be directly associated with cholesterol levels. Given loss-of-function of PCSK9 can significantly reduce the risk of of coronary heart diseases, PCSK9 has been a potential drug target in the therapeutic strategy of coronary heart diseases.