ELISA/assay

Human PCSK9/Proprotein Convertase 9 ELISA Kit PicoKine®

EK1147

96 wells/kit, with removable strips.

369 USD

Human PCSK9/Proprotein Convertase 9 ELISA Kit PicoKine®

96 wells/kit, with removable strips.

369 USD

Human PCSK9/Proprotein Convertase 9 ELISA Kit PicoKine® (96 Tests). Quantitate Human PCSK9 in cell culture supernatants, cell lysates, serum and plasma (heparin, EDTA). Sensitivity: 10pg/ml.

Human

ELISA

PCSK9

Q8NBP7

Expression system for standard: NS0; Immunogen sequence: S153-Q692

There is no detectable cross-reactivity with other relevant proteins.

156 pg/ml - 10,000 pg/ml

<10 pg/ml

cell culture supernatants, cell lysates, serum and plasma (heparin, EDTA)

monoclonal antibody from mouse, polyclonal antibody from goat

Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles (Ships with gel ice, can store for up to 3 days in room temperature. Freeze upon receiving.)

Proprotein convertase subtilisin/kexin type 9

Proprotein convertase subtilisin/kexin type 9;3.4.21.-;Neural apoptosis-regulated convertase 1;NARC-1;Proprotein convertase 9;PC9;Subtilisin/kexin-like protease PC9;PCSK9;NARC1;PSEC0052;

Proprotein convertase subtilisin/kexin type 9

74286 MW

Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments (PubMed:18039658). Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation (PubMed:18799458, PubMed:17461796, PubMed:18197702, PubMed:22074827). Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non- acetylated intermediates of BACE1 in the early secretory pathway (PubMed:18660751). Inhibits epithelial Na (+) channel (ENaC)- mediated Na (+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.

Cytoplasm. Secreted. Endosome. Lysosome. Cell surface. Endoplasmic reticulum. Golgi apparatus. Autocatalytic cleavage is required to transport it from the endoplasmic reticulum to the Golgi apparatus and for the secretion of the mature protein. Localizes to the endoplasmic reticulum in the absence of LDLR and colocalizes to the cell surface and to the endosomes/lysosomes in the presence of LDLR. The sorting to the cell surface and endosomes is required in order to fully promote LDLR degradation.

Expressed in neuro-epithelioma, colon carcinoma, hepatic and pancreatic cell lines, and in Schwann cells.

Belongs to the peptidase S8 family.

Proprotein convertase subtilisin/kexin type 9, also known as PCSK9, is an enzyme that in humans is encoded by the PCSK9 gene. This gene encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. By genomic sequence analysis, the PCSK9 gene was mapped to chromosome 1p32. This protein plays a major regulatory role in cholesterol homeostasis. PCSK9 binds to the epidermal growth factor-like repeat A (EGF-A) domain of the low-density lipoprotein receptor (LDLR), inducing LDLR degradation. Reduced LDLR levels result in decreased metabolism of low-density lipoproteins (LDL), which could lead to hypercholesterolemia. PCSK9 may also have a role in the differentiation of cortical neurons.

Amino Acid Metabolism, Amino Acids, Cancer, Cardiovascular, Cell Biology, Cholesterol Metabolism, Intracellular, Lipid And Lipoprotein Metabolism, Lipid Metabolism, Lipids / Lipoproteins, Metabolic Signaling Pathways, Metabolism, Neural Stem Cells, Pathways And Processes, Proteolysis / Ubiquitin, Proteolytic Enzymes, Signal Transduction, Stem Cells