Recombinant human PCSK9 protein (Active) (Biotin) is a Human Full Length protein, in the 31 to 692 aa range, expressed in HEK 293, with >=80% purity and suitable for SDS-PAGE, FuncS.
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Application | Reactivity | Dilution info | Notes |
---|---|---|---|
Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info - | Notes - |
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:17461796, PubMed:18197702, PubMed:18799458, 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.
NARC1, PSEC0052, PCSK9, Proprotein convertase subtilisin/kexin type 9, Neural apoptosis-regulated convertase 1, Proprotein convertase 9, Subtilisin/kexin-like protease PC9, NARC-1, PC9
Recombinant human PCSK9 protein (Active) (Biotin) is a Human Full Length protein, in the 31 to 692 aa range, expressed in HEK 293, with >=80% purity and suitable for SDS-PAGE, FuncS.
pH: 8
Constituents: 20% Glycerol (glycerin, glycerine), 0.64% Sodium chloride, 0.48% Tris, 0.02% Potassium chloride
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:17461796, PubMed:18197702, PubMed:18799458, 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.
Belongs to the peptidase S8 family.
Cleavage by furin and PCSK5 generates a truncated inactive protein that is unable to induce LDLR degradation.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Enzymatically biotin-labeled using Avi-tag™ technology
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a protein responsible for the regulation of cholesterol levels by binding to low-density lipoprotein receptors (LDLR) on hepatocytes. This interaction marks the LDLRs for degradation reducing the liver's ability to clear LDL cholesterol from the blood. PCSK9 has a molecular weight of approximately 74 kDa. The protein is mainly expressed in the liver but is also found in the intestine and kidneys. PCSK9 is referred to as NARC-1 standing for neural apoptosis-regulated convertase 1 highlighting its role in the liver's cholesterol management system.
PCSK9 influences cholesterol homeostasis by its important role in degrading LDL receptors. It functions independently rather than as part of larger protein complexes. PCSK9 gains particular interest in therapeutic contexts where its inhibition can lead to increased LDLR levels and enhanced clearance of LDL cholesterol. Biotinylated PCSK9 and mouse PCSK9 variants provide significant tools for experimental study. Kits such as the PCSK9 ELISA kit enable detailed measurement of PCSK9 levels in blood samples providing insights into cholesterol metabolism dynamics.
PCSK9 operates within the lipid metabolism pathway and the cholesterol biosynthesis pathway. The protein's activity affects the fate of LDL cholesterol within these pathways. It interacts with proteins such as apolipoprotein B (ApoB) which plays a central role in the structural component of LDL particles. The modulation of these pathways by PCSK9 highlights the significance of its function in maintaining cardiovascular health and managing cholesterol levels.
PCSK9 is closely linked to hypercholesterolemia and coronary artery disease. Mutations in PCSK9 can lead to autosomal dominant hypercholesterolemia due to its effect on LDL receptor degradation. Other proteins such as ApoB and LDLR are involved in these conditions tightly interacting with PCSK9's regulatory function. A better understanding of PCSK9's role offers potential therapeutic targets for cardiovascular disease interventions especially through the development of PCSK9 antibodies and PCSK9 assays that adjust cholesterol levels.
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Specific activity of ab271653.
SDS-PAGE analysis of 4 μg ab271653.
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