ELISA/assay

Monkey Proprotein Convertase Subtilisin/Kexin Type 9 ELISA Kit

MBS040633

48-Strip-Wells

435 USD

ELISA Kit

Monkey Proprotein Convertase Subtilisin/Kexin Type 9 ELISA Kit

Proprotein Convertase Subtilisin/Kexin Type 9

proprotein convertase subtilisin/kexin type 9 preproprotein; Proprotein convertase subtilisin/kexin type 9; proprotein convertase subtilisin/kexin type 9; subtilisin/kexin-like protease PC9; neural apoptosis regulated convertase 1; convertase subtilisin/kexin type 9 preproprotein; proprotein convertase subtilisin/kexin type 9; Neural apoptosis-regulated convertase 1; NARC-1; Proprotein convertase 9; PC9; Subtilisin/kexin-like protease PC9

PCSK9

PCSK9; PCSK9; FH3; PC9; NARC1; LDLCQ1; NARC-1; HCHOLA3; NARC1; NARC-1; PC9

PCSK9_HUMAN

Monkey

No significant cross-reactivity or interference between Monkey PCSK9 and analogues was observed.

Store all reagents at 2-8 degree C

Samples: Serum, Plasma, Tissue Homogenate, Feces, Urine and Body Fluids. Assay Type: Sandwich. Detection Range: 62.5 ng/ml - 2000 ng/ml. Sensitivity: 10 ng/ml.

Intended Uses: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated PCSK9 concentrations in Monkey serum, plasma and other body fluids. Using Purified Monkey PCSK9 antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add PCSK9 and PCSK9 antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of PCSK9 in the samples is then determined by comparing the O.D. of the samples to the standard curve. Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100]

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated PCSK9 concentrations in Monkey serum, plasma and other body fluids. Using Purified Monkey PCSK9 antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add PCSK9 and PCSK9 antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of PCSK9 in the samples is then determined by comparing the O.D. of the samples to the standard curve.

31317307

NP_777596.2

NM_174936.3

Q8NBP7

74,286 Da

This gene encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. The encoded protein is synthesized as a soluble zymogen that undergoes autocatalytic intramolecular processing in the endoplasmic reticulum. The protein may function as a proprotein convertase. This protein plays a role in cholesterol homeostasis and may have a role in the differentiation of cortical neurons. Mutations in this gene have been associated with a third form of autosomal dominant familial hypercholesterolemia (HCHOLA3). [provided by RefSeq, Jul 2008]

PCSK9: 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. 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. 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. 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. Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3). A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins. Belongs to the peptidase S8 family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted; Secreted, signal peptide; Protease; EC 3.4.21.-; Cell development/differentiation. Chromosomal Location of Human Ortholog: 1p32.3. Cellular Component: Golgi apparatus; extracellular space; cell surface; rough endoplasmic reticulum; endoplasmic reticulum; lysosome; early endosome; ER to Golgi transport vesicle; extrinsic to external side of plasma membrane; perinuclear region of cytoplasm; late endosome; cytoplasm; plasma membrane. Molecular Function: sodium channel inhibitor activity; very-low-density lipoprotein binding; protein binding; protein self-association; low-density lipoprotein receptor binding; serine-type endopeptidase activity; low-density lipoprotein binding; apolipoprotein binding; apolipoprotein receptor binding. Biological Process: cholesterol metabolic process; lysosomal transport; apoptosis; positive regulation of receptor internalization; lipoprotein metabolic process; regulation of low-density lipoprotein receptor catabolic process; proteolysis; liver development; cellular response to starvation; neuron differentiation; protein autoprocessing; cholesterol homeostasis; triacylglycerol metabolic process; neurogenesis; cellular response to insulin stimulus; positive regulation of neuron apoptosis; phospholipid metabolic process; regulation of neuron apoptosis; negative regulation of receptor recycling; low-density lipoprotein receptor catabolic process; regulation of receptor activity; kidney development. Disease: Hypercholesterolemia, Autosomal Dominant, 3

48-Strip-Wells

435 USD

96-Strip-Wells

600