ELISA/assay

Canine Proprotein Convertase Subtilisin/Kexin Type 9 ELISA Kit

MBS751361

48-Strip-Wells

470 USD

ELISA Kit

Canine 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; PSEC0052; NARC-1; PC9

PCSK9_HUMAN

Canine

This assay has high sensitivity and excellent specificity for detection of PCSK-9. No significant cross-reactivity or interference between PCSK-9 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between PCSK-9 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 pg/mL.

Intended Uses: This PCSK-9 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Canine PCSK-9. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Principle of the assay: PCSK-9 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-PCSK-9 antibody and an PCSK-9-HRP conjugate. The assay sample and buffer are incubated together with PCSK-9-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the PCSK-9 concentration since PCSK-9 from samples and PCSK-9-HRP conjugate compete for the anti-PCSK-9 antibody binding site. Since the number of sites is limited, as more sites are occupied by PCSK-9 from the sample, fewer sites are left to bind PCSK-9-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The PCSK-9 concentration in each sample is interpolated from this standard curve.

31317307

NP_777596.2

NM_174936.3

20,827 Da

This gene encodes a member of the subtilisin-like proprotein convertase family, which includes proteases that process protein and peptide precursors trafficking through regulated or constitutive branches of the secretory pathway. The encoded protein undergoes an autocatalytic processing event with its prosegment in the ER and is constitutively secreted as an inactive protease into the extracellular matrix and trans-Golgi network. It is expressed in liver, intestine and kidney tissues and escorts specific receptors for lysosomal degradation. It plays a role in cholesterol and fatty acid metabolism. Mutations in this gene have been associated with autosomal dominant familial hypercholesterolemia. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2014]

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: EC 3.4.21.-; Cell development/differentiation; Secreted; Secreted, signal peptide; Protease. 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: very-low-density lipoprotein binding; sodium channel inhibitor activity; 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; cellular response to starvation; proteolysis; liver development; neuron differentiation; protein autoprocessing; cholesterol homeostasis; triacylglycerol metabolic process; neurogenesis; cellular response to insulin stimulus; phospholipid metabolic process; positive regulation of neuron apoptosis; 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

470 USD

96-Strip-Wells

675