ELISA/assay

Mouse Apolipoprotein E ELISA Kit

MBS721115

48-Strip-Wells

470 USD

ELISA Kit

Mouse Apolipoprotein E ELISA Kit

Apolipoprotein E

apolipoprotein E; Apolipoprotein E; apolipoprotein E; apo-E; apolipoprotein E3; apolipoprotein E

APOE

APOE; APOE; AD2; LPG; LDLCQ5; Apo-E

APOE_HUMAN

Mouse

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive

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

Neurobiology

Principle of the Assay: Apo-E ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-Apo-E antibody and an Apo-E-HRP conjugate. The assay sample and buffer are incubated together with Apo-E-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 Apo-E concentration since Apo-E from samples and Apo-E-HRP conjugate compete for the anti-Apo-E antibody binding site. Since the number of sites is limited, as more sites are occupied by Apo-E from the sample, fewer sites are left to bind Apo-E-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The Apo-E concentration in each sample is interpolated from this standard curve.

4557325

NP_000032.1

NM_000041.2

36,154 Da

Alzheimer's Disease Pathway (83097); Alzheimer's Disease Pathway (509); Alzheimers Disease Pathway (672448); Binding And Uptake Of Ligands By Scavenger Receptors Pathway (771599); Chylomicron-mediated Lipid Transport Pathway (106157); Disease Pathway (530764); Diseases Associated With Visual Transduction Pathway (771581); HDL-mediated Lipid Transport Pathway (106158); Lipid Digestion, Mobilization, And Transport Pathway (106111); Lipoprotein Metabolism Pathway (106156)

Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly removed from the circulation by receptor-mediated endocytosis in the liver. Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells. ApoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. The APOE gene is mapped to chromosome 19 in a cluster with APOC1 and APOC2. Defects in apolipoprotein E result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants. [provided by RefSeq, Jul 2008]

APOE: Mediates the binding, internalization, and catabolism of lipoprotein particles. It can serve as a ligand for the LDL (apo B/E) receptor and for the specific apo-E receptor (chylomicron remnant) of hepatic tissues. Defects in APOE are a cause of hyperlipoproteinemia type 3 (HLPP3); also known as familial dysbetalipoproteinemia. Individuals with HLPP3 are clinically characterized by xanthomas, yellowish lipid deposits in the palmar crease, or less specific on tendons and on elbows. The disorder rarely manifests before the third decade in men. In women, it is usually expressed only after the menopause. The vast majority of the patients are homozygous for APOE*2 alleles. More severe cases of HLPP3 have also been observed in individuals heterozygous for rare APOE variants. The influence of APOE on lipid levels is often suggested to have major implications for the risk of coronary artery disease (CAD). Individuals carrying the common APOE*4 variant are at higher risk of CAD. Genetic variations in APOE are associated with Alzheimer disease type 2 (AD2). It is a late-onset neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated in neuronal death. The APOE*4 allele is genetically associated with the common late onset familial and sporadic forms of Alzheimer disease. Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE*4 alleles in 42 families with late onset AD. Thus APOE*4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE*4 was virtually sufficient to cause AD by age 80. The mechanism by which APOE*4 participates in pathogenesis is not known. Defects in APOE are a cause of sea-blue histiocyte disease (SBHD); also known as sea-blue histiocytosis. This disorder is characterized by splenomegaly, mild thrombocytopenia and, in the bone marrow, numerous histiocytes containing cytoplasmic granules which stain bright blue with the usual hematologic stains. The syndrome is the consequence of an inherited metabolic defect analogous to Gaucher disease and other sphingolipidoses. Defects in APOE are a cause of lipoprotein glomerulopathy (LPG). LPG is an uncommon kidney disease characterized by proteinuria, progressive kidney failure, and distinctive lipoprotein thrombi in glomerular capillaries. It mainly affects people of Japanese and Chinese origin. The disorder has rarely been described in Caucasians. Belongs to the apolipoprotein A1/A4/E family. Protein type: Secreted; Secreted, signal peptide; Lipid-binding. Chromosomal Location of Human Ortholog: 19q13.2. Cellular Component: Golgi apparatus; microtubule; extracellular space; lysosome; endoplasmic reticulum; early endosome; dendrite; extracellular region; nuclear envelope; extracellular matrix; chylomicron; extrinsic to external side of plasma membrane; cell soma; membrane; cytoplasm; late endosome; plasma membrane; nucleus; vesicle. Molecular Function: lipid transporter activity; heparin binding; identical protein binding; protein homodimerization activity; metal chelating activity; beta-amyloid binding; cholesterol binding; antioxidant activity; protein binding; low-density lipoprotein receptor binding; cholesterol transporter activity; hydroxyapatite binding; phospholipid binding; tau protein binding; lipid binding. Biological Process: phototransduction, visible light; lipoprotein catabolic process; negative regulation of MAP kinase activity; cGMP-mediated signaling; positive regulation of axon extension; axon regeneration in the peripheral nervous system; positive regulation of membrane protein ectodomain proteolysis; synaptic transmission, cholinergic; intracellular transport; triacylglycerol catabolic process; oligodendrocyte differentiation; negative regulation of neuron apoptosis; cholesterol catabolic process; long-chain fatty acid transport; cholesterol metabolic process; regulation of Cdc42 protein signal transduction; positive regulation of nitric-oxide synthase activity; negative regulation of blood coagulation; lipoprotein metabolic process; positive regulation of lipid biosynthetic process; regulation of axon extension; negative regulation of blood vessel endothelial cell migration; maintenance of cellular localization; response to reactive oxygen species; cholesterol homeostasis; response to ethanol; positive regulation of cGMP biosynthetic process; regulation of gene expression; lipoprotein biosynthetic process; protein import; negative regulation of endothelial cell proliferation; nitric oxide mediated signal transduction; regulation of neuronal synaptic plasticity; response to dietary excess; vasodilation; response to insulin stimulus; positive regulation of low-density lipoprotein receptor catabolic process; phospholipid efflux; negative regulation of cholesterol biosynthetic process; retinoid metabolic process; aging; receptor-mediated endocytosis; response to retinoic acid; negative regulation of lipid biosynthetic process; neurite regeneration; cholesterol efflux; cytoskeleton organization and biogenesis; cellular calcium ion homeostasis; G-protein coupled receptor protein signaling pathway; triacylglycerol metabolic process; reverse cholesterol transport; negative regulation of inflammatory response; fatty acid homeostasis; artery morphogenesis. Disease: Macular Degeneration, Age-related, 1; Alzheimer Disease 2; Alzheimer Disease 4; Lipoprotein Glomerulopathy; Sea-blue Histiocyte Disease

48-Strip-Wells

470 USD

96-Strip-Wells

675