product summary
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company name :
MyBioSource
product type :
ELISA/assay
product name :
Rabbit ApoE(Apolipoprotein E)ELISA Kit
catalog :
MBS2513934
quantity :
48-Strip-Wells
price :
450 USD
more info or order :
product information
catalog number :
MBS2513934
products type :
ELISA Kit
products full name :
Rabbit ApoE(Apolipoprotein E)ELISA Kit
products short name :
ApoE
other names :
apolipoprotein E isoform b; Apolipoprotein E; apolipoprotein E; apolipoprotein E3; apolipoprotein E
products gene name :
ApoE
other gene names :
APOE; APOE; AD2; LPG; APO-E; LDLCQ5; Apo-E
uniprot entry name :
APOE_HUMAN
reactivity :
Rabbit
sequence length :
317
specificity :
This kit recognizes natural and recombinant Rabbit ApoE. No significant cross-reactivity or interference between Rabbit ApoE and analogues was observed.
storage stability :
Store at 4 degree C.
other info1 :
Samples: Serum, plasma and other biological fluids. Assay Type: Sandwich. Detection Range: 0.625-40ng/mL. Sensitivity: 0.375ng/mL
products description :
Intended Uses: This ELISA kit applies to the in vitro quantitative determination of Rabbit ApoE concentrations in serum, plasma and other biological fluids. Principle of the Assay This ELISA kit uses Sandwich-ELISA as the method. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to ApoE. Standards or samples are added to the appropriate micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for ApoE and Avidin-Horseradish Peroxidase (HRP) conjugate is added to each micro plate well successively and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain ApoE, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of ApoE. You can calculate the concentration of ApoE in the samples by comparing the OD of the samples to the standard curve.
ncbi gi num :
4557325
ncbi acc num :
NP_000032.1
ncbi gb acc num :
NM_000041.3
uniprot acc num :
P02649
ncbi mol weight :
36,154 Da
ncbi pathways :
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)
ncbi summary :
The protein encoded by this gene is a major apoprotein of the chylomicron. It binds to a specific liver and peripheral cell receptor, and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. This gene maps to chromosome 19 in a cluster with the related apolipoprotein C1 and C2 genes. Mutations in this gene 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. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2014]
uniprot summary :
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: Lipid-binding; Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: 19q13.2. Cellular Component: Golgi apparatus; microtubule; extracellular space; endoplasmic reticulum; lysosome; dendrite; early endosome; extracellular region; nuclear envelope; extracellular matrix; chylomicron; extrinsic to external side of plasma membrane; cell soma; membrane; late endosome; cytoplasm; plasma membrane; nucleus; vesicle. Molecular Function: heparin binding; lipid transporter activity; identical protein binding; protein homodimerization activity; metal chelating activity; beta-amyloid binding; cholesterol binding; antioxidant activity; protein binding; low-density lipoprotein receptor binding; hydroxyapatite binding; cholesterol transporter activity; phospholipid binding; tau protein binding; lipid binding. Biological Process: lipoprotein catabolic process; phototransduction, visible light; 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; regulation of axon extension; positive regulation of lipid biosynthetic process; 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; lipoprotein biosynthetic process; regulation of gene expression; 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; retinoid metabolic process; negative regulation of cholesterol biosynthetic process; aging; receptor-mediated endocytosis; response to retinoic acid; negative regulation of lipid biosynthetic process; neurite regeneration; cytoskeleton organization and biogenesis; cholesterol efflux; cellular calcium ion homeostasis; G-protein coupled receptor protein signaling pathway; reverse cholesterol transport; triacylglycerol metabolic process; 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
size1 :
48-Strip-Wells
price1 :
450 USD
size2 :
96-Strip-Wells
price2 :
535
more info or order :
company information
MyBioSource
P.O. Box 153308
San Diego, CA 92195-3308
sales@mybiosource.com
https://www.mybiosource.com
1-888-627-0165
headquarters: USA
MyBioSource, LLC was orginally founded in Vancouver by three enthusiastic scientists who are passionate about providing the world with the best reagents available. Together, they form a company with a big vision known as MyBioSource. MyBioSource is now located in San Diego, California, USA.

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