Human Apo E ELISA Kit (RMEK-0152372)
Cat. No.: RMEK-0152372
Category: ELISA Kits
INQUIRY
1 x 96 tests
Human Apo E ELISA Kit is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of Apo E protein in cit plasma, edta plasma, hep plasma, milk, and serum. The technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time.
Product Features
| Species Reactivity | Human |
|---|---|
| Detection Method | Colorimetric |
| Assay Duration | One step assay |
| Assay Time | 1.5 h |
| Assay Type | Sandwich (quantitative) |
| Precision | Intra-Assay-Serum-3-1.6%; Inter-Assay-Serum-8-9.5% |
| Sensitivity | 10.8 pg/mL |
| Range | 31.25 pg/mL - 2000 pg/mL |
| Sample Type | Cit plasma, EDTA Plasma, Hep Plasma, Milk, Serum |
| Recovery | Milk-109-95% - 119%; Serum-108-89% - 122%; Hep Plasma-114-96% - 123%; EDTA Plasma-108-100% - 117%; Cit plasma-117-106% - 125% |
| Key Features | One-wash 90 minute protocol; Sensitivity: 10.8 pg/mL; Range: 31.25 pg/mL - 2000 pg/mL; Sample type: Cit plasma, EDTA Plasma, Hep Plasma, Milk, Serum; Detection method: Colorimetric; Assay type: Sandwich (quantitative); Reacts with: Human |
Target Information
| Target Symbol | APOE |
|---|---|
| UniProt ID | P02649 |
| Biomarker of SCs/CSCs | Luminal A Breast Cancer |
| Function | 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. |
| Cellular Localization | Secreted. |
| Post-transcriptional Modifications | Synthesized with the sialic acid attached by O-glycosidic linkage and is subsequently desialylated in plasma. O-glycosylated with core 1 or possibly core 8 glycans. Thr-307 is a minor glycosylation site compared to Ser-308.Glycated in plasma VLDL of normal subjects, and of hyperglycemic diabetic patients at a higher level (2-3 fold).Phosphorylation sites are present in the extracelllular medium. |
| Involvement in Disease | 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. |
Storage & Shipping
| Storage | Store at 2-8°C |
|---|---|
| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
