Anti-Apolipoprotein E (Human)

apoLipoprotein E

This product was assayed by immunoblot and found to be reactive against apoLipoprotein E at a dilution of 1:5 000 to 1:10 000. This product was also assayed against 1. 0 ug of apoLipoprotein E in a standard sandwich ELISA using Peroxidase conjugated Affinity Purified anti-Goat IgG [H& L] (Rabbit) catalog # 25-732-294061 and (ABTS (2 2\' -azino-bis-[3-ethylbenthiazoline-6-sulfonic acid]) as a substrate for 30 minutes at room temperature. A working dilution of 1:4 000 to 1:8 000 of the stock concentration is suggested for this product. For immunohistochemistry on paraffin embedded tissue dilute the product 1:50 to 1:200. Optimal titers for other applications should be determined by the researcher. Physical State: Liquid (sterile filtered)Purity and

1. 0 mg/ml (by UV absorbance at 280 nm)

None

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.

Occurs in all lipoprotein fractions in plasma. It constitutes 10-20% of very low density lipoproteins (VLDL) and 1-2% of high density lipoproteins (HDL). APOE is produced in most organs. Significant quantities are produced in liver brain spleen lung adrenal ovary kidney and muscle.

Glycated in plasma VLDL of normal subjects and of hyperglycemic diabetic patients at a higher level (2-3 fold).

Defects in APOE are a cause of hyperlipoproteinemia type III [MIM:107741]; also known as familial dysbetalipoproteinemia. Individuals with hyperlipoproteinemia type III 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 hyperlipoproteinemia type III 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.

Defects in APOE are a cause of sea-blue histiocyte disease [MIM:269600]; also called 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.

Belongs to the apolipoprotein A1/A4/E family.