Merck, AB947-K, Anti-Apolipoprotein E (1L)

General description
34 kDa
FUNCTION: SwissProt: P02649 # 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.
SIZE: 317 amino acids; 36154 Da
SUBCELLULAR LOCATION: Secreted.
TISSUE SPECIFICITY: 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.
PTM: Synthesized with the sialic acid attached by O-glycosidic linkage and is subsequently desialylated in plasma. & Glycated in plasma VLDL of normal subjects, and of hyperglycemic diabetic patients at a higher level (2-3 fold).
DISEASE: SwissProt: P02649 # 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. & The APOE*4 allele is associated with late onset Alzheimer disease 2 (AD2) [MIM:104310]. The APOE*4 allele is genetically associated with the common late onset familial and sporadic forms of Alzheimer disease (AD). 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 [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.
SIMILARITY: SwissProt: P02649 ## Belongs to the apolipoprotein A1/A4/E family.
Recombinant human apolipoprotein E.
Application
Western blot (Schwab, 1996): 1:1,000-1:2,000

Immunohistochemistry (Summers, 1998; Wisniewski & Frangione, 1992; Schwab, 1996)

Optimal working dilutions must be determined by the end user.
Biochem/physiol Actions
Monospecific for Apolipoprotein E by immunoelectrophoresis when tested against pooled human plasma and twice concentrated pooled human serum. Reacts with Apo E isoforms E2, E3 and E4 by Western blot.
Physical form
Delipidated goat antiSerum, 0.2 μm filtered. Liquid in Tris-saline, pH 7.4 with 0.1% sodium azide as preservative.
Preparation Note
Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Other Notes
Liver tissue
Disclaimer
This product is intended for use by IVD manufacturers.
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