AD2; LPG; LDLCQ5; Apolipoprotein E; Apo-E; apolipoprotein E

For Research Use Only. Not for use in diagnostic procedures.

Liquid

200 ug/mL (lot specific)

Store APO-E peptide at -20 degree C, stable for one year.

Small volumes of APOE blocking peptide vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Blocking (BL)

APO-E peptide is used for blocking the activity of APO-E antibody. It usually blocks the antibody activity completely in Western blot by incubating the peptide with equal volume of antibody for 30 min at 37 degree C.

36,154 Da

apolipoprotein E

apolipoprotein E; apolipoprotein E3

Apolipoprotein E

Apo-E??[Similar Products]

APOE_HUMAN

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]

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; extracellular space; microtubule; 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: 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; 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; regulation of gene expression; lipoprotein biosynthetic process; negative regulation of endothelial cell proliferation; protein import; 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

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