Rabbit APOE Polyclonal Antibody | anti-APOE antibody

APOE antibody - N-terminal region

Cat. Num. AAA3211574

• Gene Names: APOE; AD2; LPG; APO-E; ApoE4; LDLCQ5
• Reactivity: Human, Mouse, Rat, Zebrafish
• Applications: Immunohistochemistry, Western Blot
• Purity: Affinity Purified
• Synonyms: APOE; Polyclonal Antibody; APOE antibody - N-terminal region; anti-APOE antibody

• Host: Rabbit
• Reactivity: Human, Mouse, Rat, Zebrafish
• Clonality: Polyclonal
• Purity/Purification: Affinity Purified
• Form/Format: Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
• Sequence: Synthetic peptide located within the following region: LMDETMKELKAYKSELEEQLTPVAEETRARLSKELQAAQARLGADMEDVC
• Sequence Length: 317

• Applicable Applications for anti-APOE antibody: Immunohistochemistry (IHC), Western Blot (WB)
• Homology: Human: 100%; Mouse: 93%; Rat: 93%; Zebrafish: 77%
• Preparation and Storage: For short term use, store at 2-8 degree C up to 1 week. For long term storage, store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Immunohistochemistry (IHC)

(Researcher: Dr. Yuzhi Chen, University of Arkansas for Medical ScienceApplication: IHCSpecies+tissue/cell type: Mouse brain stem cellsPrimary antibody dilution: 1:500Secondary antibody: Goat anti-rabbit Alexa-Fluor 594Secondary antibody dilution: 1:1000)

Western Blot (WB)

(Sample Type: Mouse BrainSample Type:2. mouse brain extracts (80ug) 3. rat brain extract(80ug) Primary Antibody Dilution:2ug/ml Secondary Antibody: IRDye 800CW goat anti-rabbit from Li-COR Bioscience Secondary Antibody Dilution:1: 20,000 Image Submitted by: Yuzhi Chen University of Arkansas for Medical Science)

Western Blot (WB)

(Sample Type: Human 721_BAPOE antibody - N-terminal region validated by WB using 721_B cell lysate at 1.0ug/ml.There is BioGPS gene expression data showing that APOE is expressed in 721_B)

Related Product Information for anti-APOE antibody

This is a rabbit polyclonal antibody against APOE. It was validated on Western Blot

Target Description: Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly removed from the circulation by receptor-mediated endocytosis in the liver. Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells. ApoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. The APOE gene is mapped to chromosome 19 in a cluster with APOC1 and APOC2. Defects in apolipoprotein E 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.

Product Categories/Family for anti-APOE antibody

Polyclonal; Lymphocyte Signaling; Drugs and Drug Metabolism; Mitochondria; Meiosis/Mitosis/Cell Cycle; Immunohistochemistry; GPCR

NCBI and Uniprot Product Information

• NCBI GI #: 4557325
• NCBI GeneID: 348
• NCBI Accession #: NP_000032
• NCBI GenBank Nucleotide #: NM_000041
• UniProt Accession #: P02649
• Molecular Weight: 34kDa
• NCBI Official Full Name: apolipoprotein E isoform b
• NCBI Official Synonym Full Names: apolipoprotein E
• NCBI Official Symbol: APOE
• NCBI Official Synonym Symbols: AD2; LPG; APO-E; ApoE4; LDLCQ5
• NCBI Protein Information: apolipoprotein E
• UniProt Protein Name: Apolipoprotein E
• Protein Family: Apolipoprotein
• UniProt Gene Name: APOE
• UniProt Synonym Gene Names: Apo-E
• UniProt Entry Name: APOE_HUMAN

NCBI Description

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. [provided by RefSeq, Jun 2016]

Uniprot Description

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; extracellular space; microtubule; lysosome; endoplasmic reticulum; 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: lipid transporter activity; heparin binding; 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; lipid binding; tau protein binding

Biological Process: lipoprotein catabolic process; phototransduction, visible light; negative regulation of MAP kinase activity; cGMP-mediated signaling; positive regulation of axon extension; positive regulation of membrane protein ectodomain proteolysis; axon regeneration in the peripheral nervous system; 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; positive regulation of lipid biosynthetic process; regulation of axon extension; negative regulation of blood vessel endothelial cell migration; maintenance of cellular localization; cholesterol homeostasis; response to reactive oxygen species; response to ethanol; positive regulation of cGMP biosynthetic process; regulation of gene expression; lipoprotein biosynthetic process; 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; negative regulation of cholesterol biosynthetic process; retinoid metabolic 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; triacylglycerol metabolic process; reverse cholesterol transport; fatty acid homeostasis; negative regulation of inflammatory response; artery morphogenesis

Disease: Macular Degeneration, Age-related, 1; Alzheimer Disease 2; Alzheimer Disease 4; Lipoprotein Glomerulopathy; Sea-blue Histiocyte Disease