Anti-Apolipoprotein E4 antibody [4E4] (ab169861)
Key features and details
- Mouse monoclonal [4E4] to Apolipoprotein E4
- Suitable for: WB
- Reacts with: Chinese hamster
- Isotype: IgG1
Overview
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Product name
Anti-Apolipoprotein E4 antibody [4E4]
See all Apolipoprotein E4 primary antibodies -
Description
Mouse monoclonal [4E4] to Apolipoprotein E4 -
Host species
Mouse -
Tested applications
Suitable for: WBmore details -
Species reactivity
Reacts with: Chinese hamster -
Immunogen
Synthetic peptide corresponding to Human Apolipoprotein E4 conjugated to Keyhole Limpet Haemocyanin (KLH).
Database link: P02649 -
Positive control
- CHO + Apolipoprotein E4 lysate
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General notes
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. -
Storage buffer
Preservative: 0.1% Sodium azide
Constituent: 99% PBS -
Concentration information loading...
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Purity
Protein G purified -
Clonality
Monoclonal -
Clone number
4E4 -
Myeloma
x63-Ag8.653 -
Isotype
IgG1 -
Research areas
Associated products
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Compatible Secondaries
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Conjugation kits
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Isotype control
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab169861 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB |
1/64000. Predicted molecular weight: 36 kDa.
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Notes |
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WB
1/64000. Predicted molecular weight: 36 kDa. |
Target
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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. -
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. -
Involvement in disease
Defects in APOE are a cause of hyperlipoproteinemia type 3 (HLPP3) [MIM:107741]; 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) [MIM:104310]. 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. Note=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) [MIM:269600]; 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) [MIM:611771]. 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. -
Sequence similarities
Belongs to the apolipoprotein A1/A4/E family. -
Post-translational
modificationsSynthesized 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. -
Cellular localization
Secreted. - Information by UniProt
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Alternative names
- AD2 antibody
- Alzheimer disease 2 (APOE*E4 associated, late onset) antibody
- Apo E4 antibody
see all
Images
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Lane 1 : 169861 at 1/8000 dilution
Lane 2 : 169861 at 1/16000 dilution
Lane 3 : 169861 at 1/32000 dilution
Lane 4 : 169861 at 1/64000 dilution
Lane 5 : 169861 at 1/128000 dilution
All lanes : CHO + Apolipoprotein E4 lysate
Predicted band size: 36 kDaCHO + Apolipoprotein E4 lysate was run on 4-12% His-Tris 2D gel in 1x MOPS buffer. Transfer to 0.45 um nitrocellulose. Membrane probed with anti Apolipoprotein E4 anti-mouse IgG (whole molecule) AP-conjugate (1/2000 dilution). Detection with BCIP/MBT substrate.
Datasheets and documents
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SDS download
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Datasheet download
References (1)
ab169861 has been referenced in 1 publication.
- Thangavel R et al. Co-Expression of Glia Maturation Factor and Apolipoprotein E4 in Alzheimer's Disease Brain. J Alzheimers Dis 61:553-560 (2018). IF . PubMed: 29172001