Key features and details
- Expression system: Escherichia coli
- Purity: > 90% SDS-PAGE
- Tags: His tag N-Terminus
- Suitable for: SDS-PAGE, HPLC
- High batch-to-batch consistency
- Optimal bioactivity
- Guaranteed identical to human native proteins
- >95% purity
- Ultra-low endotoxin levels: <0.005 Eu/µg
- Carrier and tag free
Product nameRecombinant Human Apolipoprotein E
See all Apolipoprotein E proteins and peptides
Purity> 90 % SDS-PAGE.
Purity is greater than 90% as determined by HPLC adn SDS-PAGE. Endotoxin level is <0.1 ng per µg of ApoE2.
Expression systemEscherichia coli
Protein lengthFull length protein
Predicted molecular weight34 kDa
Amino acids19 to 317
TagsHis tag N-Terminus
Our Abpromise guarantee covers the use of ab123749 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Additional notesEndotoxin Level: <0.1 ng/µg.
Concentration information loading...
Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at -20ºC.
ReconstitutionReconstitute in sterile dH2O to a concentration of 0.1-1.0 mg/ml. The solution can then be diluted into other aqueous buffers and store at 4°C for 1 week or –20°C for future use.
FunctionMediates 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 specificityOccurs 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 diseaseDefects 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 similaritiesBelongs to the apolipoprotein A1/A4/E family.
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.
- Information by UniProt
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab123749 has not yet been referenced specifically in any publications.