Key features and details
- Expression system: Escherichia coli
- Purity: >= 90% SDS-PAGE
- Endotoxin level: < 1.000 Eu/µg
- Active: Yes
- Suitable for: SDS-PAGE
Product nameRecombinant human Apolipoprotein E3
See all Apolipoprotein E3 proteins and peptides
Determined by its ability to stimulate the proliferation of human SH-SY5Y cells.
Purity>= 90 % SDS-PAGE.
ab50242 purity is greater than 90% by SDS-PAGE gel and HPLC analyses.
Endotoxin level< 1.000 Eu/µg
Expression systemEscherichia coli
Protein lengthFull length protein
SequenceMKVEQAVETE PEPELRQQTE WQSGQRWELA LGRFWDYLRW VQTLSEQVQE ELLSSQVTQE LRALMDETMK ELKAYKSELE EQLTPVAEET RARLSKELQA AQARLGADME DVCGRLVQYR GEVQAMLGQS TEELRVRLAS HLRKLRKRLL RDADDLQKRL AVYQAGAREG AERGLSAIRE RLGPLVEQGR VRAATVGSLA GQPLQERAQA WGERLRARME EMGSRTRDRL DEVKEQVAEV RAKLEEQAQQ IRLQAEAFQA RLKSWFEPLV EDMQRQWAGL VEKVQAAVGT SAAPVPSDNH
Our Abpromise guarantee covers the use of ab50242 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Concentration information loading...
Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
ReconstitutionCentrifuge the vial prior to opening. Initially reconstitute in 20mM Sodium Phosphate, pH 7.8 + 0.5mM DTT to 1.0 mg/ml. Store at 2°C to 8°C for up to 1 week or prepare for extended storage. After initial reconstitution, further dilute in a buffer containing a carrier protein or stabilizer (e.g. 0.1% BSA). Store working aliquots at -20°C to -80°C.
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.
ab50242 has been referenced in 2 publications.
- Calero O et al. A fast and cost-effective method for apolipoprotein E isotyping as an alternative to APOE genotyping for patient screening and stratification. Sci Rep 8:5969 (2018). PubMed: 29654261
- Young EK et al. HDL-ApoE content regulates the displacement of hepatic lipase from cell surface proteoglycans. Am J Pathol 175:448-57 (2009). SDS-PAGE . PubMed: 19528346