Full Product Name
APOE siRNA (Human)
Product Synonym Names
Apolipoprotein E; Apo-E
Product Gene Name
APOE sirna
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Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
3D Structure
ModBase 3D Structure for P02649
Specificity
APOE siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
Purity/Purification
> 97%
Form/Format
Lyophilized powder
Quality Control
Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
Directions for Use
We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
Components
We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human APOE gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
Preparation and Storage
Shipped at 4 degree C. Store at -20 degree C for one year.
Negative Control
siRNA Negative Control (Catalog# MBS8241404) is a non-targeting 21 nt siRNA recommended as a negative control for experiments using targeted siRNA transfection.
Other Notes
Small volumes of APOE sirna 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.
Related Product Information for
APOE sirna
siRNA to inhibit APOE expression using RNA interference
Applications Tested/Suitable for APOE sirna
RNA Interference (RNAi)
NCBI/Uniprot data below describe general gene information for APOE. It may not necessarily be applicable to this product.
NCBI Accession #
NP_000032.1
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NCBI GenBank Nucleotide #
NM_000041.3
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UniProt Primary Accession #
P02649
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UniProt Secondary Accession #
Q9P2S4; B2RC15; C0JYY5[Other Products]
UniProt Related Accession #
P02649[Other Products]
Molecular Weight
36,154 Da
NCBI Official Full Name
apolipoprotein E isoform b
NCBI Official Synonym Full Names
apolipoprotein E
NCBI Official Symbol
APOE [Similar Products]
NCBI Official Synonym Symbols
AD2; LPG; APO-E; LDLCQ5
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NCBI Protein Information
apolipoprotein E
UniProt Protein Name
Apolipoprotein E
Protein Family
Apolipoprotein
UniProt Gene Name
APOE [Similar Products]
UniProt Synonym Gene Names
Apo-E [Similar Products]
UniProt Entry Name
APOE_HUMAN
NCBI Summary for APOE
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]
UniProt Comments for APOE
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, signal peptide; Secreted; Lipid-binding
Chromosomal Location of Human Ortholog: 19q13.2
Cellular Component: Golgi apparatus; extracellular space; microtubule; lysosome; endoplasmic reticulum; early endosome; dendrite; extracellular region; nuclear envelope; extracellular matrix; chylomicron; extrinsic to external side of plasma membrane; membrane; cell soma; cytoplasm; late endosome; 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: negative regulation of MAP kinase activity; lipoprotein catabolic process; phototransduction, visible light; 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; lipoprotein biosynthetic process; regulation of gene expression; 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; triacylglycerol metabolic process; reverse cholesterol transport; 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
Research Articles on APOE
1. results suggest that elastase-like proteases in the microglial cells surrounding Abeta plaques are responsible for ApoE degradation in the brain.
Precautions
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