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APOE Recombinant Mouse mAb

APOE Recombinant Mouse mAb

     
  • 1 - APOE Recombinant Mouse mAb AP94424
    Blocking buffer: 5% NFDM/TBST Primary ab dilution: 1:1000 Primary ab incubation condition: room temperature 2h Secondary ab: Goat Anti-Mouse IgG H&L (HRP) Lysate: Mouse serum Protein loading quantity: 20 µg Exposure time: 10 s Predicted MW: 34-36 kDa Observed MW: 34-36 kDa
  • 1 - APOE Recombinant Mouse mAb AP94424
    Blocking buffer: 5% NFDM/TBST Primary ab dilution: 1:5000 Primary ab incubation condition: room temperature 2h Secondary ab: Goat Anti-Mouse IgG H&L (HRP) Lysate: Human serum Protein loading quantity: 20 µg Exposure time: 10 s Predicted MW: 34-36 kDa Observed MW: 34-36 kDa
  • 1 - APOE Recombinant Mouse mAb AP94424
    Cell line: HepG2 Fixative: 100% Ice-cold methanol Permeabilization: 0.1% TritonX-100 Primary ab dilution: 1:50 Primary incubation condition: 4°C overnight Secondary ab: Goat Anti-Mouse IgG Nuclear counter stain: DAPI (Blue) Comment: Color green is the positive signal for AP94424
  • 14 - APOE Recombinant Mouse mAb AP94424
    Tissue: Human brain Section type: Formalin fixed & Paraffin -embedded section Retrieval method: High temperature and high pressure Retrieval buffer: Tris/EDTA buffer, pH 9.0 Primary ab dilution: 1:100 Primary ab incubation condition: 1 hour at room temperature Secondary ab: SP Kit(Mouse)(sp-0024) Counter stain: Hematoxylin (Blue) Comment: Color brown is the positive signal for AP94424
  • 14 - APOE Recombinant Mouse mAb AP94424
    Tissue: Mouse brain Section type: Formalin fixed & Paraffin -embedded section Retrieval method: High temperature and high pressure Retrieval buffer: Tris/EDTA buffer, pH 9.0 Primary ab dilution: 1:100 Primary ab incubation condition: 1 hour at room temperature Secondary ab: SP Kit(Mouse)(sp-0024) Counter stain: Hematoxylin (Blue) Comment: Color brown is the positive signal for AP94424
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IHC-P, IHC-F, IF, ICC
Host Rabbit
Clonality Recombinant
Physical State Liquid
Isotype IgG1, Kappa
Purity affinity purified by Protein G
Buffer 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
SUBCELLULAR LOCATION Secreted.
SIMILARITY Belongs to the apolipoprotein A1/A4/E family.
Post-translational modifications Synthesized 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 extracellular medium.
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.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
Background Descriptions Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. ApoE exists in three major isoforms; E2, E3, and E4, which differ from one another by a single amino-acid substitution. Compared with E3 and E4, E2 exhibits the lowest receptor binding affinity. Defects in ApoE are a cause of hyperlipoproteinemia type III due to increased plasma cholesterol and triglycerides levels which are the consequence of impaired clearance of chylomicron and VLDL remnants.
Additional Information
Target/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.
Dilution WB=1:500-1:2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:50-1:100,IF=1:50-1:100
Format0.01M TBS(pH7.4) with 1% BSA, 0.09% (W/V) sodium azide and 50% Glyce
StorageStore at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

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