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Anti-Apolipoprotein E antibody [D6E10] (ab1906)

Overview

  • Product nameAnti-Apolipoprotein E antibody [D6E10]See all Apolipoprotein E primary antibodies ...
  • Description
    Mouse monoclonal [D6E10] to Apolipoprotein E
  • Tested applicationsICC/IF, IP, WB, IHC-P, IHC-Fr, Flow Cyt more details
  • Species reactivity
    Reacts with: Mouse, Human
  • Immunogen

    Synthetic peptide spanning the polymorphic amino acid position 158 of ApoE.

Applications

Our Abpromise guarantee covers the use of ab1906 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Notes
ICC/IF ICC/IF: Use at an assay dependent dilution. PubMed: 21163940
IP IP: Use at an assay dependent dilution. PubMed: 21163940
WB WB: 1/100 - 1/1000. Predicted molecular weight: 38 kDa.
IHC-P IHC-P: 1/100 - 1/10000. Antigen retrieval is not essential but may optimise staining.
IHC-Fr IHC-Fr: 1/100 - 1/10000.
Flow Cyt Flow Cyt: Use at an assay dependent concentration. PubMed: 22896615

Target

  • 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.
  • 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 extracelllular medium.
  • Cellular localizationSecreted.
  • Target information above from: UniProt accession P02649 The UniProt Consortium
    The Universal Protein Resource (UniProt) in 2010
    Nucleic Acids Res. 38:D142-D148 (2010) .

    Information by UniProt
  • Database links
  • Alternative names
      AD2 antibodyAlzheimer disease 2 antibodyApo E antibody
      Apo-E antibodyApoE antibodyAPOE_HUMAN antibodyAPOEA antibodyApolipoprotein E antibodyApolipoprotein E3 antibodyApolipoproteinE antibodyApoprotein antibodyLDLCQ5 antibodyLPG antibodyMGC1571 antibody
    see all

Anti-Apolipoprotein E antibody [D6E10] images

  • IHC-P using ab1906 showing senile plaques. (x200)
  • IHC-P using ab1906. Strong immunoreactivity to Apo E of vascular amyloid ß. Down syndrome. Orig. magn. X 100.


  • Predicted band size : 38 kDa


    Western blot using ab1906, on 1 µl of human serum

References for Anti-Apolipoprotein E antibody [D6E10] (ab1906)

This product has been referenced in:
  • Da Costa D  et al. Reconstitution of the entire hepatitis C virus life cycle in nonhepatic cells. J Virol 86:11919-25 (2012). WB, Flow Cyt ; Human . Read more (PubMed: 22896615) »
  • Soler-López M  et al. Interactome mapping suggests new mechanistic details underlying Alzheimer's disease. Genome Res 21:364-76 (2011). WB, ICC/IF, IP ; Human . Read more (PubMed: 21163940) »

See all 7 Publications for this product

Product Wall

Displaying 1 - 10 of 18 results for Abreviews and Q&A

Application Western blot
Sample Human Serum (serum)
Loading amount 100 µg
Specification serum
Gel Running Conditions Reduced Denaturing
Blocking step Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 20°C
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Application Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)
Sample Human Tissue sections (Testis)
Specification Testis
Fixative Formaldehyde
Antigen retrieval step Heat mediated - Buffer/Enzyme Used: Citric acid
Permeabilization No
Blocking step BSA as blocking agent for 10 minute(s) · Concentration: 1% · Temperature: 21°C
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Submitted Sep 07 2012

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