Anti-Apolipoprotein A I antibody [12C8] (ab17278)

Overview

  • Product nameAnti-Apolipoprotein A I antibody [12C8]See all Apolipoprotein A I primary antibodies ...
  • Description
    Mouse monoclonal [12C8] to Apolipoprotein A I
  • SpecificityNo cross reactivity is seen with human apolipoprotein B.
  • Tested applicationsWB, IHC-P, ELISAmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Full length native Apolipoprotein A1, isolated from human plasma.

Applications

Our Abpromise guarantee covers the use of ab17278 in the following tested applications.

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

Application Abreviews Notes
WB Use at an assay dependent dilution. Predicted molecular weight: 24 kDa.
IHC-P Use a concentration of 2 µg/ml. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
ELISA 1/6500.

Target

  • FunctionParticipates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT). As part of the SPAP complex, activates spermatozoa motility.
  • Tissue specificityMajor protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine.
  • Involvement in diseaseDefects in APOA1 are a cause of high density lipoprotein deficiency type 2 (HDLD2) [MIM:604091]; also known as familial hypoalphalipoproteinemia (FHA). Inheritance is autosomal dominant.
    Defects in APOA1 are a cause of the low HDL levels observed in high density lipoprotein deficiency type 1 (HDLD1) [MIM:205400]; also known as analphalipoproteinemia or Tangier disease (TGD). HDLD1 is a recessive disorder characterized by the absence of plasma HDL, accumulation of cholesteryl esters, premature coronary artery disease, hepatosplenomegaly, recurrent peripheral neuropathy and progressive muscle wasting and weakness. In HDLD1 patients, ApoA-I fails to associate with HDL probably because of the faulty conversion of pro-ApoA-I molecules into mature chains, either due to a defect in the converting enzyme activity or a specific structural defect in Tangier ApoA-I.
    Defects in APOA1 are the cause of amyloid polyneuropathy-nephropathy Iowa type (AMYLIOWA) [MIM:107680]; also known as amyloidosis van Allen type or familial amyloid polyneuropathy type III. AMYLIOWA is a hereditary generalized amyloidosis due to deposition of amyloid mainly constituted by apolipoprotein A1. The clinical picture is dominated by neuropathy in the early stages of the disease and nephropathy late in the course. Death is due in most cases to renal amyloidosis. Severe peptic ulcer disease can occurr in some and hearing loss is frequent. Cataracts is present in several, but vitreous opacities are not observed.
    Defects in APOA1 are a cause of amyloidosis type 8 (AMYL8) [MIM:105200]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.
  • Sequence similaritiesBelongs to the apolipoprotein A1/A4/E family.
  • Post-translational
    modifications
    Palmitoylated.
    Phosphorylation sites are present in the extracelllular medium.
  • Cellular localizationSecreted.
  • Information by UniProt
  • Database links
  • Alternative names
    • Apo AI antibody
    • Apo-AI antibody
    • ApoA I antibody
    • ApoA-I antibody
    • APOA1 antibody
    • APOA1/APOC3 fusion gene antibody
    • APOA1_HUMAN antibody
    • Apolipoprotein A I precursor antibody
    • Apolipoprotein A-I(1-242) antibody
    • Apolipoprotein A1 antibody
    • Apolipoprotein AI antibody
    • Apolipoprotein of high density lipoprotein antibody
    • ApolipoproteinAI antibody
    • Brp14 antibody
    • Ltw1 antibody
    • Lvtw1 antibody
    • MGC117399 antibody
    • Sep1 antibody
    • Sep2 antibody
    see all

Anti-Apolipoprotein A I antibody [12C8] images

  • All lanes : Anti-Apolipoprotein A I antibody [12C8] (ab17278) at 5 µg/ml

    Lane 1 : Ovary (Human) Tissue Lysate - adult normal tissue (ab30222)
    Lane 2 : Lung (Human) Tissue Lysate

    Lysates/proteins at 10 µg per lane.

    Secondary
    Lane 1 : Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
    Lane 2 : Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution


    Predicted band size : 24 kDa
    Observed band size : 25 kDa (why is the actual band size different from the predicted?)
    Additional bands at : 260 kDa,45 kDa,55 kDa,75 kDa. We are unsure as to the identity of these extra bands.
  • Ab17278 staining human normal skeletal muscle. Staining is localised to the cytoplasm.
    Left panel: with primary antibody at 2 ug/ml. Right panel: isotype control.
    Sections were stained using an automated system DAKO Autostainer Plus , at room temperature. Sections were rehydrated and antigen retrieved with the Dako 3-in-1 AR buffer EDTA pH 9.0 in a DAKO PT Link. Slides were peroxidase blocked in 3% H2O2 in methanol for 10 minutes. They were then blocked with Dako Protein block for 10 minutes (containing casein 0.25% in PBS), then incubated with primary antibody for 20 minutes, and detected with Dako Envision Flex amplification kit for 30 minutes. Colorimetric detection was completed with diaminobenzidine for 5 minutes. Slides were counterstained with Haematoxylin and coverslipped under DePeX. Please note that for manual staining we recommend to optimize the primary antibody concentration and incubation time (overnight incubation), and amplification may be required.

References for Anti-Apolipoprotein A I antibody [12C8] (ab17278)

This product has been referenced in:
  • Johnson LA  et al. Diabetic atherosclerosis in APOE*4 mice: synergy between lipoprotein metabolism and vascular inflammation. J Lipid Res 54:386-96 (2013). Mouse . Read more (PubMed: 23204275) »
  • Yvan-Charvet L  et al. Inhibition of cholesteryl ester transfer protein by torcetrapib modestly increases macrophage cholesterol efflux to HDL. Arterioscler Thromb Vasc Biol 27:1132-8 (2007). Read more (PubMed: 17322101) »

See all 3 Publications for this product

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