Recombinant
RabMAb

Recombinant Anti-Apolipoprotein A I antibody [EPSISR27] - BSA and Azide free (ab232048)

Overview

  • Product name

    Anti-Apolipoprotein A I antibody [EPSISR27] - BSA and Azide free
    See all Apolipoprotein A I primary antibodies
  • Description

    Rabbit monoclonal [EPSISR27] to Apolipoprotein A I - BSA and Azide free
  • Host species

    Rabbit
  • Tested applications

    Suitable for: WB, ICC/IFmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Synthetic peptide within Human Apolipoprotein A I. The exact sequence is proprietary.
    Database link: P02647

  • Positive control

    • ICC/IF: HepG2 cells.
  • General notes

    ab232048 is the carrier-free version of ab151710 This format is designed for use in antibody labeling, including fluorochromes, metal isotopes, oligonucleotides, enzymes.

     

    Our carrier-free formats are supplied in a buffer free of BSA, sodium azide and glycerol for higher conjugation efficiency.

    Use our conjugation kits  for antibody conjugates that are ready-to-use in as little as 20 minutes with <1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.

    Ab232048 is compatible with the Maxpar® Antibody Labeling Kit from Fluidigm.

    Maxpar® is a trademark of Fluidigm Canada Inc.

    Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.

    Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.

    This product is a recombinant rabbit monoclonal antibody.

Applications

Our Abpromise guarantee covers the use of ab232048 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 concentration. Predicted molecular weight: 30 kDa.
ICC/IF Use at an assay dependent concentration.

Target

  • Function

    Participates 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 specificity

    Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine.
  • Involvement in disease

    Defects 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 similarities

    Belongs to the apolipoprotein A1/A4/E family.
  • Post-translational
    modifications

    Palmitoylated.
    Phosphorylation sites are present in the extracelllular medium.
  • Cellular localization

    Secreted.
  • Information by UniProt
  • Database links

  • Alternative names

    • Apo-AI antibody
    • ApoA I antibody
    • ApoA-I antibody
    • APOA1 antibody
    • APOA1_HUMAN antibody
    • Apolipoprotein A-I(1-242) antibody
    • Apolipoprotein A1 antibody
    • Apolipoprotein AI antibody
    • Apolipoprotein of high density lipoprotein antibody
    • ApolipoproteinAI antibody
    • Brp14 antibody
    • high density lipoprotein uptake antibody
    • Ltw1 antibody
    • Lvtw1 antibody
    • MGC117399 antibody
    • Sep1 antibody
    • Sep2 antibody
    see all

Images

  • Immunofluorescent analysis of HepG2 (Human liver hepatocellular carcinoma cell line) cells labeling Apolipoprotein A I with ab151710 at 1/250 dilution.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab151710).

References

ab232048 has not yet been referenced specifically in any publications.

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