Overview

  • Product nameAnti-Apolipoprotein A I antibodySee all Apolipoprotein A I primary antibodies ...
  • Description
    Goat polyclonal to Apolipoprotein A I
  • SpecificityTypically less than 1% cross reactivity against other types of apoLipoprotein was detected by ELISA. This antibody reacts with human apoLipoprotein A-I and has negligible cross-reactivity with Type A-II, B, C-I, C-II, C-III, E and J apoLipoproteins.
  • Tested applicationsIHC-P, WB, ELISA, IPmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Full length native apoLipoprotein Type A-I (purified).

  • Positive control
    • FFPE human normal liver tissue sections
  • General notesThis antibody has been used to determine that atherosclerotic lesions in the human aorta contain considerable amounts of lipoproteins. These lipoproteins were observed to be complexed with components of the extracellular matrix (especially LDL and proteoglycans). The role of these matrix-lipoprotein complexes is not entirely clear, however, animal models of atherosclerosis have shown that increased cellular proliferation and increased production of extracellular matrix components occur following injury to the intimal layer of the aorta.

Properties

Applications

Our Abpromise guarantee covers the use of ab7613 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
IHC-P Use a concentration of 1 µg/ml. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
WB 1/5000 - 1/10000.
ELISA 1/4000 - 1/8000.
IP Use at an assay dependent dilution.

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 images

  • IHC image of Apolipoprotein A I staining in human normal liver formalin fixed paraffin embedded tissue section, performed on a Leica BondTM system using the standard protocol B. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH6, epitope retrieval solution 1) for 20 mins. The section was then incubated with ab7613, 1µg/ml, for 15 mins at room temperature. A donkey anti-goat biotinylated secondary antibody was used to detect the primary, and visualized using an HRP conjugated ABC system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.

    For other IHC staining systems (automated and non-automated) customers should optimize variable parameters such as antigen retrieval conditions, primary antibody concentration and antibody incubation times.

References for Anti-Apolipoprotein A I antibody (ab7613)

This product has been referenced in:
  • Röhrl C  et al. Endoplasmic reticulum stress impairs cholesterol efflux and synthesis in hepatic cells. J Lipid Res 55:94-103 (2014). WB . Read more (PubMed: 24179149) »
  • Park KH  et al. Dysfunctional lipoproteins from young smokers exacerbate cellular senescence and atherogenesis with smaller particle size and severe oxidation and glycation. Toxicol Sci 140:16-25 (2014). Read more (PubMed: 24798380) »

See all 11 Publications for this product

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Thank you for contacting Abcam.

We havenot tested ab7613specifically against plasminogen, and cross-reaction with plasminogen is not detectable by our QC Testing.

Please let me know if you have any further.

Abcam guarantees this product to work in the species/application used in this Abreview.
Application Western blot
Sample Human Purified protein (purified apoAI (BIODESIGN))
Loading amount 0.5 µg
Specification purified apoAI (BIODESIGN)
Gel Running Conditions Reduced Denaturing
Blocking step 5%milk+1%BSA as blocking agent for 12 hour(s) and 0 minute(s) · Concentration: 100% · Temperature: 4°C
Username

Abcam user community

Verified customer

Submitted Jan 23 2008

Abcam guarantees this product to work in the species/application used in this Abreview.
Application Western blot
Sample Human Purified protein (human plasma)
Loading amount 50 µg
Specification human plasma
Treatment Plama was separated into different bands by agarose electrophoresis, and alphaHDL was cut and protein was extracted for 2nd dimensional SDS-PAGE
Gel Running Conditions Non-reduced Denaturing
Blocking step Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 22°C
Username

Dr. xuefei li

Verified customer

Submitted Sep 19 2007

Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"