Anti-Apolipoprotein A I antibody (HRP) (ab8946)

Overview

• Product nameAnti-Apolipoprotein A I antibody (HRP)See all Apolipoprotein A I primary antibodies ...
• Description
  Sheep polyclonal to Apolipoprotein A I (HRP)
• ConjugationHRP
• SpecificityThe unconjugated immunoglobulin gives a single arc when tested by immunoelectrophoresis against Humanplasma. Identity has been confirmed by double diffusion (Ouchterlony) against Human plasma and an anti-Humanapolipoprotein A-1 of known specificity.
• Tested applicationsELISA more details
• Species reactivity
  Reacts with: Human
  
• Immunogen

  Human Apolipoprotein A-1 purified from plasma and shown to be homogeneous by SDS-PAGE.

Properties

• FormLiquid
• Storage instructionsStore at +4°C.
• Storage bufferPBS pH7.2,ProclinTM300 (0.05%),Methylisothiazolone (0.002%), Bromonitrodioxane (0.002%).
• Concentration information loading...
• PurityIgG fraction
• Purification notesAntiserum is prepared by immunisation of sheep with Apolipoprotein A-1 and if necessary, adsorped. Following adsorption, an immunoglobulin fraction is produced by ion-exchange chromatography and zone electrophoresis is performed to ensure that only a gamma-mobility component is present. The antibody is then conjugated with horseradish peroxidase activated by periodate. Preservatives are added and the product is then 0.2µm filtered.
• Clonality Polyclonal
• IsotypeIgG
• Light chain typeunknown
• Research Areas
  • Metabolism
  • Types of disease
  • Heart disease

  • Metabolism
  • Pathways and Processes
  • Metabolic signaling pathways
  • Lipid and lipoprotein metabolism
  • Lipoprotein metabolism

  • Metabolism
  • Pathways and Processes
  • Metabolic signaling pathways
  • Lipid and lipoprotein metabolism
  • Lipid metabolism

  • Metabolism
  • Types of disease
  • Cancer

  • Cancer
  • Cancer Metabolism
  • Metabolic signaling pathway
  • Metabolism of lipids and lipoproteins

  • Signal Transduction
  • Metabolism
  • Lipid metabolism

  • Cardiovascular
  • Atherosclerosis
  • Lipoprotein metabolism

  • Cardiovascular
  • Lipids / Lipoproteins
  • Lipoproteins/Apolipoproteins
  • Apolipoproteins

  • Neuroscience
  • Neurology process
  • Neurodegenerative disease
  • Other

Applications

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
  modificationsPalmitoylated.
  Phosphorylation sites are present in the extracelllular medium.
• Cellular localizationSecreted.

Target information above from: UniProt accession P02647 The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010) .

Information by UniProt
• Database links
  • Entrez Gene: 335 Human
  • Omim: 107680 Human
  • SwissProt: P02647 Human
  • Unigene: 93194 Human

• Alternative names
  Apo AI antibodyApo-AI antibodyApoA I antibody

  ApoA-I antibodyAPOA1 antibodyAPOA1/APOC3 fusion gene antibodyAPOA1_HUMAN antibodyApolipoprotein A I precursor antibodyApolipoprotein A-I(1-242) antibodyApolipoprotein A1 antibodyApolipoprotein AI antibodyApolipoprotein of high density lipoprotein antibodyApolipoproteinAI antibodyBrp14 antibodyLtw1 antibodyLvtw1 antibodyMGC117399 antibodySep1 antibodySep2 antibody

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