The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Immobilized Human Apolipoprotein A I at 10 µg/mL (100 µl/well) can bind biotinylated Human SCARB1.
The EC50 of biotinylated human SCARB1 is 10-100 ng/mL.
< 1.000 Eu/µg
>95% by SDS-PAGE . ab155731 was lyophilized from 0.22 µm filtered solution.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
pH: 7.40 Constituents: 95% PBS, 5% Trehalose
This product is an active protein and may elicit a biological response in vivo, handle with caution.
It is recommended to reconstitute the lyophilized protein in sterile deionized water to a final concentration of 400 µg/mL. Solubilize for 30 to 60 minutes at room temperature with occasional gentle mixing. Carrier protein (0.1% HSA or BSA) is strongly recommended for further dilution and long term storage.
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.
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.
Belongs to the apolipoprotein A1/A4/E family.
Palmitoylated. Phosphorylation sites are present in the extracelllular medium.