ApoA-1, human recombinant

A protein promoting cholesterol efflux from tissues to the liver 
Catalog #: 4693 | abID: ab285632

Product Details

abID ab285632
Alternate Name APOA1, MGC117399, Apoa1, Alp-1, Apoa-1, Brp-14, Ltw-1, Lvtw-1, apolipoprotein, apolipoproteins, MGC102525, Sep-1, Sep-2, Sep2, Human ApoA-1, ApoA-1, ApoA1, Apo A1, h-ApoA-1, rh-ApoA-1, recombinant human ApoA-1, ApoA1,recombinant ApoA-1, Apo, ApoA1, Apolip
Gene Symbol ApoA1
Gene ID 335
Accession # NM_000039
Source E. coli
Appearance Lyophilized protein
Physical Form Description Sterile filtered and lyophilized with no additives
Molecular Weight 28.2 kDa
Purity by SDS-PAGE ≥97%
Endotoxin Level <0.1 ng/μg
Biological Activity Test in process
Reconstitution Instructions Reconstitute in H₂O to a concentration of 0.1-1.0 mg/ml. The solution can then be diluted into other aqueous buffers and store at 4°C for 1 week or –20°C for future use.
Handling Centrifuge the vial prior to opening.
Storage Conditions -20°C
USAGE For Research Use Only! Not to be used in humans


ApoA-I is a 29.0 kDa protein produced in the liver and intestine, and secreted as the predominant constituent of nascent high-density lipoprotein (HDL) particle. ApoA-I, which is found exclusively in HDL, has a unique ability to capture and solubilize free cholesterol. This apoA-I ability enables HDL to remove excess peripheral cholesterol and return it to the liver for recycling and excretion. This process, called reverse cholesterol transport, is though to inhibit atherogenesis. For this reason HDL is also known as the “good cholesterol.” The therapeutic potential of apoA-I has been recently assessed in patients with acute coronary syndromes, using a recombinant form of a naturally occurring variant of apoA-I (called apoA-I Milano). The availability of recombinant normal apoA-I should facilitate further investigation into the potential usefulness of apoA-I in preventing atherosclerotic Vascular diseases. Recombinant human ApoA-I is a 28.2 kDa protein of 244 amino acid residues.

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Haan et al., Hepatic ABCA1 Expression Improves β-Cell Function and Glucose Tolerance. Diabetes, Dec 2014; 63: 4076 - 4082.
Omar Saeed  et al., Pharmacological Suppression of Hepcidin Increases Macrophage Cholesterol Efflux and Reduces Foam Cell Formation and Atherosclerosis, Arterioscler Thromb Vasc Biol, Feb 2012; 32: 299 - 307.
Barlic J et al (2009) J. Immunol.; 182: 7928 - 7936.
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