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Human CellExp™ ApoA-1, human recombinant

Promotes cholesterol efflux from tissues to the liver for excretion.
Catalog #: 7403

In stock

$220.00

Product Details

Cat # +Size 7403-10
Size 10 μg
Alternate Name Apolipoprotein A-I, APOA1, MGC117399
Gene Symbol ApoA1
Gene ID 335
Accession # P02647
Source HEK293 cells
Appearance Lyophilized
Physical Form Description Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Generally 5-8% Mannitol or trehalose is added as a protectant before lyophilization.
Molecular Weight This protein is fused with polyhistidine tag at the C-terminus, and has a calculated MW of 29 kDa. The predicted N-terminus is Asp 25. DTT-reduced Protein migrates as 26-30 kDa in SDS-PAGE.
Purity by SDS-PAGE ≥95%
Endotoxin Level <1 EU/μg by LAL method
Biological Activity Immobilized Human ApoAI at 10 μg/mL (100 μl/well) can bind biotinylated human SCARB1. The EC50 of biotinylated human SCARB1 is 10-100 ng/mL.
Reconstitution Instructions Centrifuge the vial prior to opening. Reconstitute in sterile deionized water to a concentration of 50 µg/ml. Solubilize for 30 to 60 min. at RT with occasional gentle mixing. Do not vortex. Carrier protein (0.1% HSA or BSA) is strongly recommended for fu
Handling Centrifuge the vial prior to opening.
Storage Conditions -20°C
Shipping Conditions Gel Pack
USAGE For Research Use Only! Not to be used in humans

Details

ApoA1 is also known as apolipoprotein A-I, ApoA-I , and is the major protein component of high density lipoprotein (HDL) in plasma. It has a specific role in lipid metabolism. Chylomicrons secreted from the intestinal enterocyte also contain ApoA1 but it is quickly transferred to HDL in the bloodstream. The protein promotes cholesterol efflux from tissues to the liver for excretion. It is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. ApoA-I was also isolated as a prostacyclin (PGI2) stabilizing factor, and thus may have an anticlotting effect. Defects in the gene encoding it are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis. In addition, it has been shown that ApoA1 is implicated in the anti-endotoxin function of HDL via interaction with lipopolysaccharide or endotoxin.


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