|Application ||WB, E|
|Description||APOA1: apolipoprotein A-I, it is the major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion, and it is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. Defects in the Apolipoprotein A I gene are associated with HDL deficiency and Tangier disease. 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. The availability of recombinant normal apoA-I should facilitate further investigation into the potential usefulness of apoA-I in preventing atherosclerotic vascular diseases.|
|Immunogen||Purified recombinant fragment of human APOA1 expressed in E. Coli.|
|Formulation||Ascitic fluid containing 0.03% sodium azide.|
|Other Names||Apolipoprotein A-I, Apo-AI, ApoA-I, Apolipoprotein A1, Proapolipoprotein A-I, ProapoA-I, Truncated apolipoprotein A-I, Apolipoprotein A-I(1-242), APOA1|
|Dilution||WB~~1/500 - 1/2000|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||APOA1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Tissue Location||Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine. The oxidized form at Met-110 and Met-136 is increased in individuals with increased risk for coronary artery disease, such as in carrier of the eNOSa/b genotype and exposure to cigarette smoking It is also present in increased levels in aortic lesions relative to native ApoA-I and increased levels are seen with increasing severity of disease.|
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1. J Mol Med. 2006,Jul, 84(7):561-72. Epub 2006 May 17. 2. Clin Endocrinol (Oxf). 2006,Mar, 64(3):260-4.
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