|Reactivity||Human, Mouse, Rat|
|Calculated MW||62521 Da|
|Other Names||Liver carboxylesterase 1, Acyl-coenzyme A:cholesterol acyltransferase, ACAT, Brain carboxylesterase hBr1, Carboxylesterase 1, CE-1, hCE-1, Cocaine carboxylesterase, Egasyn, HMSE, Methylumbelliferyl-acetate deacetylase 1, Monocyte/macrophage serine esterase, Retinyl ester hydrolase, REH, Serine esterase 1, Triacylglycerol hydrolase, TGH, CES1, CES2, SES1|
|Target/Specificity||A synthetic peptide corresponding to residues on the C-terminus of human ACAT was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|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||ACAT Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acyl-CoA ester. Hydrolyzes the methyl ester group of cocaine to form benzoylecgonine. Catalyzes the transesterification of cocaine to form cocaethylene. Displays fatty acid ethyl ester synthase activity, catalyzing the ethyl esterification of oleic acid to ethyloleate.|
|Cellular Location||Endoplasmic reticulum lumen|
|Tissue Location||Expressed predominantly in liver with lower levels in heart and lung.|
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Provided below are standard protocols that you may find useful for product applications.
Triacylglycerol hydrolase is a microsomal enzyme that hydrolyzes stored cytoplasmic triacylglycerol in the liver and participates in the lipolysis/re-esterification cycle during the assembly of very-low-density lipoproteins. Expression of human TGH in Escherichia coli yields a protein without enzymatic activity, which suggests that posttranslational processing is necessary for the catalytic activity (1). ACAT esterifies free cholesterol and stores cholesteryl esters in lipid droplets. Macrophage ACAT1 deficiency results in increased atherosclerotic lesion area in hyperlipidemic mice via disrupted cholesterol efflux, increased lipoprotein uptake, accumulation of intracellular vesicles, and accelerated apoptosis (2). Data show that macrophage ACAT1 influences the efflux of both cellular and lipoprotein-derived cholesterol and propose a pathway for the pro-atherogenic transformation of ACAT1(-/-) macrophages (3).
1. Alam M, et al. Biochemistry 41(21):6679-87, 2002.
2. Dove DE, et al. Atherosclerosis 186(2):267-74, 2006.
3. Sone DE, et al. Arterioscler Thromb Vasc Biol 25(1): 128-34, 2005.
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