SOAT-1/ACAT-1 Polyclonal Antibody

Sterol O-acyltransferase 1 (SOAT-1), also known as acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1), is an enzyme encoded by ACAT1 in humans that catalyzes the intracellular formation of cholesterol esters from cholesterol and long-chain fatty acyl-coenzyme A.¹ It is ubiquitously expressed and localized to the rough endoplasmic reticulum where it preferentially utilizes oleic acid (Item Nos. 90260 | 24659) or palmitic acid (Item No. 10006627) as fatty acid substrates for the synthesis of cholesterol esters, which are stored intracellularly or packaged into chylomicrons or VLDL and secreted into the blood stream. SOAT-1/ACAT-1 protein levels are increased in macrophages under various pathological conditions, including atherosclerosis.² SOAT-1/ACAT-1 activity is increased by cholesterol in vitro, and ACAT1 expression is increased by stimulation with the pro-inflammatory cytokines TNF-α or IFN-γ in isolated human and THP-1 monocytes, respectively.^3,1 ACAT1 silencing in human H4 neuroglioma cells overexpressing amyloid-β precursor protein (APP) reduces secretion of soluble amyloid-β (Aβ) and Aβ42 (Item No. 20574).⁴ Genome-wide deletion of Acat1 reduces macrophage infiltration and neutral lipid deposition in atherosclerotic aortic lesions and decreases serum total cholesterol levels, but increases brain cholesterol deposition, in ApoE^-/- mice fed a Western diet.⁵ Cayman's SOAT-1/ACAT-1 Polyclonal Antibody can be used for immunoflouresence (IF) immunohistochemistry (IHC) and Western blot (WB) applications. The antibody recognizes the N-terminus to detect full-length SOAT-1/ACAT-1 at approximately 65 kDa from human, mouse, porcine, and rat samples.

WARNING This product is not for human or veterinary use.

1. Pramfalk, C., Eriksson, M., and Parini, P. Cholesteryl esters and ACAT. Eur. J. Lipid Sci. Technol. 114(6), 624-633 (2012).

2. Sakashita, N., Miyazaki, A., Chang, C.C.Y., et al. Acyl-coenzyme A:cholesterol acyltransferase 2 (ACAT2) is induced in monocyte-derived macrophages: In vivo and in vitro studies. Lab. Invest. 83(11), 1569-1581 (2003).

3. Chang, T.-Y., Li, B.-L., Chang, C.Y., et al. Acyl-coenzyme A:cholesterol acyltransferases. Am. J. Physiol. Endocrinol. Metab. 297(1), E1-E9 (2009).

4. Huttunen, H.J., Greco, C., and Kovacs, D.M. Knockdown of ACAT-1 reduces amyloidogenic processing of APP. FEBS Lett. 581(8), 1688-1692 (2007).

5. Accad, M., Smith, S.J., Newland, D.L., et al. Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1. J. Clin. Invest. 105(6), 711-719 (2000).

Addabbo, F., Ratliff, B., Park, H.-C., et al. The Krebs cycle and mitochondrial mass are early victims of endothelial dysfunction. Am. J. Pathol. 174(1), 34-43 (2009).

Ikenoya, M., Yoshinaka, Y., Kobayashi, H., et al. A selective ACAT-1 inhibitor, K^-604, suppresses fatty streak lesions in fat-fed hamsters without affecting plasma cholesterol levels. Atherosclerosis 191(2), 290-297 (2007).