Related references
Note: Only part of the references are listed.Direct intestinal cholesterol secretion contributes significantly to total fecal neutral sterol excretion in mice
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Dietary fat-induced alterations in atherosclerosis are abolished by ACAT2-deficiency in ApoB100 only, LDLr-/- mice
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Liver-specific inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 with antisense oligonucleotides limits atherosclerosis development in apolipoprotein B100-only low-density lipoprotein receptor-/- mice
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ACAT2 is a target for treatment of coronary heart disease associated with hypercholesterolemia
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ACAT2 contributes cholesteryl esters to newly secreted VLDL, whereas LCAT adds cholesteryl ester to LDL in mice
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Plasma cholesteryl esters provided by lecithin:cholesterol acyltransferase and acyl-coenzyme A:: Cholesterol acyltransferase 2 have opposite atherosclerotic potential
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ACAT2 deficiency limits cholesterol absorption in the cholesterol-fed mouse: Impact on hepatic cholesterol homeostasis
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ACAT2 is localized to Hepatocytes and is the major cholesterol-esterifying enzyme in human liver
P Parini et al.
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Targeted deletion of the ileal bile acid transporter eliminates enterohepatic cycling of bile acids in mice
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Sterol absorption by the small intestine
SD Turley et al.
CURRENT OPINION IN LIPIDOLOGY (2003)
Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice
EL Willner et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2003)
Increased hepatobiliary and fecal cholesterol excretion upon activation of the liver X receptor is independent of ABCA1
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SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver
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Control of cholesterol turnover in the mouse
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JOURNAL OF BIOLOGICAL CHEMISTRY (2002)
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NATURE MEDICINE (2000)