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Journal of Lipid Research, Vol. 50, 676-684, April 2009 Molecular cloning of hamster lipid transfer inhibitor protein (apolipoprotein F) and regulation of its expression by hyperlipidemia*
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 * This research was supported in part by Grant HL-60934 from the National Heart, Lung and Blood Institute, National Institutes of Health. Published, JLR Papers in Press, November 13, 2008.
1 To whom correspondence should be addressed. e-mail: mortonr{at}ccf.org
Lipid transfer inhibitor protein (LTIP) is a regulator of cholesteryl ester transfer protein (CETP) function. Factors affecting plasma LTIP levels are poorly understood. In humans, plasma LTIP is elevated in hypercholesterolemia. To define possible mechanisms by which hyperlipidemia modifies LTIP, we investigated the effects of hypercholesterolemic diets on plasma LTIP and mRNA levels in experimental animals. The hamster, which naturally expresses CETP, was shown to express LTIP. Hamster LTIP mRNA, exclusively detected in the liver, defined a predicted LTIP protein that is 69% homologous to human, with an isoelectric point of 4.15 and Mr =
Supplementary key words rabbit cholesterol hydrogenated coconut oil Abbreviations: apoF, apolipoprotein F; CETP, cholesteryl ester transfer protein; HCO, hydrogenated coconut oil; LTIP, lipid transfer inhibitor protein; LXR, liver X receptor
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