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Soat-1 role in atherosclerosis
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Several residues in one subunit closely interact with the same residues in the other subunit; mutating these res. to Cys does not lead to loss in enzyme activity. Mutating residues F453, A457, or H460 to Cys causes large loss in enzyme activity.
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increase in the in vitro ACAT1 activity in PC-3 prostate cancer cells treated with androgen
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The results suggest that rs1044925 polymorphism in ACAT1 gene is not only associated with serum LDL-C and nHDLC levels in healthy Chinese subjects in Chengdu area, but also with HDL-C level in subjects with endogenous hypertriglyceridemia.
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RNA secondary structures located in the vicinity of the GGC(1274-1276) codon are required for production of the 56-kDa isoform.
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ACAT inhibition may stimulate cholesterol-catabolic (cytochrome P450) pathway in lesion-macrophages.
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Angiotensin II enhances foam cell formation by upregulating ACAT1 expression predominantly through the actions of AT(1) receptor via the G protein/c-Src/PKC/MAPK pathway in human monocyte-macrophages
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Docosahexaenoic acid can act as a substrate for ACAT1. In the manner of a poor substrate, docosahexaenoic acid also inhibited the activity of ACAT1.
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Results suggest that the ERK, p38MAPK and JNK signaling pathways may be involved in insulin-mediated regulation of ACAT1, but no PI3K and PLC-gamma signaling pathways were involved in the present study.
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Leptin accelerates cholesteryl ester accumulation in human monocyte-derived macrophages by increasing ACAT-1 expression.
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High ACAT1 expression is associated with estrogen receptor negative basal-like breast cancer.
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Macrophages cope with cholesterol loading by using a novel mechanism: they produce more ER-derived vesicles with elevated ACAT1 enzyme activity without having to produce more ACAT1 protein.
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the plaque-modulating effects of K-604 can be explained by stimulation of procollagen production independent of ACAT inhibition in addition to potent inhibition of macrophage ACAT-1
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Visfatin may down-regulate the ABCA1 expression and up-regulate the ACAT1 expression via PPARgamma signal transduction pathway, which decreases the outflow of free cholesterol, increases the content of cholesterol esters, and then induces foam cell formation.
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In THP-1-derived macrophages and foam cells, the expression level of ACAT-1 and cellular cholesterol content increased significantly in response to asymmetric dimethylarginine treatment in a time- and concentration-dependent manner.
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The present study shows that the C allele carriers of ACAT-1 rs1044925 SNP in male hyperlipidemic subjects had higher serum total cholesterol, HDL-cholesterol and ApoAI levels than the C allele noncarriers.
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Essential oil of Pinus koraiensis leaves significantly inhibited hACAT1 levels in HepG2 cells.
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Several lipid-related gene polymorphisms interact with overweight/obesity to modulate blood pressure levels.
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ABCA1 and ACAT1 DNA methylation induced by homocysteine may play a potential role in ABCA1 and ACAT1 expression and the accumulation of cholesterol in monocyte-derived foam cells
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The molecular mechanism of insulin action is mediated via interaction of the functional IRE upstream of the ACAT1 P1 promoter with C/EBPalpha and is MAPK-dependent.
