EC Number   |
General Information |
Reference |
|---|
   2.3.1.26 | evolution |
along with acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), ACAT1 and ACAT2 are founding members of the membrane-bound O-acyltransferase (MBOAT) enzyme family. MBOATs are multispan membrane enzymes that use long-chain or medium-chain fatty acyl-CoA as the first substrate, and catalyze the transfer of the fatty acyl group to the 3beta-hydroxyl moiety of a certain hydrophobic substance as the second substrate. An MBOAT contains two active sites: a histidine within a long hydrophobic peptide region, and an asparagine located within a long hydrophilic peptide region |
736702 |
| 2.3.1.26 | malfunction |
ACAT1 deficiency significantly increases free cholesterol levels in hepatic stellate cells, augmenting Toll-like receptor 4, TLR4, protein and downregulating expression of transforming growth factor-beta (TGFbeta) pseudoreceptor Bambi (bone morphogenetic protein and activin membrane-bound inhibitor), leading to sensitization of hepatic stellate cells to TGFbeta activation. Exacerbation of liver fibrosis by ACAT1 deficiency is dependent on free cholesterol accumulation-induced enhancement of TLR4 signaling, effects of ACAT1 deficiency on induced liver fibrosis, overview. ACAT1 deficiency does not affect hepatocellular damage |
-, 736580 |
| 2.3.1.26 | malfunction |
ACAT1 deficiency significantly increases free cholesterol levels in hepatic stellate cells, augmenting Toll-like receptor 4, TLR4, protein and downregulating expression of transforming growth factor-beta (TGFbeta) pseudoreceptor Bambi (bone morphogenetic protein and activin membrane-bound inhibitor), leading to sensitization of hepatic stellate cells to TGFbeta activation. Exacerbation of liver fibrosis by ACAT1 deficiency is dependent on free cholesterol accumulation-induced enhancement of TLR4 signaling. ACAT1 deficiency does not affect hepatic ACAT2 expression, effects of ACAT1 deficiency on induced liver fibrosis, overview |
736580 |
| 2.3.1.26 | malfunction |
aortic atherosclerosis development is significantly lower in all mice with global or tissue-restricted SOAT2 gene deletions. Nevertheless, liver-specific and complete SOAT2-/-LDLr-/- knockout mice have less aortic cholesterol esters accumulation and smaller aortic lesions than intestine-specific SOAT2SI-/SI-LDLr-/- mice |
735970 |
| 2.3.1.26 | malfunction |
blocking ACAT enzyme activity with ACAT inhibitors, or with genetic ablation of ACAT1, significantly increases macrophage apoptosis |
736702 |
| 2.3.1.26 | malfunction |
genetic deficiency, antisense oligonucleotide, or small molecule inhibitors of enzyme SOAT2 can effectively reduce atherosclerotic cardiovascular disease progression, and even promote regression of established cardiovascular disease, also causing compensatory upregulation of ABCA1 in the liver of mice. SOAT2 inhibition can also stabilize highly advanced plaques when given in the late phases of atherosclerosis progression. The ability of SOAT2 inhibitors to protect against atherosclerosis can be in part attributed to decreased intestinal cholesterol absorption, reduced hepatic very low density lipoprotein, and blunted retention of low density lipoprotein in the artery wall. Either chronic or acute inhibition of SOAT2 promotes a non-biliary pathway of reverse cholesterol transport called transintestinal cholesterol excretion. Intestine or liver specific deletion of SOAT2 is not sufficient to enhance LXR-stimulated fecal neutral sterol loss, and SOAT2 only modestly alters XR-driven reorganization of cholesterol-sensitive gene expression in the liver and small intestine |
736719 |
| 2.3.1.26 | malfunction |
mice lacking ACAT1 or ACAT2 do not have a decreased PREG ester contents in adrenals, nor do they have altered levels of the three major secreted adrenal steroids in serum |
720018 |
| 2.3.1.26 | malfunction |
mice lacking ACAT1 or ACAT2 do not have a decreased pregnenolone ester contents in adrenals, nor do they have altered levels of the three major secreted adrenal steroids in serum |
720018 |
| 2.3.1.26 | malfunction |
mice lacking sterol O-acyltransferase 2 have less hepatic cholesterol entrapment and improved liver function. mRNA expression levels for several markers of inflammation are all significantly lower in mutants lacking sterol O-acyltransferase 2 |
755767 |
| 2.3.1.26 | metabolism |
the enzyme converts cholesterol to cholesteryl esters and plays key roles in the regulation of cellular cholesterol homeostasis. It metabolizes diverse substrates including both sterols and certain steroids, and it contains two different binding sites for steroidal molecules |
736702 |
