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Literature summary extracted from

  • Warrier, M.; Zhang, J.; Bura, K.; Kelley, K.; Wilson, M.D.; Rudel, L.L.; Brown, J.M.
    Sterol O-acyltransferase 2-driven cholesterol esterification opposes liver X receptor-stimulated fecal neutral sterol loss (2016), Lipids, 51, 151-157.
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
2.3.1.26 drug development selective inhibitors of the cholesterol esterifying enzyme sterol-O acyltransferase 2 (SOAT2) hold great promise as effective atherosclerotic cardiovascular disease therapeutics Mus musculus

Protein Variants

EC Number Protein Variants Comment Organism
2.3.1.26 additional information generation of enzyme knockout SOAT2-/- mice Mus musculus

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.3.1.26 acyl-CoA + cholesterol Mus musculus
-
 CoA + cholesterol ester
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
2.3.1.26 Mus musculus O88908
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
2.3.1.26 enterocyte
-
 Mus musculus
-
2.3.1.26 hepatocyte
-
 Mus musculus
-
2.3.1.26 liver
-
 Mus musculus
-
2.3.1.26 small intestine
-
 Mus musculus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.3.1.26 acyl-CoA + cholesterol
-
 Mus musculus CoA + cholesterol ester
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.3.1.26 ACAT2
-
 Mus musculus
2.3.1.26 acyl-coA:cholesterol o-acyl transferase 2
-
 Mus musculus
2.3.1.26 Soat2
-
 Mus musculus
2.3.1.26 sterol O-acyltransferase 2
-
 Mus musculus

General Information

EC Number General Information Comment Organism
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 Mus musculus
2.3.1.26 metabolism the enzyme plays a major role in the cholesterol ester cycle, and has a potential role as a regulator of reverse cholesterol transport (RCT) called transintestinal cholesterol excretion. Combination of SOAT2 inhibition with LXR agonist treatment results in a marked negative cholesterol balance. SOAT2's key role in promoting intestinal cholesterol absorption and suppressing the non-biliary TICE pathway are both likely contributing mechanisms underlying SOAT2's ability to oppose LXR-stimulated fecal cholesterol disposal Mus musculus
2.3.1.26 physiological function sterol O-acyltransferase 2-driven cholesterol esterification can alter both the packaging and retention of atherogenic apoB-containing lipoproteins and opposes liver X receptor-stimulated fecal neutral sterol loss. Enzyme SOAT2-driven cholesterol esterification interplays with fecal cholesterol disposal and high density lipoprotein metabolism. Potential role for SOAT2 as a regulator of reverse cholesterol transport (RCT) called transintestinal cholesterol excretion Mus musculus