thiolase


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a·ce·tyl-CoA a·ce·tyl·trans·fer·ase

an acetyltransferase forming acetoacetyl-CoA from two molecules of acetyl-CoA, releasing one CoA. A key step in ketogenesis and sterol synthesis.

thiolase

An obsolete generic term for any enzyme (e.g., acetyl CoA acetyltransferase [EC 2.3.1.9]) which catalyses a reaction between a compound, R–R’, and a thiol, R’–SH, forming R–S–R’ and R'–H.
References in periodicals archive ?
Fatty acid [beta]-oxidation: acyl-CoA oxidase, bifunctional protein (hydratase-dehydrogenase), thiolase 3.
The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase.
During the conversion of acetyl-CoA into butyryl-CoA thiolase crotonase 3-hydroxybutyryl-CoA dehydrogenase and butyryl-CoA dehydrogenase are played vital roles as key enzymes.
Trimetazidine slows down the oxidation of fatty acids due to the selective inhibition of the long-chain 3-ketoacyl-CoA thiolase, leading to an increase in glucose oxidation and the restoration of interface between the glycolysis and the oxidative decarboxylation and causes the myocardial protection against ischemia.
Initially, three units of acetyl-CoA are condensed into mevalonate by means of three sequential steps involving the enzymes acetoacetylCoA thiolase (THIOL), HMG-CoA synthase (HMGS), and HMGCoA reductase(HMGR).
13 TMZ acts by optimizing cardiac metabolism by reducing fatty acid oxidation through the selective inhibition of mitochondrial 3-ketoacyl CoA thiolase.
Modulation of fatty acids oxidation in heart failure by selective pharmacological inhibition of 3-ketoacyl coenzyme-A thiolase.
19) In addition to its effect on palmitoyl-CoA and acyl coenzyme A oxidase, sesamin was also noted to amplify the action of numerous other hepatic fatty acid oxidation enzymes, including carnitine palmitoyltransferase, acyl-CoA dehydrogenase, 3-hydroxyacyl-CoA dehydrogenase, enoyi-CoA hydratase and 3-ketoaeyl-CoA thiolase, as well as to improve, in a dose-dependent manner, the activity of 2,4-dienoyl-CoA reductase and [DELTA]3, [DELTA]2-enoyl-CoA isomerase, both of which are involved in the auxiliary pathway for beta-oxidation of unsaturated fatty acids.
After the fourth step in which a 3-ketoacyl-CoA thiolase is involved, cycling continues until the final thiolytic cleavage with the production of two acetylCoA molecules.
Specifically, very long chain acylcoenzyme A (CoA) dehydrogenase (VLCAD), medium chain acyl-CoA dehydrogenase (MCAD), peroxisomal bifunctional protein (hydratase + 3-hydroxyacyl-CoA dehydrogenase) (PH), peroxisomal thiolase (PT), diacylglicerol acyltransferase 1 (DGAT1), and p52 mRNA levels were higher in hPPAR[alpha] mice than in mPPAR[alpha] and Ppar[alpha]-null mice.
of Unigenes IPRO13032 EGF-like region, conserved site 296 IPR006058 2Fe-2S ferredoxin, iron-sulfur 124 binding site IPR002155 Thiolase 102 IPR000020 Anaphylatoxin/fibulin 19 IPR001007 von Willebrand factor, type C 15 IPR001778 Pollen allergen Poa pIX/Phl pVl, 14 C-terminal IPR001450 4Fe-4S ferredoxin, iron-sulfur 6 binding IPR004051 Potassium channel, voltage 3 dependent, Kv1A IPR007899 CHAD 3 IPR000217 Tubulin 2 1PRO15812 Integrin beta subunit 2 IPR000104 Antifreeze protein, type I 2 IPR006081 Alpha defensin 2 IPR011142 Spider toxin CSTX, conserved site 1 IPR001316 Peptidase SIA, streptogrisin 1 IPR002049 EGF-like, laminin 1 EGF, epidermal growth factor; CHAD, Chondroadherin; CSTX, Cupiennius salei toxin.
The second genetic disorder included in this study is an organic acid disorder called Mitochondrial acetoacetyl-CoA thiolase (T2), commonly known as Beta-ketothiolase deficiency.