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 ?
Degradation of the cleaved leader peptide of thiolase by a peroxisomal proteinase.
SCP-x, a longer form of SCP-2 that is transcribed from an alternate transcription site, is a peroxisomal 3-ketoacyl-CoA thiolase [105].
The length of 3-ketoacyl-CoA thiolase was 1194 bp, which was repeated 4 times.
The core enzymes for [beta]-oxidation include acyl CoA oxidase (ACX), multifunctional protein (MFP), and 3-ketoacyl-CoA thiolase (KAT) [61].
In BMMs, IFN-[alpha] stimulation leads to the upregulation of genes associated with isoleucine (propionyl-CoA carboxylase; PPCA, 3-ketoacylCoA thiolase 1A and 2; ACAA1A/2) and valine (3hydroxyisobutyrate dehydrogenase; HIBADH) catabolism.
The [beta]-oxidation cycle consists of four reactions, catalyzed by acyl-CoA dehydrogenases (ACADs), enoyl-CoA hydratases, L-3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase, that sequentially remove two carbons--one acetyl-CoA molecule, until the acyl-CoA is completely converted to acetyl-CoA.
Lopaschuk, "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," Circulation Research, vol.
Fatty acid [beta]-oxidation: acyl-CoA oxidase, bifunctional protein (hydratase-dehydrogenase), thiolase 3.
Dyck, "Beneficial effects of trimetazidine in ex vivo working ischemic hearts are due to a stimulation of glucose oxidation secondary to inhibition of long-chain 3-ketoacyl coenzyme a thiolase," Circulation Research, vol.
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).