acetoacetyl-CoA


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ac·e·to·a·ce·tyl-CoA

(as'e-tō-a-sē'til),
Intermediate in the oxidation of fatty acids and in the formation of ketone bodies; also formed from two molecules of acetyl-CoA and in the degradation of ketogenic amino acids; major role is condensation with acetyl-CoA to form β-hydroxy-β-methylglutaryl-CoA.

ac·e·to·a·ce·tyl-CoA

(as'ĕ-tō-ă-sē'til)
Intermediate stage in the oxidation of fatty acids and in the formation of ketone bodies; also formed from two molecules of acetyl-CoA; major role is condensation with acetyl-CoA to form the important β-hydroxy-β-methylglutaryl-CoA.
Synonym(s): acetyl-coenzyme A, active acetate.
References in periodicals archive ?
In a thiolase-mediated reaction, 2 molecules of acetyl-CoA condense to form acetoacetyl-CoA, and subsequently 3-hydroxy, 3methylglutaryl-CoA (3-HMG-CoA).
3-Hydroxy-3-methylglutaryl-Coenzyme A synthase(HMGS) is the second enzyme in MVA pathway of isoprenoid biosynthesis, and catalyzes the condensation of acetyl-CoA with acetoacetyl-CoA to yield HMG-CoA.
Biological significance of plant HMGS in the MVA pathway: As an important condensing enzyme in the MVA pathway, HMGS can catalyze condensation of acetyl-CoA and acetoacetyl-CoA to generate HMG-CoA, which is further converted into generate MVA by HMGR.
The subsequent nucleophilic attack on acetoacetyl-CoA (its second substrate) leads to the formation of HMG-CoA (Theisen et al.
Novel acetoacetyl-CoA synthesizing enzyme found in the Streptomyces MVA pathway gene clusters
35) The MVA pathway begins with the synthesis of acetoacetyl-CoA, which was first reported to be biosynthesized via a thioester-dependent Claisen condensation reaction between two molecules of acetyl-CoA, and is catalyzed by acetoacetyl-CoA thiolase (EC 2.
Acetyl-Coenzyme A acetyltransferase 2 (ACAT) transforms acetyl-CoA into acetoacetyl-CoA and can increases the rate of ketogenesis.
Purification, kinetic mechanism and regulation of different forms of mitochondrial acetoacetyl-CoA thiolases from ox liver.
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.
Activities of 3-hydroxybutyrate dehydrogenase, 3-oxoacid CoA-transferase and acetoacetyl-CoA thiolase in relation to ketone-body utilisation in muscles from vertebrates and invertebrates.
Increased lipolysis results in the overproduction of acetoacetyl-CoA, which then acts as the substrate for hepatic formation of ketone bodies.