acyl-coenzyme A

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acyl-coenzyme A

[′a·səl kō′en‚zim ′ā]
(biochemistry)
References in periodicals archive ?
Inouye, "Enzymatic and genetic characterization of firefly luciferase and Drosophila CG6178 as a fatty acyl-Coa synthetase," Bioscience, Biotechnology and Biochemistry, vol.
TMS tests: Phenylketonuria, Homocystinura, Maple Syrup Urine Disease, Arginino Succinic Aciduria, Citrullinemia, Propionic Acidemia, Methyl Malonic Acidemia, Isovaleric Acidemia, Beta Ketothiolase deficiency, Glutaric Aciduria types 1 & 2, Medium Chain Acyl-CoA Dehydrogenase deficiency, Very Long Chain Acyl CoA Dehydrogenase deficiency, HMG-CoA Lyase deficiency.
Those babies who have their newborn bloodspot sample from this month will be offered screening for medium chain acyl-CoA dehydrogenase deficiency (MCADD).
noted a "sesamin-induced increase in the gene expression of mitochondrial and peroxisomal fatty acid oxidation enzymes," with the gene expression of peroxisomal acyl-CoA oxidase and bifunctional enzyme primarily affected by sesamin (15% and 50%, respectively).
En el presente estudio se analizo la oxidacion de sustratos tritiados en fibroblastos de pacientes con deficiencia MAD (por la sigla en ingles de multiple acyl-CoA dehydrogenases) como herramienta diagnostica para estas alteraciones metabolicas.
The role of the carnitine system is to maintain homeostasis in the acyl-CoA pools of the cell, keeping the acyl-CoA/CoA pool constant even under conditions of very high turnover of the acyl-CoA (20).
As an obligate carrier for optimal mitochondrial fatty acid oxidation, it is a critical source of energy and also protects the cell from acyl-CoA accretion through the generation of acylcarnitines (4).
Ten disorders accounted for an estimated 100 or more cases (phenylketonuria, 3-methylcrotonylCoA carboxylase deficiency, medium-chain acyl-CoA dehydrogenase deficiency, Hb SS, Hb SC, Hb S/a thalassemia, congenital hypothyroidism, congenital adrenal hyperplasia, galactosemia, and cystic fibrosis).
Diagnosis of very-long chain ACYL-COA dehydrogenase deficiency using tritiated substrates
In an earlier report (3), we indicated that the posterior vacuole had properties of peroxisomes, which function primarily to process very long chain fatty acids (VLCFA) with the assistance of key enzymes, acyl-CoA oxidase (ACOX) and catalase.
Another is MCAD (medium chain acyl-CoA dehydrogenase deficiency), a disorder that affects the ability to process fat and may be responsible for up to 10 percent of deaths attributed to sudden infant death syndrome.
The acyl residues are exported to the cytoplasm and converted to acyl-CoA esters by acyl-CoA synthetase, thereby producing substrates that are further elongated in species that produce VLCs and further desaturated in species that produce polyunsaturated fatty acids.
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