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Literature summary extracted from

  • van Maldegem, B.T.; Wanders, R.J.; Wijburg, F.A.
    Clinical aspects of short-chain acyl-CoA dehydrogenase deficiency (2010), J. Inherit. Metab. Dis., 33, 507-511.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
1.3.8.1 SCAD DNA and amino acid sequence determination and analysis Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.3.8.1 mitochondrion
-
 Homo sapiens 5739
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1.3.8.1 butanoyl-CoA + acceptor Homo sapiens
-
 but-2-enoyl-CoA + reduced acceptor
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
1.3.8.1 Homo sapiens
-
-
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.3.8.1 butanoyl-CoA + acceptor
-
 Homo sapiens but-2-enoyl-CoA + reduced acceptor
-
 ?

Synonyms

EC Number Synonyms Comment Organism
1.3.8.1 SCAD
-
 Homo sapiens
1.3.8.1 short-chain acyl-CoA dehydrogenase
-
 Homo sapiens

General Information

EC Number General Information Comment Organism
1.3.8.1 additional information short-chain acyl-CoA dehydrogenase deficiency, SCADD, is an autosomal recessive inborn error of mitochondrial fatty acid oxidation due to mutations in the SCAD protein. SCADD is biochemically characterized by increased C4-carnitine in plasma and ethylmalonic acid in urine, phenotype, overview Homo sapiens
1.3.8.1 physiological function SCAD catalyzes the dehydrogenation of butyryl-CoA during the first step of the short-chain fatty acid beta-oxidation spiral Homo sapiens