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Literature summary for 1.3.8.8 extracted from

  • Clark-Taylor, T.; Clark-Taylor, B.E.
    Is autism a disorder of fatty acid metabolism? Possible dysfunction of mitochondrial beta-oxidation by long chain acyl-CoA dehydrogenase (2004), Med. Hypotheses, 62, 970-975.
    View publication on PubMed
Search for more literature for 1.3.8.8

Localization

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

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens enzyme deficiency may ba a cause of autism, physiological alterations in case of enzyme deficiency are in TCA energy metabolism, ammonia detoxification, and synthesis of omega-3 DHA, and elevated acyl-carnitine levels, the mitochondrial enzyme is responsible for beta-oxidation of branched and unsaturated fatty acids with preference for long-chain fatty acids ?
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
 8-year-old male autistic patient
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
linoleoyl-CoA + acceptor
-
 Homo sapiens 2,9,12-octadecatrienoyl-CoA + reduced acceptor
-
 ?
additional information enzyme deficiency may ba a cause of autism, physiological alterations in case of enzyme deficiency are in TCA energy metabolism, ammonia detoxification, and synthesis of omega-3 DHA, and elevated acyl-carnitine levels, the mitochondrial enzyme is responsible for beta-oxidation of branched and unsaturated fatty acids with preference for long-chain fatty acids Homo sapiens ?
-
 ?
additional information enzyme has broad substrate specificity with preference for medium- and long-chain fatty acids, overview Homo sapiens ?
-
 ?
oleoyl-CoA + acceptor
-
 Homo sapiens 2,9-octadecadienoyl-CoA + reduced acceptor
-
 ?

Synonyms

Synonyms Comment Organism
LCAD
-
 Homo sapiens
long chain acyl-CoA dehydrogenase
-
 Homo sapiens