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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Mutations of the flavin-containing monooxygenase gene ( FMO3) cause trimethylaminuria, a defect in detoxication.

Individuals with the recessive condition trimethylaminuria exhibit variation in metabolic detoxication of xenobiotics by hepatic flavin-containing monooxygenases. We show here that mutations in the human flavin-containing monooxygenase isoform 3 gene ( FMO3 ) impair N -oxygenation of xenobiotics and are responsible for the trimethylaminuria phenotype. Three disease-causing mutations in nine Australian-born probands have been identified which share a particular polymorphic haplotype. Nonsense and missense mutations are associated with a severe phenotype and are also implicated in impaired metabolism of other nitrogen- and sulfur-containing substrates including biogenic amines, both clinically and when mutated proteins expressed from cDNA are studied in vitro . These findings illustrate the critical role played by human FMO3 in the metabolism of xenobiotic substrates and endogenous amines.[1]


  1. Mutations of the flavin-containing monooxygenase gene (FMO3) cause trimethylaminuria, a defect in detoxication. Treacy, E.P., Akerman, B.R., Chow, L.M., Youil, R., Bibeau, C., Lin, J., Bruce, A.G., Knight, M., Danks, D.M., Cashman, J.R., Forrest, S.M. Hum. Mol. Genet. (1998) [Pubmed]
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