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Literature summary for 2.1.1.1 extracted from

  • van Driel, L.M.; Smedts, H.P.; Helbing, W.A.; Isaacs, A.; Lindemans, J.; Uitterlinden, A.G.; van Duijn, C.M.; de Vries, J.H.; Steegers, E.A.; Steegers-Theunissen, R.P.
    Eight-fold increased risk for congenital heart defects in children carrying the nicotinamide N-methyltransferase polymorphism and exposed to medicines and low nicotinamide (2008), Eur. Heart J., 29, 1424-1431.
    View publication on PubMed

Application

Application Comment Organism
medicine epidemiologic study to analyze risk factors for complex congenital heart defects (CHDs) and multifactorial aetiology Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P40261
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Source Tissue

Source Tissue Comment Organism Textmining
blood
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Homo sapiens
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Specific Activity [micromol/min/mg]

Specific Activity Minimum [µmol/min/mg] Specific Activity Maximum [µmol/min/mg] Comment Organism
additional information
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study population, DNA analysis and allelic discrimination assay of the NNMT gene, distribution of nicotinamide N-methyltransferase genotypes in families, children carrying the NNMT A allele face additional risk of congenital heart defects (CHDs) in combination with peri-conception exposure to medicines and/or a low dietary nicotinamide intake Homo sapiens

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
S-adenosyl-L-methionine + nicotinamide polymorphism in the nicotinamide N-methyltransferase (NNMT) gene as risk factor for complex congenital heart defects (CHDs) Homo sapiens S-adenosyl-L-homocysteine + 1-methylnicotinamide
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?

Synonyms

Synonyms Comment Organism
NNMT
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Homo sapiens