FMO1

饮食衍生的氨基三甲胺（TMA）的代谢N-氧化是由含黄素的单加氧酶介导的，并受遗传性FMO3基因多态性的影响，导致小的亚群减少TMA N-氧化能力，导致鱼类气味综合征三甲胺尿症。这种酶的三种形式，在胎儿肝脏中发现的FMO1，在成人肝脏中发现的FMO2，和FMO3是由聚集在1q23-q25区域的基因编码的含黄素单加氧酶是NADPH依赖的黄素酶，它催化药物、农药和外来物质中软亲核杂原子中心的氧化。已经发现了一些编码不同亚型的转录变体。[由RefSeq提供，2013年9月]
Metabolic N-oxidation of the diet-derived amino-trimethylamine (TMA) is mediated by flavin-containing monooxygenase and is subject to an inherited FMO3 polymorphism in man resulting in a small subpopulation with reduced TMA N-oxidation capacity resulting in fish odor syndrome Trimethylaminuria. Three forms of the enzyme, FMO1 found in fetal liver, FMO2 found in adult liver, and FMO3 are encoded by genes clustered in the 1q23-q25 region. Flavin-containing monooxygenases are NADPH-dependent flavoenzymes that catalyzes the oxidation of soft nucleophilic heteroatom centers in drugs, pesticides, and xenobiotics. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2013]