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Flavin containing monooxygenase 3

Flavin-containing monooxygenases (FMO) are an important class of drug-metabolizing enzymes that catalyze the NADPH-dependent oxygenation of various nitrogen-,sulfur-, and phosphorous-containing xenobiotics such as therapeutic drugs, dietary compounds, pesticides, and other foreign compounds. The human FMO gene family is composed of 5 genes and multiple pseudogenes. FMO members have distinct developmental- and tissue-specific expression patterns. The expression of this FMO3 gene, the major FMO expressed in adult liver, can vary up to 20-fold between individuals. This inter-individual variation in FMO3 expression levels is likely to have significant effects on the rate at which xenobiotics are metabolised and, therefore, is of considerable interest to the pharmaceutical industry. This transmembrane protein localizes to the endoplasmic reticulum of many tissues. Alternative splicing of this gene results in multiple transcript variants encoding the same protein. Mutations in this gene cause the disorder trimethylaminuria (TMAu) which is characterized by the accumulation and excretion of unmetabolized trimethylamine and a distinctive body odor. In healthy individuals, trimethylamine is primarily converted to the non odorous trimethylamine N-oxide.[provided by RefSeq, Aug 2009] (from NCBI)
Top mentioned proteins: FMO2, FMO5, ACID, CAN, HAD
Papers on FMO3
Oxidative stress-responsive transcription factor NRF2 is not indispensable for the human hepatic Flavin-containing monooxygenase-3 (FMO3) gene expression in HepG2 cells.
Manautou et al., United States. In Toxicol In Vitro, Mar 2016
The hepatic expression of FMO3 is highly variable and until recently, it was thought to be uninducible.
L-Carnitine intake and high trimethylamine N-oxide plasma levels correlate with low aortic lesions in ApoE(-)(/-) transgenic mice expressing CETP.
Bellamine et al., United States. In Atherosclerosis, Jan 2016
Male ApoE(-/-) mice transfected with human cholesteryl ester transfer protein (hCETP) were fed l-carnitine and/or methimazole, a flavin monooxygenase 3 (FMO3) inhibitor that prevents the formation of TMAO.
Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease.
Kim et al., London, Canada. In Dig Dis Sci, Dec 2015
No intergroup variation existed in plasma TMAO levels based on FMO3 genotype.
Emerging roles of flavin monooxygenase 3 in cholesterol metabolism and atherosclerosis.
Brown et al., Cleveland, United States. In Curr Opin Lipidol, Oct 2015
The goal of this review is to discuss emerging evidence that the hepatic enzyme that generates TMAO, flavin monooxygenase 3 (FMO3), plays a regulatory role in maintaining whole body cholesterol balance and atherosclerosis development.
Association of Flavin Monooxygenase Gene E158K Polymorphism with Chronic Heart Disease Risk.
Polonikov et al., Kursk, Russia. In Bull Exp Biol Med, Oct 2015
We studied the relationship between the risk of chronic heart disease and FMO3 gene polymorphism E158K analyzed by PCR and restriction fragment length polymorphism (RFLP) analysis.
[Genetic polymorphism of FMO3 and its role in drug metabolism and toxicity].
Wang et al., In Zhongguo Zhong Yao Za Zhi, Jul 2015
The flavin-containing monooxygenase 3 (FMO3) is an important hepatic microsomal enzyme.
Antioxidant-related gene polymorphisms associated with the cardio-ankle vascular index in young Russians.
Polonikov et al., Kursk, Russia. In Cardiol Young, Jul 2015
A total of 89 patients (mean age, 21.6 years) were examined by the cardio-ankle vascular index and for 15 gene polymorphisms related to antioxidant enzymes including FMO3 (flavin-containing monooxygenase 3), GPX1 (glutathione peroxidase 1), and GPX4 (glutathione peroxidase 4).
Escherichia coli Overexpressing a Baeyer-Villiger Monooxygenase from Acinetobacter radioresistens Becomes Resistant to Imipenem.
Sadeghi et al., Torino, Italy. In Antimicrob Agents Chemother, 2014
Ar-BVMO not only is capable of oxidizing two anticancer drugs metabolized by human FMO3, danusertib and tozasertib, but also can oxidize other synthetic drugs, such as imipenem.
The contributory role of gut microbiota in cardiovascular disease.
Hazen et al., In J Clin Invest, 2014
A meta-organismal pathway was elucidated involving gut microbiota-dependent formation of TMA and host hepatic flavin monooxygenase 3-dependent (FMO3-dependent) formation of TMA-N-oxide (TMAO), a metabolite shown to be both mechanistically linked to atherosclerosis and whose levels are strongly linked to cardiovascular disease (CVD) risks.
Pharmacogenetics of olanzapine metabolism.
Dahl et al., Huddinge, Sweden. In Pharmacogenomics, 2013
The formation of the various olanzapine metabolites is influenced by polymorphisms in the genes coding for CYP1A2, CYP1A expression regulator AHR, UGT1A4 and UGT2B10, as well as FMO3.
Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation.
Lusis et al., Los Angeles, United States. In Cell Metab, 2013
We demonstrate that two flavin mono-oxygenase family members, FMO1 and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to TMAO.
Fragment Molecular Orbital Molecular Dynamics with the Fully Analytic Energy Gradient.
Gordon et al., Ames, United States. In J Chem Theory Comput, 2013
An FMO-MD simulation that includes the fully analytic energy gradient and two body corrections (FMO2) gives improved energy conservation compared with a previously calculated FMO-MD simulation with an approximate energy gradient and including up to three body corrections (FMO3).
Flavin-containing monooxygenase 3 gene polymorphisms in Turkish population.
Alpertunga et al., ─░stanbul, Turkey. In Toxicol Mech Methods, 2012
It was found that FMO3 158K, 257M and 308G alleles, demonstrate impaired metabolism toward many FMO3 substrates, were observed frequently in Turkish population similar to the other populations
FAD-dependent enzymes involved in the metabolic oxidation of xenobiotics.
Strolin Benedetti, Colombes, France. In Ann Pharm Fr, 2011
What have we here? A man or a fish?
Jakobs et al., Amsterdam, Netherlands. In Lancet, 2010
patient heterozygous for 4 FMO3 mutations
A common FMO3 polymorphism may amplify the effect of nicotine exposure in sudden infant death syndrome (SIDS).
Bajanowski et al., Essen, Germany. In Int J Legal Med, 2010
This study is the first to demonstrate a gene-environment interaction in SIDS. The findings suggest that the common polymorphism G472A of FMO3 could act as an additional genetic SIDS risk factor in children whose mothers smoke.
A novel mutation in the flavin-containing monooxygenase 3 gene (FMO3) of a Norwegian family causes trimethylaminuria.
Shephard et al., London, United Kingdom. In Mol Genet Metab, 2009
The identification in a family from northern Norway of a novel causative mutation of FMO3 gene causing trimethylaminuria, is described.
Flavin-containing monooxygenase 3 polymorphisms in 13 ethnic populations from Europe, East Asia and sub-Saharan Africa: frequency and linkage analysis.
Dahl et al., Uppsala, Sweden. In Pharmacogenomics, 2009
Distribution of functionally relevant FMO3 polymorphisms varies not only between ethnicities but also within
Mild trimethylaminuria caused by common variants in FMO3 gene.
Mayatepek et al., In Lancet, 1999
Mild to transient trimethylaminuria is caused by common variants in the FMO3 gene leading to greatly reduced enzyme activity in vivo.
Missense mutation in flavin-containing mono-oxygenase 3 gene, FMO3, underlies fish-odour syndrome.
Phillips et al., London, United Kingdom. In Nat Genet, 1997
TMA oxidation is catalyzed by flavin-containing mono-oxygenase (FMO; refs 7,8), and tissue localization and functional studies have established FMO3 as the form most likely to be defective in fish-odour syndrome.
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