أحادي الأكسيجيناز المحتوي على الفلافين 3
مراجع

↑  Shephard EA، Dolphin CT، Fox MF، Povey S، Smith R، Phillips IR (يونيو 1993). "Localization of genes encoding three distinct flavin-containing monooxygenases to human chromosome 1q". Genomics. ج. 16 ع. 1: 85–9. DOI:10.1006/geno.1993.1144. PMID:8486388.
↑  Dolphin CT، Riley JH، Smith RL، Shephard EA، Phillips IR (فبراير 1998). "Structural organization of the human flavin-containing monooxygenase 3 gene (FMO3), the favored candidate for fish-odor syndrome, determined directly from genomic DNA". Genomics. ج. 46 ع. 2: 260–7. DOI:10.1006/geno.1997.5031. PMID:9417913.
↑  "Entrez Gene: FMO3 flavin containing monooxygenase 3". مؤرشف من الأصل في 2021-12-11.
1 2 3 4 5  Trimethylamine monooxygenase (Homo sapiens). Technische Universität Braunschweig. يوليو 2016. مؤرشف من الأصل في 2023-07-25. اطلع عليه بتاريخ 2016-09-18. {{استشهاد بموسوعة}}: |عمل= تُجوهل (مساعدة)
1 2 3 4 5 6  Krueger SK، Williams DE (يونيو 2005). "Mammalian flavin-containing monooxygenases: structure/function, genetic polymorphisms and role in drug metabolism". Pharmacol. Ther. ج. 106 ع. 3: 357–387. DOI:10.1016/j.pharmthera.2005.01.001. PMC:1828602. PMID:15922018. A second precaution with respect to predicting FMO enzyme substrate specificity is that factors other than size and charge must play a role, but these parameters are not well understood. An example is the high selectivity observed with human FMO3, compared to the other FMO enzymes, in the N-oxygenation of the important constitutive substrate trimethylamine (Lang et al., 1998). ... The most efficient human FMO in phenethylamine N-oxygenation is FMO3, the major FMO present in adult human liver; the Km is between 90 and 200 μM (Lin & Cashman, 1997b). ... Of particular significance for this review is that individuals homozygous for certain FMO3 allelic variants (e.g., null variants) also demonstrate impaired metabolism toward other FMO substrates including ranitidine, nicotine, thio-benzamide, and phenothiazine derivatives (Table 4; Cashman et al., 1995, 2000; Kang et al., 2000; Cashman, 2002; Park et al., 2002; Lattard et al., 2003a, 2003b). ... The metabolic activation of ethionamide by the bacterial FMO is the same as the mammalian FMO activation of thiobenzamide to produce hepatotoxic sulfinic and sulfinic acid metabolites. Not surprisingly, Dr. Ortiz de Montellano's laboratory and our own have found ethionamide to be a substrate for human FMO1, FMO2, and FMO3 (unpublished observations).
Table 5: N-containing drugs and xenobiotics oxygenated by FMO
Table 6: S-containing drugs and xenobiotics oxygenated by FMO
Table 7: FMO activities not involving S- or N-oxygenation
1 2 3  Hisamuddin IM، Yang VW (يونيو 2007). "Genetic polymorphisms of human flavin-containing monooxygenase 3: implications for drug metabolism and clinical perspectives". Pharmacogenomics. ج. 8 ع. 6: 635–643. DOI:10.2217/14622416.8.6.635. PMC:2213907. PMID:17559352.
1 2  Cashman JR (سبتمبر 2000). "Human flavin-containing monooxygenase: substrate specificity and role in drug metabolism". Curr. Drug Metab. ج. 1 ع. 2: 181–191. DOI:10.2174/1389200003339135. PMID:11465082.
↑  Zhou S، Kestell P، Paxton JW (يوليو 2002). "6-methylhydroxylation of the anti-cancer agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA) by flavin-containing monooxygenase 3". Eur J Drug Metab Pharmacokinet. ج. 27 ع. 3: 179–183. DOI:10.1007/bf03190455. PMID:12365199. S2CID:21583717. Only FMO3 formed 6-OH-MXAA at a similar rate to that in cDNA-expressed cytochromes P-450 (CYP)1A2. The results of this study indicate that human FMO3 has the capacity to form 6-OH-MXAA, but plays a lesser important role for this reaction than CYP1A2 that has been demonstrated to catalyse 6-OH-MXAA formation.
↑  Tang WH، Hazen SL (أكتوبر 2014). "The contributory role of gut microbiota in cardiovascular disease". J. Clin. Invest. ج. 124 ع. 10: 4204–4211. DOI:10.1172/JCI72331. PMC:4215189. PMID:25271725.
↑  Bennett BJ، de Aguiar Vallim TQ، Wang Z، Shih DM، Meng Y، Gregory J، Allayee H، Lee R، Graham M، Crooke R، Edwards PA، Hazen SL، Lusis AJ (2013). "Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation". Cell Metab. ج. 17 ع. 1: 49–60. DOI:10.1016/j.cmet.2012.12.011. PMC:3771112. PMID:23312283.
↑  Dolphin CT، Janmohamed A، Smith RL، Shephard EA، Phillips IR (1997). "Missense mutation in flavin-containing mono-oxygenase 3 gene, FMO3, underlies fish-odour syndrome". Nat. Genet. ج. 17 ع. 4: 491–4. DOI:10.1038/ng1297-491. PMID:9398858. S2CID:24732203.
↑  Glennon RA (2013). "Phenylisopropylamine stimulants: amphetamine-related agents". Foye's principles of medicinal chemistry (ط. 7th). Philadelphia, USA: Wolters Kluwer Health/Lippincott Williams & Wilkins. ص. 646–648. ISBN:9781609133450. The simplest unsubstituted phenylisopropylamine, 1-phenyl-2-aminopropane, or amphetamine, serves as a common structural template for hallucinogens and psychostimulants. Amphetamine produces central stimulant, anorectic, and sympathomimetic actions, and it is the prototype member of this class (39). ... The phase 1 metabolism of amphetamine analogs is catalyzed by two systems: cytochrome P450 and flavin monooxygenase.
↑  Cashman JR، Xiong YN، Xu L، Janowsky A (مارس 1999). "N-oxygenation of amphetamine and methamphetamine by the human flavin-containing monooxygenase (form 3): role in bioactivation and detoxication". J. Pharmacol. Exp. Ther. ج. 288 ع. 3: 1251–1260. PMID:10027866.
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التصنيفات الطبية:  دليل الوراثة المندلية عند البشر (OMIM): 136132  
المعرفات الخارجية:  Ensembl Transcript ID: ENST00000530212  نظام اللغة الطبية الموحدة (UMLS CUI): C1414645  
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