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Differential gene expression by SFRP2(+), FMO1(+), and COL11A1(+) fibroblasts suggests roles in matrix deposition, inflammatory cell retention, and connective tissue cell differentiation, respectively.
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Report developmental regulation of hepatic FMO1 expression.
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Study tested the genetic effects of three FMOs genes (FMO1, FMO3, and FMO6P) on nicotine dependence by performing targeted sequencing on 2,852 nicotine-dependent and nondependent smokers; identified significant association signals for gene FMO1 and FMO6P
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data support the role of FMO3 in the N-oxidation of OLA and implicate for the first time the contribution of FMO1 and its functional *6 variant in OLA disposition
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polymorphisms in FMO1 are significant risk factors in the development of nicotine dependence and that the mechanism may involve variation in nicotine pharmacology.
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The results of this study suggested that the alteration of FMO gene expression is a consequence of the pathological environment linked to oxidative stress related to mutated SOD1.
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FMO1 expression is restricted to the fetus; FMO1 suppression occurred within 3 d postpartum in a process tightly coupled to birth, but not gestational age.
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data from transient expression assays in HepG2 cells suggested this SNP could account for a 2- to 3-fold loss of FMO1 promoter activity.
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"...in fetal liver, where FMO1 predominates attaining expression levels of (about) 32% of expressed CYP3A4." p. 574 "...recent examples indicate that FMOs play a prominent role in the metabolism ...of important drugs." p. 575
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FMO1 was found to be down-regulated in human adult brain tissue.
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Early studies described in this review document that FMO1 is the most abundant FMO enzyme in the human fetal liver, whereas FMO3 is essentially absent.
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Specific allelic variants of the FMO1 gene might be associated to susceptibility to develop ALS.
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The resulting data showed that N,N-dimethylamphetamine N-oxidation is mainly mediated by FMO1.