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- Table of Contents
Facts about Dimethylaniline monooxygenase [N-oxide-forming] 5.
Human | |
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Gene Name: | FMO5 |
Uniprot: | P49326 |
Entrez: | 2330 |
Belongs to: |
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FMO family |
dimethylaniline monooxygenase [N-oxide-forming] 5; Dimethylaniline oxidase 5; EC 1.14.13.8; flavin containing monooxygenase 5; FMO 5; Hepatic flavin-containing monooxygenase 5
Mass (kDA):
60.221 kDA
Human | |
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Location: | 1q21.1 |
Sequence: | 1; NC_000001.11 (147183963..147225798, complement) |
Expressed in fetal and adult liver.
Microsome membrane. Endoplasmic reticulum membrane.
There are many advantages to using FMO5 markers in biological research. These benefits include:
The FMO5 marker can be used in vivo for many purposes. It enhances mammalian cell responses to larger stresses. FMOs are a set of genes that regulate cell metabolism and stress resistance. They play an important role in the regulation and maintenance of major cellular metabolic activities, as well as cellular aging. Here are some of the ways in which this marker is being used in research.
The first study used human data on pharmacokinetics for 10 FMO substrates. To calculate unbound CLint (the fraction of a drug that is bound to the enzyme), the plasma protein binding, blood/plasma and plasma clearance data for each FMO substrate were combined. The data were then analyzed to determine the effect on in vivo CL. The results showed that the FMO5 marker increased AO-mediated cellular toxicity in mice, whereas it did not have a significant effect on ND-NDI.
In vitro tests have shown that FMO5 markers are highly responsive to multiple stresses including cadmium. This marker increases the body's tolerance to oxidative stress and extends lifespan in C. elegans. FMO5 also stimulates JNK/p38, two proteins involved in the insulin signaling pathway. These molecules work in parallel and provide a more robust response to multiple stressesors.
The FMOs participate in energy production metabolism. In particular, FMO expression regulates carbohydrate, energy, and amino acid metabolism. They also regulate lipid and vitamin metabolism. These in-vivo studies indicate that FMOs are essential for energy metabolism regulation. FMOs can also be found in human cells and other cell types. These studies also highlighted the functional significance of FMOs in energy metabolism.
Research in the field of alcoholic liver disease is crucial for the FMO5 marker. Its role in AFLD is still unknown. Two possible mediators are the dysfunction of the intestinal microflora or liver injury. The FMO5 marker could help us understand AFLD better. This study will help us understand how the FMO5 proteins can affect the development of apoptosis.
Recent studies have shown that liver protection against AFLD-induced damage is possible by co-expression Fmo5/PPARa. Co-expression of these genes results in a reduction of activation of NF-kB signaling pathway. This result provides a unique perspective on how FMO5 is expressed in the liver. FMO5 expression can help protect the liver. It also helps evaluate the effects of AFLD mediated inflammation on liver.
The FMO5 marker may be useful in assessing the role of the mitochondria in metabolism in cancer. Overexpression of FMO reduces overall glycolytic activity. The overall glycolytic ability is measured by measuring ECAR after glucose, oligomycin, 2DG were administered sequentially over the indicated times. These changes in ECAR can be used to calculate glycolysis, glycolytic potential, and glycolytic reserve.
FMOs can improve liver stress resistance by increasing liver stress resistance in HepG2 or HEK293A cell lines. These experiments have shown that FMO1-5 has a higher stress resistance than an empty vector of pDEST. FMO1-5 is stable in expressing FMO1-5 while OE cells are stable in expressing pDEST.
In L02 cells, Fmo5 and PPARa overexpression inhibits AFLD-induced nuclear transfer of NF-kB p65. The siRNAs siRNAs Fmo5 and siRNAs PPARa cotransfection also increase TG, TNFa, IL-6. These experiments yielded similar results to human liver.
The FMO5 marker can be used in a wide range of applications. In vivo data from hepatocytes demonstrate its use in assessing hepatic drug clearance. These studies also show the usefulness of FMO5 markers as biomarkers of liver function. The FMO5 marker can also be used to evaluate the effect of intravenous drugs.
In vitro uses of the FMO5 gene markers can improve the resistance of cells to a variety of stressors. Studies have shown that FMOs enhance cell metabolism in both HEK 293A and HepG2 cells. FMOs are also effective in increasing stress resistance in many mammalian lineages. Further research is needed to determine whether FMO5 is useful in determining disease susceptibility or prevention.
Moreover co-expressions of Fmo5/PPARa marked prevented AFLD induced apoptosis. Liver injury, and inflammatory responses. Fmo5-PPARa co-expression also inhibited nuclear transfer of NFkB p65. This is a signaling pathway related to inflammation. Moreover, AFLD induced apoptosis significantly decreased when Fmo5 was co-expressed with PPARa.
FMO5 in the blood is useful for monitoring drug metabolic rate. This marker is very sensitive and specific in drug development. It has been shown to be effective in screening drugs using in vitro studies. It is a sensitive marker that can be used to determine drug metabolism in mice. The FMO5 marker has many applications, including drug discovery and development. The FMO5 marker can be used in vitro for a variety of purposes.
Researchers were able to analyze PPARa expression using human bactosomes in E. coli and human suprasomes in insect cells. Inhibiting Fmo5 decreased PPARa expression and upregulated cleaved caspase-3 expression. Fmo5 expression in excess reduced NF-kB P65 phosphorylation, and this cell line model showed an increase in PPARa.
The FMO5 gene is involved with carbohydrate and amino acids metabolism. These pathways are controlled via FMOs. FMOs play an important part in energy metabolism. Moreover, FMOs regulate energy metabolism, as well as the energetic pathways. These processes are crucial for a human cell's survival.
Several studies have shown that cadmium increases JNK activity in FMO-OE cells. C.elegans have a shorter lifespan due to increased JNK activity. In addition, JNK phosphorylates the transcriptional factor DAF-16/FOXO, which is responsible for forkhead gene expression. It has also been shown that it can increase G-protein coupled receptor (EGFR), activity, which results in enhanced cell growth.
Studies have shown that FMO5 gene has been beneficial in assessing liver health. The effects of alcohol on intestinal flora have been shown. In addition, the FMO5 gene expression was significantly reduced in aging mice. The FMO5 genes is closely associated with intestinal flora balance. The FMO5 gene can be used as a sensor for intestinal bacteria.
Studies have shown FMO gene exclusion reduces HepG2 cell glycolytic activity. The extracellular acidification rates (ECAR) are used to calculate glycolysis. ECAR results can be used for calculating glycolysis reserve and capacity. ECAR variations represent the average + SEM from two experiments. This marker is useful in predicting cells' energy balance.
PMID: 7872795 by Overby L.H., et al. Characterization of flavin-containing monooxygenase 5 (FMO5) cloned from human and guinea pig: evidence that the unique catalytic properties of FMO5 are not confined to the rabbit ortholog.
PMID: 12527699 by Furnes B., et al. Identification of novel variants of the flavin-containing monooxygenase gene family in African Americans.