FMO3
Reactivity: Human
ELISA, IHC
Host: Rabbit
Polyclonal
unconjugated
Application Notes
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,IHC: 1:100-1:300,ELISA 1:20000,IF 1:50-200
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
-20 °C
Storage Comment
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Expiry Date
12 months
Target
FMO3
(Flavin Containing Monooxygenase 3 (FMO3))
Alternative Name
FMO3
Background
FMO3, Dimethylaniline monooxygenase [N-oxide-forming] 3, Dimethylaniline oxidase 3, FMO II, FMO form 2, Hepatic flavin-containing monooxygenase 3, FMO 3, Trimethylamine monooxygenaseFlavin-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 different isoforms. 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.