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|Recombinant Human FDPS / Farnesyl Diphosphate Synthase protein (Catalog#13229-H07E)|
|This antibody was obtained from a rabbit immunized with purified, recombinant Human FDPS / Farnesyl Diphosphate Synthase (rh FDPS / Farnesyl Diphosphate Synthase; Catalog#13229-H07E; NP_001129294.1; Met1-Lys353).|
|Human FDPS / Farnesyl Diphosphate Synthase|
|WB, ELISA, ICC/IF, IF, FCM, IP|
ELISA: 0.1-0.2 μg/mL
This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human FDPS / Farnesyl Diphosphate Synthase. The detection limit for Human FDPS / Farnesyl Diphosphate Synthase is 0.0012 ng/well.
FCM: 0.5-2 μg/Test
ICC/IF: 10-25 μg/mL
IP: 1-4 μg/mg of lysate
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Z-farnesyl diphosphate synthase (FDPS) is an enzyme belonging to the family of transferases, specifically those transferring aryl or alkyl groups other than methyl groups. Z-farnesyl diphosphate synthase (FDPS) functions as key enzyme in isoprenoid biosynthesis which catalyzes the formation of farnesyl diphosphate, a precurcor for several classes of essential metabolites. FDPS catalyzes the production of geranyl pyrophosphate and farnesyl pyrophosphate from isopentenyl pyrophosphate and dimethylallyl pyrophosphate. The resulting product, farnesyl pyrophosphate, is a key intermediate in cholesterol and sterol biosynthesis, a substrate for protein farnesylation and geranylgeranylation, and a ligand or agonist for certain hormone receptors and growth receptors. Drugs that inhibit this enzyme prevent the post-translational modifications of small GTPases and have been used to treat diseases related to bone resorption. Functions of FDPS may be inactivated by interferon-induced RSAD2. This inactivation may result of disruption of lipid rafts at the plasma membrane, and thus have an antiviral effect since many enveloped viruses need lipid rafts to bud efficiently out of the cell.