Recombinant Human CART/CARTPT Protein
SKU: PKSH030681-100
Recombinant Human CART/CARTPT Protein
SKU # | PKSH030681 |
Expression Host | HEK293 Cells |
Description
Synonyms | CART |
Species | Human |
Expression Host | HEK293 Cells |
Sequence | Met 1-Leu116 |
Accession | NP_004282.1 |
Calculated Molecular Weight | 10.6 kDa |
Observed Molecular Weight | 11 kDa |
Tag | None |
Bio-activity | Not validated for activity |
Properties
Purity | > 90 % as determined by reducing SDS-PAGE. |
Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
Storage | Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months. |
Shipping | This product is provided as lyophilized powder which is shipped with ice packs. |
Formulation | Lyophilized from sterile PBS, pH 7.4 Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual. |
Reconstitution | Please refer to the printed manual for detailed information. |
Background
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.