Recombinant Mouse FGF-9 (N-6His)(Cat. No.:CR12) novoprotein
$105.00
In stock
SKU
CR12
10μg: $105
50μg: $315
500μg: $1260
1mg: $1800
Description
Recombinant Mouse Fibroblast Growth Factor 9 is produced by our E.coli expression system and the target gene encoding Met1Ser208 is expressed with a 6His tag at the N-terminus.
Product Details
| Item | Details |
| Known As | Fibroblast growth factor 9; FGF-9; Glia-activating factor; GAF; heparin-binding growth factor-9; HBGF-9; Fgf9; Fgf-9 |
| Mol Mass | 24.4 KDa |
| APMol Mass | 25 KDa, reducing conditions |
| Formulation Description | Supplied as a 0.2 μm filtered solution of 20mM Tris-HCl, 150mM NaCl, 5% Trehalose, 1mM EDTA, 20% Glycerol, 1mM DTT, pH 8.5. |
| Endotoxin | < 0.01 EU/µg as determined by LAL test. |
| Storage | Store at ≤-70°C, stable for 6 months after receipt. Store at ≤-70°C, stable for 3 months under sterile conditions after opening. Please minimize freeze-thaw cycles. |
| Shipping | The product is shipped on dry ice/polar packs. Upon receipt, store it immediately at the temperature listed below. |
Background
Fibroblast growth factor-9 (FGF-9) is an approximately 26 kDa secreted glycoprotein of the FGF family. Secreted mouse FGF-9 lacks the N-terminal 1-3 aa and shares >98% sequence identity with rat, human, equine, porcine and bovine FGF-9. FGF-9 plays an important role in the regulation of embryonic development, cell proliferation, cell differentiation and cell migration. In the mouse embryo the location and timing of FGF-9 expression affects development of the skeleton, cerebellum, lungs, heart, vasculature, digestive tract, and testes .It may have a role in glial cell growth and differentiation during development, gliosis during repair and regeneration of brain tissue after damage, differentiation and survival of neuronal cells, and growth stimulation of glial tumors. Deletion of mouse FGF-9 is lethal at birth due to lung hypoplasia, and causes rhizomelia, or shortening of the proximal skeleton. An unusual constitutive dimerization of FGF 9 buries receptor interaction sites which lowers its activity, and increases heparin affinity which inhibits diffusion. A spontaneous mouse mutant, Eks, interferes with dimerization, resulting monomeric, diffusible FGF-9 that causes elbow and knee synostoses (joint fusions) due to FGF-9 misexpression in developing joints.
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