Warehouse Overstock Promotion |  Save 10%  on Premium Lab Supplies |  Shop Now

Menu

This product has been added to the cart.

Recombinant Mouse FGF-9/FGF9 Protein (His Tag)(Active)

SKU: PKSM041022-50

  • $ 62195


Request a Quote

Recombinant Mouse FGF-9/FGF9 Protein (His Tag)(Active)

 

SKU # PKSM041022
Expression Host E.coli

 

 

Description

Synonyms FGF-9, Fgf-9, Fgf9, Fibroblast growth factor 9, GAF, Glia-activating factor, HBGF-9, heparin-binding growth factor-9
Species Mouse
Expression Host E.coli
Sequence Met1-Ser208
Accession P54130
Calculated Molecular Weight 24.4 kDa
Observed Molecular Weight 25 kDa
Tag N-His
Bio-activity Not validated for activity
  

 

Properties

Purity > 95 % as determined by reducing SDS-PAGE.
Endotoxin < 0.01 EU per μg of the protein as determined by the LAL method.
Storage Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
Shipping This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C.
Formulation 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.
Reconstitution Not Applicable



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.