Recombinant Human FGF-23 (RMPP-00231547)
Cat. No.: RMPP-00231547
Category: Growth Factors & Cytokines
INQUIRY
5 μg
20 μg
The FGF family plays a central role during prenatal development, postnatal growth and regeneration of a variety of tissues, by promoting cellular proliferation and differentiation. FGF-23, FGF-21 and FGF-19 constitute an atypical FGF subfamily whose ligands act as circulating hormones and require the participation of a Klotho protein as a co-receptor for their signaling. FGF-23 is a bone-derived hormone that acts in the kidney to regulate phosphate homeostasis and vitamin D metabolism. The signaling receptor for FGF-23, a Klotho-FGFR1 (IIIc) complex, is an essential regulator of the renal sodium phosphate co-transporter and key vitamin D-metabolizing enzymes CYP27B1 and CYP24A1. Recombinant Human FGF-23 is a 25.5 kDa globular protein containing 228 amino acid residues.
Product Features
| Source | E.coli |
|---|---|
| Purity | ≥ 95% by SDS-PAGE gel and HPLC analyses. |
| Nature | Recombinant |
| Endotoxin Level | < 1 Eu/μg |
| Cross Reactivity | Mouse, Rat |
Protein Information
| UniProt ID | Q9GZV9 |
|---|---|
| Molecular Weight | 25.5 kDa |
| Molecular Weight Information | Predicted MW is 25389.60 Da (+/- 10 Da by ESI-TOF). Observed MW is 25390.94 |
| Sequence Similarities | Belongs to the heparin-binding growth factors family. |
| Protein Length | Full length protein |
| Cellular Localization | Secreted. Secretion is dependent on O-glycosylation. |
| Tissue Specificity | Expressed in osteogenic cells particularly during phases of active bone remodeling. In adult trabecular bone, expressed in osteocytes and flattened bone-lining cells (inactive osteoblasts). |
| Function | Regulator of phosphate homeostasis. Inhibits renal tubular phosphate transport by reducing SLC34A1 levels. Upregulates EGR1 expression in the presence of KL (By similarity). Acts directly on the parathyroid to decrease PTH secretion (By similarity). Regulator of vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization. |
| Involvement in Disease | Defects in FGF23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR). ADHR is characterized by low serum phosphorus concentrations, rickets, osteomalacia, leg deformities, short stature, bone pain and dental abscesses.Defects in FGF23 are a cause of hyperphosphatemic familial tumoral calcinosis (HFTC). HFTC is a severe autosomal recessive metabolic disorder that manifests with hyperphosphatemia and massive calcium deposits in the skin and subcutaneous tissues. |
| Post-translational Modifications | Following secretion this protein is inactivated by cleavage into a N-terminal fragment and a C-terminal fragment. The processing is effected by proprotein convertases.O-glycosylated by GALT3. Glycosylation is necessary for secretion; it blocks processing by proprotein convertases when the O-glycan is alpha 2,6-sialylated. Competition between proprotein convertase cleavage and block of cleavage by O-glycosylation determines the level of secreted active FGF23. |
Storage & Shipping
| Shipping and Storage | Shipped on Dry Ice. |
|---|
For research use only. Not for clinical use.
