Key features and details
- Expression system: HEK 293 cells
- Purity: > 90% SDS-PAGE
- Endotoxin level: < 0.100 Eu/µg
- Active: Yes
- Tags: Fc tag C-Terminus
- Suitable for: Functional Studies, SDS-PAGE
Product nameRecombinant human FGF 23 protein
See all FGF 23 proteins and peptides
Biological activityActivates ERK and FRS2alpha phosphorylation in Klotho expressing cells.
Purity> 90 % SDS-PAGE.
ab108553 is 0.2µm filtered.
Endotoxin level< 0.100 Eu/µg
Expression systemHEK 293 cells
Protein lengthFull length protein
Predicted molecular weight60 kDa including tags
Amino acids25 to 251
TagsFc tag C-Terminus
Additional sequence informationFGF23 is cleaved between aa179 and aa180 (~40kDa).
Our Abpromise guarantee covers the use of ab108553 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Additional notesWorking aliquots are stable for up to 3 months when stored at -20°C.
Concentration information loading...
Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
FunctionRegulator 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.
Tissue specificityExpressed in osteogenic cells particularly during phases of active bone remodeling. In adult trabecular bone, expressed in osteocytes and flattened bone-lining cells (inactive osteoblasts).
Involvement in diseaseDefects in FGF23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR) [MIM:193100]. 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) [MIM:211900]. HFTC is a severe autosomal recessive metabolic disorder that manifests with hyperphosphatemia and massive calcium deposits in the skin and subcutaneous tissues.
Sequence similaritiesBelongs to the heparin-binding growth factors family.
modificationsFollowing 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.
Cellular localizationSecreted. Secretion is dependent on O-glycosylation.
- Information by UniProt
ERK and FRS2aplha phosphorylation induced by FGF 23 in Klotho expressing cells.
Klotho expressing HEK 293EBNA cells were serum starved for 16hr and then stimulated with hFGF 23-His, FGF 23-Fc (ab108553), mCD137-Fc (Fc control) and FGF-b (positive control) for 10 min, respectively.
Antibodies against pFRS2alpha, pERK1/2 & total ERK1/2 were used for immunoblotting.
Lane 1: Mock (non-treated)
Lane 2: Mock + hFGF 23-Fc (ab108553) 1µg/ml
Lane 3: Mock + hFGF 23-His 1µg/ml
Lane 4: Klotho + hFGF 23-Fc (ab108553) 1µg/ml
Lane 5: Klotho + hFGF 23-Fc (ab108553) 4µg/ml
Lane 6: Klotho + mCD137-Fc 1µg/ml
Lane 7: Klotho (non-treated)
Lane 8: Klotho + 100ng/ml FGF-b
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab108553 has not yet been referenced specifically in any publications.