The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Activates ERK and FRS2alpha phosphorylation in Klotho expressing cells.
< 0.100 Eu/µg
% SDS-PAGE. ab108942 is 0.2µm filtered
Working 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.
Fibroblast growth factor 23
Fibroblast growth factor 23 C-terminal peptide
Fibroblast growth factor 23 precursor
Tumor derived hypophosphatemia inducing factor
Tumor-derived hypophosphatemia-inducing factor
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.
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).
Involvement in disease
Defects 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.
Belongs to the heparin-binding growth factors family.
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.
Secreted. Secretion is dependent on O-glycosylation.
Functional Studies - Recombinant mouse FGF 23 protein (ab108942)
ERK and FRS2alpha phosphorylation induced by FGF 23 in Klotho expressing cells.
Klotho expressing HEK 293EBNA cells were serum starved for 16hr and then stimulated with mFGF 23-Fc (ab108942), and FGF-b (100ng/ml) (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: Klotho + ab108942 1ng/ml
Lane 3: Klotho + ab108942 10ng/ml
Lane 4: Klotho + ab108942 100ng/ml
Lane 5: Klotho + ab108942 500ng/ml
Lane 6: Klotho + ab108942 1000ng/ml
Lane 7: Klotho + 100ng/ml FGF-b
has not yet been referenced specifically in any publications.
Publishing research using ab108942? Please let us know so that we can cite the reference in this datasheet.
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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"
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