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| Cat.No | ACP19002 | Target Name | FGF23 |
|---|---|---|---|
| Form | Lyophilized powder | Expression System | Custom Production. Please inquire and provide the desire expression system. |
| Expression Range | 25-251 | Protein Length | Full Length of Mature Protein |
| Purity | >85% (SDS-PAGE) | Storage Buffer | 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0. |
| Target Species | Human | Uniprot ID | Q9GZV9 |
|---|
Uniprot Id
Q9GZV9
Target Species
Human
Target Name
FGF23
Target Full Name
Fibroblast growth factor 23
Target Function
Regulator of phosphate homeostasis. Inhibits renal tubular phosphate transport by reducing SLC34A1 levels. Upregulates EGR1 expression in the presence of KL. Acts directly on the parathyroid to decrease PTH secretion. Regulator of vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization.
Target Involvement
Hypophosphatemic rickets, autosomal dominant (ADHR); Tumoral calcinosis, hyperphosphatemic, familial (HFTC)
Target Subcellular Location
Secreted. Note=Secretion is dependent on O-glycosylation.
Target Protein Families
Heparin-binding growth factors family
Target 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).
Target Synonyms
ADHR ; FGF-23; Fgf23; FGF23_HUMAN; FGFN; Fibroblast growth factor 23 ; Fibroblast growth factor 23 C-terminal peptide; Fibroblast growth factor 23 precursor ; HPDR2 ; HYPF ; Phosphatonin; PHPTC ; Tumor derived hypophosphatemia inducing factor; Tumor-derived hypophosphatemia-inducing factor
Target Background
This gene encodes a member of the fibroblast growth factor family of proteins, which possess broad mitogenic and cell survival activities and are involved in a variety of biological processes. The product of this gene regulates phosphate homeostasis and transport in the kidney. The full-length, functional protein may be deactivated via cleavage into N-terminal and C-terminal chains. Mutation of this cleavage site causes autosomal dominant hypophosphatemic rickets (ADHR). Mutations in this gene are also associated with hyperphosphatemic familial tumoral calcinosis (HFTC).
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