FGF23 Rabbit pAb
- 产品详情
- 实验流程
Application
| WB |
|---|---|
| Reactivity | Mouse |
| Predicted | Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 27 KDa |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from mouse FGF23 |
| Epitope Specificity | 81-180/251 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SIMILARITY | Belongs to the heparin-binding growth factors family. |
| SUBUNIT | Interacts with FGFR1, FGFR2, FGFR3 and FGFR4. Affinity between fibroblast growth factors (FGFs) and their receptors is increased by KL and heparan sulfate glycosaminoglycans that function as coreceptors. |
| 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. |
| 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. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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). [provided by RefSeq, Feb 2013] |
| Other Names | ADHR; FGFN; HFTC2; HPDR2; HYPF; PHPTC; FGF23_HUMAN; FGF23; FGF-23; Phosphatonin; Tumor-derived hypophosphatemia-inducing factor; fibroblast growth factor 23 |
|---|---|
| Dilution | WB=1:500-2000 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | FGF23 Rabbit pAb |
| 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. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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