Recombinant Human FGF-23
| Code | Size | Price |
|---|
| LEI-F1109-25ug | 25 ug | £512.00 |
Quantity:
Prices exclude any Taxes / VAT
Overview
Host Type: Human
Regulatory Status: RUO
Shipping:
Ambient
Storage:
This lyophilized protein is stable for six to twelve months when stored desiccated at -20°C to -70°C. After aseptic reconstitution this protein may be stored at 2°C to 8°C for one month or at -20°C to -70°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles. See Product Insert for exact lot specific storage instructions.
Further Information
Format:
This recombinant protein was lyophilized from a 0.2 um filtered solution in MOPS, sodium sulphate (Na2SO4), ethylenediaminetetraacetic acid (EDTA), and dithiothreitol (DTT).
Formulation:
This recombinant protein was lyophilized from a 0.2 um filtered solution in MOPS, sodium sulphate (Na2SO4), ethylenediaminetetraacetic acid (EDTA), and dithiothreitol (DTT).
Long Description:
Fibroblast growth factor-23 (FGF-23), also known as ADHR and HYPF, is a secreted, non-glycosylated protein and member of the FGF family. The FGF family plays a central role during prenatal development and postnatal growth and regeneration of a variety of tissues, by promoting cellular proliferation and differentiation (1). FGF-23 is mostly expressed in bone and connective tissue and exerts its effects through a ternary complex that includes Klotho and an FGF receptor (FGF R4 or the ?c? isoforms of FGF R1 or FGF R3); however, Klotho has a restricted distribution that limits FGF-23 activity (2). This complex is an essential regulator of the renal sodium phosphate co-transporter which is accomplished by modulating SLC34A1 levels (3). FGF-23 also inhibits 1-hydroxylase which is responsible for the conversion of calcifediol to calcitriol (the biologically active form of Vitamin D) (4). It up-regulates EGR1 expression in the presence of KL and acts directly on the parathyroid to decrease PTH secretion. Additionally, FGF-23 negatively regulates osteoblast differentiation and matrix mineralization. FGF-23 was identified by its mutations associated with autosomal dominant hypophosphatemic rickets (ADHR), an inherited phosphate wasting disorder (5). Abnormally high level expression of FGF-23 was found in oncogenic hypophosphatemic osteomalacia (OHO), a phenotypically similar disease caused by abnormal phosphate metabolism (6). Mutations in this gene have also been shown to cause familial tumoral calcinosis with hyperphosphatemia.
NCBI Gene:
8074
Purity:
>95% by SDS-PAGE and analyzed by silver stain.
Target:
FGF-23
References
1. Yamashita, T. et al. (2000) Biochem. Biophys. Res. Commun. 277:494
2. Frishberg, Y. et al. (2007) J. Bone Miner. Res. 22:235
3. Bowe, AE. et al. (2001) Biochem. Biophys. Res. Commun. 284:977
4. Saito, H. et al. (2005) J. Biol. Chem. 280:2543
5. White, KE. et al. (2001) J. Clin. Endocrinol. Metab. 86:497
6. Shimada, T. et al. (2001) Proc. Natl. Acad. Sci. (USA) 98:6500
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