fibroblast growth factor 23
fibroblast growth factor 23 Basic information
- Product Name:
- fibroblast growth factor 23
- Synonyms:
-
- Anti-FGF23 antibody produced in rabbit
- Anti-Fgf23 antibody produced in goat
- fibroblast growth factor 23
- DI1
- PHPTC
- Antidiuretic hormone receptor
- Avp2r
- AVPR V2
- MW:
- 0
- Mol File:
- Mol File
fibroblast growth factor 23 Chemical Properties
- storage temp.
- -20°C
- form
- buffered aqueous solution
- biological source
- rabbit
fibroblast growth factor 23 Usage And Synthesis
Biological Activity
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. Fibroblast growth factor-23, -21 and -19 (FGF-23, FGF-21 and FGF-19) act as circulating hormones and require the participation of a Klotho protein as a co-receptor for their signaling. The signaling receptor for FGF-23, a Klotho-FGFR1 (IIIc) complex, is an essential regulator of the renal sodium phosphate co-transporter and key vitamin D-metabolizing enzymes cytochrome P450 family 27 subfamily B member 1 (CYP27B1) and cytochrome P450 family 24 subfamily A member 1 (CYP24A1). FGF-23 acts in the kidney to regulate phosphate homeostasis and vitamin D metabolism.
Description
Fibroblast Growth Factor-23 Human Recombinant produced in E.Coli is a single, non-glycosylated polypeptide chain containing a total of 228 amino acids and having a molecular mass of 22.5kDa.
The FGF-23 is and purified by chromatographic techniques.
Source
Escherichia Coli
Background
FGF-23 is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities and are involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF-23 inhibits renal tubular phosphate transport. The FGF-23 gene was identified by its mutations associated with autosomal dominant hypophosphatemic rickets (ADHR), an inherited phosphate wasting disorder. Abnormally high level expression of FGF-23 was found in oncogenic hypophosphatemic osteomalacia (OHO), a phenotypically similar disease caused by abnormal phosphate metabolism. FGF-23 mutations have also been shown to cause familial tumoral calcinosis with hyperphosphatemia.
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