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Key Documents

SAB1406641

Sigma-Aldrich

Anti-FGF23 antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

Synonyme(s) :

ADHR, HPDR2, HYPF, PHPTC

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~28 kDa

Espèces réactives

human

Technique(s)

proximity ligation assay: suitable
western blot: 1 μg/mL

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... FGF23(8074)

Description générale

The protein encoded by this gene 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. The product of this gene inhibits renal tubular phosphate transport. This gene was identified by its mutations associated with autosomal dominant hypophosphatemic rickets (ADHR), an inherited phosphate wasting disorder. Abnormally high level expression of this gene was found in oncogenic hypophosphatemic osteomalacia (OHO), a phenotypically similar disease caused by abnormal phosphate metabolism. Mutations in this gene have also been shown to cause familial tumoral calcinosis with hyperphosphatemia. (provided by RefSeq)

Immunogène

FGF23 (NP_065689.1, 1 a.a. ~ 251 a.a) full-length human protein.

Sequence
MLGARLRLWVCALCSVCSMSVLRAYPNASPLLGSSWGGLIHLYTATARNSYHLQIHKNGHVDGAPHQTIYSALMIRSEDAGFVVITGVMSRRYLCMDFRGNIFGSHYFDPENCRFQHQTLENGYDVYHSPQYHFLVSLGRAKRAFLPGMNPPPYSQFLSRRNEIPLIHFNTPIPRRHTRSAEDDSERDPLNVLKPRARMTPAPASCSQELPSAEDNSPMASDPLGVVRGGRVNTHAGGTGPEGCRPFAKFI

Actions biochimiques/physiologiques

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.

Forme physique

Solution in phosphate buffered saline, pH 7.4

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Daniela Spichtig et al.
Kidney international, 85(6), 1340-1350 (2014-01-10)
Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis and is linked to cardiovascular disease and all-cause mortality in chronic kidney disease. FGF23 rises in patients with CKD stages 2-3, but in patients with autosomal dominant polycystic kidney disease, the increase
Interplay between vitamin D and the drug metabolizing enzyme CYP3A4.
Wang Z
The Journal of Steroid Biochemistry and Molecular Biology, 136, 54-58 (2013)
Fibroblast growth factor 23 and bone mineralisation.
Guo YC and Yuan Q
International Journal of Oral Science, 7(1), 8-13 (2015)
Klotho converts canonical FGF receptor into a specific receptor for FGF23.
Urakawa I
Nature, 444(7120), 770-774 (2006)
Xu Guan et al.
The Journal of pathology, 234(4), 560-572 (2014-08-19)
Increased basic fibroblast growth factor-2 (FGF2) and reduced Klotho have both been reported to be closely associated with renal fibrosis. However, the relationship between Klotho and FGF2 remains unclear. We demonstrate that FGF2 induced tubulo-epithelial plasticity in cultured HK-2 cells

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