Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
Human FGF23 ELISA Kit for Sandwich ELISA - ABIN416862
Oikonomou, Orfanidou, Vlychou, Kapsoritakis, Tsezou, Malizos, Potamianos: Lower fibroblast growth factor 23 levels in young adults with Crohn disease as a possible secondary compensatory effect on the disturbance of bone and mineral metabolism. in Journal of clinical densitometry : the official journal of the International Society for Clinical Densitometry 2014
Show all 7 Pubmed References
Human FGF23 ELISA Kit for Sandwich ELISA - ABIN368019
Xu, Yang, Sun, Yuan, Cheng, Wei, Li, Cheng, Brann, Wang: A new antifibrotic target of Ac-SDKP: inhibition of myofibroblast differentiation in rat lung with silicosis. in PLoS ONE 2012
Show all 4 Pubmed References
Mouse (Murine) FGF23 ELISA Kit for Sandwich ELISA - ABIN415718
Chen, Feng, Bao, Li, Zhang, Shen, Zhao, Guo, Jing, Lin, Zong: Adverse Effects of Osteocytic Constitutive Activation of ß-Catenin on Bone Strength and Bone Growth. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2015
Show all 2 Pubmed References
Rat (Rattus) FGF23 ELISA Kit for Sandwich ELISA - ABIN367437
Lind, Sundqvist, Hu, Pejler, Andersson, Jacobson, Melhus: Vitamin a is a negative regulator of osteoblast mineralization. in PLoS ONE 2013
Show all 2 Pubmed References
FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1 (show STC1 ELISA Kits))modulates cation levels in trpm7 (show TRPM7 ELISA Kits) mutants and in the wild type; levels of cations are restored to normal in trpm7 (show TRPM7 ELISA Kits) mutants when stc1 (show STC1 ELISA Kits) activity is blocked.
Elevated levels of interleukin-6 (show IL6 ELISA Kits), C-reactive protein (show CRP ELISA Kits), and FGF23 are independent risk factors for mortality in chronic kidney disease.
Main demonstrable effect of FGF23 in the setting of preserved renal function is suppression of 1,25-dihydroxyvitamin D3 rather than stimulation of renal phosphate excretion.
An overview of FGF23 biology and physiology is provided, clinical outcomes that have been associated with FGF23 are summarized, potential mechanisms for these observations are discussed.
Sclerostin (show SOST ELISA Kits) levels in KTR are normal and influenced more by bone turnover than by eGFR (show EGFR ELISA Kits). Its involvement with other hormones of mineral homeostasis (FGF23/Klotho (show KL ELISA Kits) and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney
High serum FGF23 expression is associated with acute decompensated heart failure.
High FGF-23 expression is associated with cardiovascular disease.
high i-FGF23 levels may be associated with prolongation of low levels of ferritin (show FTL ELISA Kits), resulting in increased usages of iron supplementation in HD patients
There might be a strong correlation between FGF-23 and ghrelin (show GHRL ELISA Kits) levels irrespective of the stage of chronic kidney disease and the dialysis modality
Results showed that human endothelial cells differentially express functional full-length alpha-Klotho (show KL ELISA Kits) protein. And that it is this full-length alpha-Klotho (show KL ELISA Kits) protein that modulates endothelial cells response to FGF-23.
In men with low-to-moderate CVD risk, serum FGF23 levels were associated independently and positively with carotid intima-media thickness. As a complementary index, serum FGF23 levels strengthen the capacity of the Framingham risk score to identify subclinical atherosclerosis.
FGF23 may be an important modulator of PTH (show PTH ELISA Kits) signaling in bone and kidney.
EPO (show EPO ELISA Kits) dependent regulation pathway of FGF23 gene expression
Klotho (show KL ELISA Kits) in bone is crucial for inducing FGF23 production upon renal failure
dietary iron content and chronic kidney disease affected FGF23 production and metabolism
Dmp1 (show DMP1 ELISA Kits) mutation creates a lower set point for extracellular phosphate and maintains it through the regulation of Fgf23 cleavage and expression
Although FGF23 is present in the fetal circulation at levels that may equal adult values, and there is robust expression of FGF23 target genes in placenta and fetal kidneys, FGF23 itself is not an important regulator of fetal phosphorous metabolism.
Annexin A7 (show ANXA7 ELISA Kits) deficiency upregulates FGF23 plasma levels, an effect paralleled by increased corticosterone plasma levels, as well as decreased 1,25(OH)2 D3 and PTH (show PTH ELISA Kits) plasma levels.
FGF23 regulates osteopontin (show SPP1 ELISA Kits) secretion indirectly by suppressing alkaline phosphatase transcription and phosphate production in osteoblastic cells, acting through FGF receptor-3 (show FGFR3 ELISA Kits) in a Klotho (show KL ELISA Kits)-independent manner
AHSG (show AHSG ELISA Kits) is produced in bone, mainly in osteocytes and also show for the first time that its production is modulated by FGF23.
Data suggest that Fgf23 level in serum is up-regulated by three forms of exercise (acute exercise, exhaustive exercise, and chronic exercise); however, only chronic exercise up-regulates FGF23 mRNA and protein expression in skeletal muscle.
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).
fibroblast growth factor 23
, tumor-derived hypophosphatemia inducing factor