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anti-Human FGF23 Antibodies:
anti-Rat (Rattus) FGF23 Antibodies:
anti-Mouse (Murine) FGF23 Antibodies:
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Human Polyclonal FGF23 Primary Antibody for IP, ELISA - ABIN188699
Orfanidou, Malizos, Varitimidis, Tsezou et al.: 1,25-Dihydroxyvitamin D(3) and extracellular inorganic phosphate activate mitogen-activated protein kinase pathway through fibroblast growth factor 23 contributing to hypertrophy and mineralization ... in Experimental biology and medicine (Maywood, N.J.) 2012
Show all 2 Pubmed References
Mouse (Murine) Polyclonal FGF23 Primary Antibody for ELISA, WB - ABIN4311599
Mirza, Alsiö, Hammarstedt, Erben, Michaëlsson, Tivesten, Marsell, Orwoll, Karlsson, Ljunggren, Mellström, Lind, Ohlsson, Larsson: Circulating fibroblast growth factor-23 is associated with fat mass and dyslipidemia in two independent cohorts of elderly individuals. in Arteriosclerosis, thrombosis, and vascular biology 2010
Human Polyclonal FGF23 Primary Antibody for IF (p), IHC (p) - ABIN714461
Andersen, Huntley, Sandberg, Heublein, Burnett: Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2016
Human Polyclonal FGF23 Primary Antibody for IF, ELISA - ABIN1534408
Sun, Zou, Yang, Morita, Gong, Shiba, Akagawa, Yuan: Inorganic polyphosphates stimulate FGF23 expression through the FGFR pathway. in Biochemical and biophysical research communications 2012
FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1 (show STC1 Antibodies))modulates cation levels in trpm7 (show TRPM7 Antibodies) mutants and in the wild type; levels of cations are restored to normal in trpm7 (show TRPM7 Antibodies) mutants when stc1 (show STC1 Antibodies) activity is blocked.
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 Antibodies) levels in KTR are normal and influenced more by bone turnover than by eGFR (show EGFR Antibodies). Its involvement with other hormones of mineral homeostasis (FGF23/Klotho (show KL Antibodies) 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 Antibodies), resulting in increased usages of iron supplementation in HD patients
There might be a strong correlation between FGF-23 and ghrelin (show GHRL Antibodies) 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 Antibodies) protein. And that it is this full-length alpha-Klotho (show KL Antibodies) 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.
Enhanced myocardial expression of FGF23 is associated with left ventricular hypertrophy in chronic kidney disease.
Klotho (show KL Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies) plasma levels.
FGF23 regulates osteopontin (show SPP1 Antibodies) secretion indirectly by suppressing alkaline phosphatase transcription and phosphate production in osteoblastic cells, acting through FGF receptor-3 (show FGFR3 Antibodies) in a Klotho (show KL Antibodies)-independent manner
AHSG (show AHSG Antibodies) 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.
Data suggest that signal transduction via Fgf23/Fgfr1 (show FGFR1 Antibodies) and calcitriol/calcitriol receptor have opposite roles in innate immunity; Fgf23 suppresses arginase-1 (show ARG1 Antibodies) expression in macrophages; calcitriol stimulates arginase-1 (show ARG1 Antibodies) expression in macrophages.
results link CYP24 (show CYP24A1 Antibodies) activity to the pathophysiology of FGF23-dependent renal phosphate wasting states and implicate pharmacologic CYP24 (show CYP24A1 Antibodies) inhibition as a therapeutic adjunct for their treatment.
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