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 and application
anti-Human FGF23 Antibodies:
anti-Rat (Rattus) FGF23 Antibodies:
anti-Mouse (Murine) FGF23 Antibodies:
Go to our pre-filtered search.
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
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
Human Polyclonal FGF23 Primary Antibody for ELISA, WB - ABIN547827
Saito, Kusano, Kinosaki, Ito, Hirata, Segawa, Miyamoto, Fukushima: Human fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and 1alpha,25-dihydroxyvitamin D3 production. in The Journal of biological chemistry 2003
Mouse (Murine) Polyclonal FGF23 Primary Antibody for WB - ABIN3044523
Ji, Ling, Zhang, Chou, Yang, Wang, Yin, Wu, Yu: MicroRNA-296 mediated corneal neovascularization in an animal model of corneal burns after alkali exposures. in Experimental and therapeutic medicine 2018
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
FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1)modulates cation levels in trpm7 mutants and in the wild type; levels of cations are restored to normal in trpm7 mutants when stc1 activity is blocked.
This study revealed a dysequilibrium of the PTH-FGF23-vitamin D axis in RRMS, with lower plasma PTH, higher plasma iFGF23 and a lower serum 1,25(OH)2D to 25OHD ratio in RRMS compared with healthy control subjects.
cFGF23 measurement may serve as a novel biomarker for incident acute kidney injury and death among critically ill patients
Levels of circulating FGF-23 but not sclerostin were related to Aortic Arch Calcification (AoAC) severity. Serum FGF-23 levels were independently associated with AoAC.
Our findings demonstrate that severely polycystic livers produce FGF23 and increase levels of circulating FGF23 in patients with autosomal polycystic kidney disease.
Increases in plasma erythropoietin and erythropoietin receptor activation are mechanisms implicated in the increase of plasma FGF23 in acute kidney injury.
The FGF23 increase related to acute kidney injury, especially in more severe stages and in patients without diuresis, is an independent risk factor for mortality.
In patients with Autosomal Dominant Polycystic Kidney Disease, as the disease stage advanced, serum FGF-23 levels increased while s-KL decreased. In ADPKD patients, the effect of serum FGF-23 on the development of AS and atherosclerosis in peripheral vessels is independent of s-KL.
In summary, our results suggest that FGF23 gene polymorphisms are associated with the risk of developing EH in Chinese Han population.
Although there are many studies suggesting the correlation between FGF23 and Insulin resistance (IR) in different populations, this study did not find any statistically significant relationship between IR and FGF23 levels in metabolic syndrome.
Data suggest that intact FGF23 level in plasma is independent predictor of cardiovascular death in patients with heart failure and provides added value to standard of care, natriuretic peptide (NT-proBNP) plasma level, for risk estimation. This study was conducted in Belgium. (FGF23 = fibroblast growth factor 23; NT-proBNP = aminoterminal pro-B-type natriuretic peptide)
In patients with heart failure, higher plasma FGF23 levels were associated with volume overload and increased risk of all-cause mortality and hospitalization.
serum level of FGF-23 was not correlated with a change in bone mineral density of maintenance hemodialysis patients, whereas the serum Klotho protein level was associated with the degree of bone mineral density
Increased insulin resistance in chronic kidney disease is a consequence of the uremic status and is intimately associated with disturbed phosphate metabolism and FGF23.
Increased serum levels of FGF23 were associated with loss of graft function in kidney transplant recipients.
Responses of FGF23 to salt intervention were more prominent in normotensive, older than 60 years, BMI <24 kg/m(2) and salt-resistant individuals. Furthermore, a significant inverse correlation was observed between 24-hour urinary sodium and serum concentrations of FGF23 after adjusting age, sex, BMI and hypertension status.
FGF23 is reduced in subjects with nephrotic syndrome compared to healthy controls. Reduced levels of Vitamin D, and urinary losses may contribute to lower levels of FGF23 in NS.
Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR and serum phosphate concentration, without significant changes in PTH.
Carboxy-terminal fragment of FGF-23 induces heart hypertrophy in sickle cell disease.
prolonged exposure to high apical calcium and calcium hyperabsorption were sensed by CaSR, which, in turn, increased FGF-23 expression to suppress calcium transport
In a Canadian Asian population with CKD, FGF23 levels obtained at 6-monthly intervals for 3 years predicted ESRD and mortality suggesting that it is also a risk marker in Asians
Although previous studies showed that increased circulating FGF23 and phosphate levels are associated with LVH, our results demonstrated that in XLH, high circulating levels of FGF23 in the setting of hypophosphatemia do not induce cardiac hypertrophy.
our data highlight a role of FGF23/FGFR4 signaling in the regulation of cardiac remodeling and function, and indicate that pharmacological interference with cardiac FGF23/FGFR4 signaling might protect from CKD- and age-related LVH.
the main physiological function of Klotho for mineral homeostasis in vivo is its role as co-receptor mediating Fgf23 action.
our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages
these results indicate that Nf1 deficiency in osteocytes dramatically increases FGF23 production and causes a mineralization defect (ie, hyperosteoidosis) via the alteration of calcium-phosphorus metabolism.
FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by myocardial infarction or ischemia/reperfusion , which is associated with the upregulation of active beta-catenin and TGF-beta
deleting FGF23 within early osteoblasts and osteocytes demonstrated that both cell types contribute to baseline circulating FGF23 concentrations, and that targeting osteoblasts/osteocytes for FGF23 production can modify systemic responses to changes in serum phosphate concentrations and rescue the Hyp genetic syndrome
Thus, monotherapy with 1,25D improves growth, skeletal microarchitecture, and bone strength in the absence of phosphate supplementation despite enhancing FGF23 expression, demonstrating that 1,25D has direct beneficial effects on the skeleton in XLH, independent of its role in phosphate homeostasis
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4
Zinc13407541 also inhibited FGF-23 signaling in isolated renal tubules ex vivo and partially reversed the hypophosphatemic effects of excess FGF-23 in a mouse model. These chemical probes provide a platform to develop lead compounds to treat disorders caused by excess FGF-23.
FGF23 may be an important modulator of PTH signaling in bone and kidney.
EPO dependent regulation pathway of FGF23 gene expression
can directly stimulate hepatic secretion of inflammatory cytokines
Klotho in bone is crucial for inducing FGF23 production upon renal failure
dietary iron content and chronic kidney disease affected FGF23 production and metabolism
Dmp1 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 deficiency upregulates FGF23 plasma levels, an effect paralleled by increased corticosterone plasma levels, as well as decreased 1,25(OH)2 D3 and PTH plasma levels.
FGF23 regulates osteopontin secretion indirectly by suppressing alkaline phosphatase transcription and phosphate production in osteoblastic cells, acting through FGF receptor-3 in a Klotho-independent manner
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