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Human FGFR3 ELISA Kit for Sandwich ELISA - ABIN417740
Siegel, Kluba, Hermanutz-Klein, Bieback, Northoff, Schäfer: Phenotype, donor age and gender affect function of human bone marrow-derived mesenchymal stromal cells. in BMC medicine 2013
Show all 2 Pubmed References
All Species FGFR3 ELISA Kit for Competition ELISA - ABIN1118060
Xiao, Li, Zhang, Hou, Lin, Gao, Luo: Combined administration of D-galactose and aluminium induces Alzheimer-like lesions in brain. in Neuroscience bulletin 2011
We present the first actionable mutation spectrum in Indian lung cancer genome. These findings implicate FGFR3 as a novel therapeutic in lung adenocarcinoma.
FGFR2 (show FGFR2 ELISA Kits), TWIST1 (show TWIST1 ELISA Kits), and FGFR3 mutations were identified in children with tracheal cartilaginous sleeve (TCS). All five children with a W290C mutation in FGFR2 (show FGFR2 ELISA Kits) had TCS, and most previously reported children with W290C had identification of TCS or early death
The Gly380Arg and Asn540Lys are hot spot mutations of the FGFR3 gene among patients with ACH/HCH (show DOCK2 ELISA Kits).
the FGFR3 gene is an infrequent target in the pathogenesis of Han Chinese urothelial cell carcinoma
Our results extend the genetic mutation spectrum of FGFR3.
Study found FGFR3 gene mutation plus GRB10 (show GRB10 ELISA Kits) gene duplication in a patient with achondroplasia plus growth delay with prenatal onset
Our family confirms the consistent and unique phenotype of this condition, and the specificity of the mutation in FGFR3.
no insertions or deletions in FGFR3 have been reported to cause thanatophoric dysplasia types 1 or 2; therefore, this represents the first report to describe such a mutation.
results suggest that FGFR3 kinase activity may regulate the papillomavirus reproductive program through phosphorylation of the E2 protein (show UBE2B ELISA Kits) although this is unlikely to occur through the Y102 residue of HPV E2.
Our data also reinforce the notion that molecular testing of FGFR3 must be included in the diagnostic approach of coronal craniosynostosis. This will allow accurate genetic counseling and optimal management of MS, which might otherwise go undiagnosed because of mild manifestations and wide variability of expression
This study for the first time genetically shows the direct positive regulation of FGFR3 on osteoclastic bone resorption.
the localization of FGF9 and its receptors at different embryonic and postnatal stages in mice testes, was examined.
Bone anabolic effects of PTH (show PTH ELISA Kits) were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH (show PTH ELISA Kits) activities.
NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK (show MAPK1 ELISA Kits), SOX9 (show SOX9 ELISA Kits), STAT1 (show STAT1 ELISA Kits), and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chondrocyte models of Achondroplasia.
data suggest that FGF2 (show FGF2 ELISA Kits) levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor (show NR3C1 ELISA Kits) expression, an effect that is likely receptor mediated, albeit not by FGFR1 (show FGFR1 ELISA Kits), FGFR2 (show FGFR2 ELISA Kits), and FGFR3.
we show that low dose of NVP-BGJ398 improves in vivo condyle growth and corrects dysmorphologies in Fgfr3(Y367C/+) mice, suggesting that postnatal treatment with NVP-BGJ398 mice might offer a new therapeutic strategy to improve mandible anomalies in achondroplasia (ACH), and others FGFR3-related disorders.
Conditional Fgfr3 deletion in mice aggravated destabilization of medial meniscus (DMM (show COL2A1 ELISA Kits))-induced cartilage degeneration. FGFR-3 activation attenuated cartilage degeneration induced by DMM (show COL2A1 ELISA Kits) surgery and age.
Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 (show HDAC6 ELISA Kits) deletion and treatment with the small molecule HDAC6 (show HDAC6 ELISA Kits) inhibitor tubacin reduced FGFR3 accumulation in the growth plate and improved endochondral bone growth
This study reveals that chondrocyte FGFR3 is involved in the regulation of bone formation and bone remodeling by a paracrine mechanism.
Results show that Fgfr3-deficient mice exhibit progressive osteoarthritis-like defects in temporomandibular Joint (TMJ) changes, indicating that FGFR3 signaling is critically involved in the maintenance of the structure integrity and function of TMJ articular cartilage during adult stage.
The ectodomain of FGFR3 is proteolytically cleaved in response to ligand-induced receptor activation by FGF1, but unlike most regulated intramembrane proteolysis target proteins, it requires endocytosis and does not involve a metalloproteinase.
Alterations in the expression of VEGF-A (show VEGFA ELISA Kits) and bFGF (show FGF2 ELISA Kits) systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
chondrodysplastic dwarfism in Japanese brown cattle is not caused by mutation in the FGFR3 gene
This gene encodes a member of the fibroblast growth factor receptor (FGFR) family, with its amino acid sequence being highly conserved between members and among divergent species. FGFR family members differ from one another in their ligand affinities and tissue distribution. A full-length representative protein would consist of an extracellular region, composed of three immunoglobulin-like domains, a single hydrophobic membrane-spanning segment and a cytoplasmic tyrosine kinase domain. The extracellular portion of the protein interacts with fibroblast growth factors, setting in motion a cascade of downstream signals, ultimately influencing mitogenesis and differentiation. This particular family member binds acidic and basic fibroblast growth hormone and plays a role in bone development and maintenance. Mutations in this gene lead to craniosynostosis and multiple types of skeletal dysplasia. Three alternatively spliced transcript variants that encode different protein isoforms have been described.
fibroblast growth factor receptor 3
, fibroblast growth factor receptor 3 variant 4
, hydroxyaryl-protein kinase
, tyrosine kinase JTK4
, heparin-binding growth factor receptor
, fibroblast growth factor receptor 3-IIIc
, tyrosine kinase (cek2)
, tyrosine kinase receptor CEK2
, fibroblast growth factor receptor 3 (achondroplasia, thanatophoric dwarfism)