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FGFR3-AS1 expression levels were higher in high grade tumors than those in low grade tumors. FGFR3-AS1 expression levels were higher in invasive tumors than those in non-invasive bladder tumors.
Disease-free survival (DFS (show FST Proteins)) was then calculated according to FGFR3 IHC expression.
The gene FGFR3 is responsible for the production of the FGFR 3 protein that converts cartilage to bone. All people with a single copy of the mutated gene FGFR3 have Achondroplasia.
genetic association studies in pediatric population in Japan: Data suggest that mutations in ACAN (aggrecan (show ACAN Proteins)), FGFR3 (fibroblast growth factor receptor-3), or GHRHR (growth- hormone-releasing-hormone receptor (show GHRHR Proteins)) are associated with idiopathic short stature in the population studied.
HPV-positive vulvar squamous cell carcinoma is characterized by oncogenic FGFR3 mutations that helps classify this subtype as a separate disease. Inhibitors of FGFR3 merit consideration as a therapeutic strategy in this neglected cancer in women
Results show that olfactory neuroblastoma (show ARHGEF16 Proteins) tumors harbor recurrent chromosomal copy-number changes, including FGFR3 amplification associated with overexpression.
FGFR3-TACC3 (show TACC3 Proteins) is a recurrent resistance mechanism, which can bypass EGFR (show EGFR Proteins) blockade by all generations of EGFR (show EGFR Proteins) TKIs in NSCLC.
Mutation in the FGFR3 gene is associated with with Klinefelter syndrome and achondroplasia.
Genetic screening of the family revealed a previously reported heterozygous c.1138 G > A (p.G380R) mutation in the coding exon 8 of FGFR3 gene
FGFR3 mutations have very limited urothelial tumorigenicity and that these mutations must collaborate with other genetic events to drive urothelial tumorigenesis.
Accelerated endochondral ossification could contribute to faster healing in Fgfr3(achondroplasia) mice.
The fractures of Fgfr3(-/-) mice healed faster with accelerated fracture callus mineralization and up-regulated expression of osteoblastogenic genes. The healing of fractures in Fgfr3(-/-) mice was accelerated in the stage of formation of cartilage and endochondral ossification
The findings suggest that the primary role of Fgfr3 and Fgfr4 (show FGFR4 Proteins) is to control the orderly formation of elastin (show ELN Proteins) fibers. In a normal lung, FGFR3 and FGFR4 (show FGFR4 Proteins) restrict the expression of MFAP5 (show MFAP5 Proteins), among other elastogenesis factors.
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 Proteins) were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH (show PTH Proteins) activities.
NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK (show MAPK1 Proteins), SOX9 (show SOX9 Proteins), STAT1 (show STAT1 Proteins), and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chondrocyte models of Achondroplasia.
data suggest that FGF2 (show FGF2 Proteins) levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor (show NR3C1 Proteins) expression, an effect that is likely receptor mediated, albeit not by FGFR1 (show FGFR1 Proteins), FGFR2 (show FGFR2 Proteins), 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.
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 Proteins) and bFGF (show FGF2 Proteins) 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)