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Mouse (Murine) FGFR3 Protein expressed in Human Cells - ABIN2007272
Lamy, Gobet, Laurent, Blanchard, Varin, Moulin, Andreou, Frebourg, Pfister: Molecular profiling of bladder tumors based on the detection of FGFR3 and TP53 mutations. in The Journal of urology 2006
Our findings show that grade heterogeneity in urothelial carcinoma is characterized by increased MIB-1 labelling, and particularly in the FGFR3 mutant pathway, with homozygous deletions of CDKN2A in low- and high-grade areas
We argue that routine use of molecular genomic tumour analysis in urothelial carcinoma may inform selection of patients for appropriate trials and we further investigate the potential of FGFR3 as a meaningful clinical target for this difficult disease
In conclusion, we identified four novel loci (TGFA (show TGFA Proteins), PIK3R1, FGFR3 and TREH (show TREH Proteins)) and confirmed two loci known to be associated with cartilage thickness.The identified associations were not caused by rare exonic variants. This is the first report linking TGFA (show TGFA Proteins) to human Osteoarthritis, which may serve as a new target for future therapies.
Case Report: FGFR3 epidermal naevus syndrome with urothelial mosaicism for activating p.Ser249Cys FGFR3 mutation.
FGFR (show FGFR2 Proteins) alterations are not frequent in low-grade gliomas, they are more common in hemispheric low-grade gliomas and are important since targeted therapies exist for FGFR (show FGFR2 Proteins) receptors.
FGFR3 gene mutations are associated with Urinary Bladder Cancer.
we identified a novel FGFR3 mutation, p.Ser348Cys, in a patient with achondroplasia. A number of different FGFR3 mutations can cause achondroplasia; therefore, if the common p.Gly380Arg mutation is not found, complete analysis of FGFR3 is indicated in patients with achondroplasia
FGFR3 promotes angiogenesis-dependent metastasis of hepatocellular carcinoma via facilitating MCP-1 (show CCL2 Proteins)-mediated vascular formation.
The expression of FGFR3-AS1 (show PTGDR Proteins) and FGFR3 is positively correlated in osteosarcoma tissues
Combined urinary FGFR3/Cyclin D3 (show CCND3 Proteins) expression shows improved detection rates for bladder cancer recurrence with high specificity and sensitivity.
Conditional Fgfr3 deletion in mice aggravated destabilization of medial meniscus (DMM (show COL2A1 Proteins))-induced cartilage degeneration. FGFR-3 activation attenuated cartilage degeneration induced by DMM (show COL2A1 Proteins) surgery and age.
Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 (show HDAC6 Proteins) deletion and treatment with the small molecule HDAC6 (show HDAC6 Proteins) 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.
loss of Fgfr3 function leads to the formation of chondroma-like lesions via downregulation of MEK (show MDK Proteins)/ERK (show EPHB2 Proteins) signaling and upregulation of IHH (show IHH Proteins).
A proliferation-independent and SOX9 (show SOX9 Proteins)-dependent differentiation block is a key driving mechanism responsible for poor endochondral bone growth in achondroplasia disorders caused by mutations in FGFR3.
This study showed constitutively active form of Fgfr3 to increase FGF signaling.
FGFR3 induces degradation of Bmpr1a (show BMPR1A Proteins) to regulate skeletal development.
microtubule formation is a major downstream effector of Fgf-receptor 3 and this pathway impacts the formation of fluid spaces in the organ of Corti.
FGFR3 plays a pivotal role in the specific uptake of BoNT/A across the cell membrane being part of a larger receptor complex involving ganglioside- and protein-protein interactions.
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)