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Human Polyclonal FGFR3 Primary Antibody für IHC (p), ELISA - ABIN544003
Lievens, Liboi et al.: The thanatophoric dysplasia type II mutation hampers complete maturation of fibroblast growth factor receptor 3 (FGFR3), which activates signal transducer and activator of transcription 1 (STAT1) ... in The Journal of biological chemistry 2003
Show all 3 Pubmed References
Human Monoclonal FGFR3 Primary Antibody für FACS - ABIN4898542
Chandesris, Soulier, Labaume, Crinquette, Repellini, Chemin, Malphettes, Fieschi, Asli, Uzunhan, Fermand, Bories, Arnulf: Detection and follow-up of fibroblast growth factor receptor 3 expression on bone marrow and circulating plasma cells by flow cytometry in patients with t(4;14) multiple myeloma. in British journal of haematology 2007
Show all 2 Pubmed References
Human Polyclonal FGFR3 Primary Antibody für IHC, ELISA - ABIN1533273
Shimizu, Ishikawa, Iwai, Ueki, Sugihara, Onishi, Kuninaka, Miyamoto, Toyama, Ijiri, Mori, Matsuzaki, Yaguchi, Nishio, Kawakami, Ikeda, Saya: Fibroblast growth factor-2 (Fgf2) is an important factor that maintains cellular immaturity and contributes to aggressiveness of osteosarcoma. in Molecular cancer research : MCR 2012
Human Polyclonal FGFR3 Primary Antibody für IHC (p), IP - ABIN153144
Scuto, Krejci, Popplewell, Wu, Wang, Kujawski, Kowolik, Xin, Chen, Wang, Kretzner, Yu, Wilcox, Yen, Forman, Jove: The novel JAK inhibitor AZD1480 blocks STAT3 and FGFR3 signaling, resulting in suppression of human myeloma cell growth and survival. in Leukemia 2011
Human Polyclonal FGFR3 Primary Antibody für IHC (p), IHC - ABIN269673
Wallenberg, Misra, Wasik, Marzano, Björnstedt, Gandin, Fernandes: Selenium induces a multi-targeted cell death process in addition to ROS formation. in Journal of cellular and molecular medicine 2014
Human Monoclonal FGFR3 Primary Antibody für IHC, WB - ABIN2717941
Winge, Nielsen, Jørgensen, Owczarek, Ewen, Nielsen, Juul, Berezin, Rajpert-De Meyts: Biglycan is a novel binding partner of fibroblast growth factor receptor 3c (FGFR3c) in the human testis. in Molecular and cellular endocrinology 2014
Human Monoclonal FGFR3 Primary Antibody für CyTOF, FACS - ABIN4900760
Stewart, Chang, Trudel, Anderson, Richardson, Alsina, Reece, Young, Sable-Hunt, Li, Keats, Van Wier, Ahmann, Price-Troska, Giusti, Bergsagel, Chesi, Fonseca: Diagnostic evaluation of t(4;14) in multiple myeloma and evidence for clonal evolution. in Leukemia 2007
Targeting activating mutations in FGFR3 assay was used for screening tumor DNA from Metastatic Relapse in Advanced Bladder Cancer patients; at least one mutation was detected in 19 of the 60 patients.
Study shows that several disease-linked mutations convert FGFR3 to a stronger client to cdc37, where the determinant underpinning client strength involves an allosteric network through the N-lobe and at the lobe interface.
FGFR3 mutations and elevated expression of ERCC1 in muscle-invasive bladder cancer are potential predictive biomarkers of the response to neoadjuvant chemotherapy.
Authors showed that in chondrocytes from human (ACH, TD) and mouse Fgfr3Y367C/+ cartilage, the constitutively active FGFR3 perturbed PC length and the sorting and trafficking of intraflagellar transport (IFT) 20 to the PC.
Authors found that, mechanistically, FGFR3-AS1 silencing decreased the activation of the PI3K/AKT signaling pathway.
Our results identified FGFR3(high)/Ki67(high) papillary pTa tumors as a subgroup with poor prognosis and encourage histological grading as high grade tumors.
Patients with FGFR3 mutations or FGFR3-TACC3 fusion may constitute potential candidates for a novel FGFR-targeted therapy in the perioperative setting.
Data suggest that FGFR3 with mutation found in SADDAN (but not FGFR3 with mutation found in TDII) affects cytoskeleton organization in chondrocytes by inducing tyrosine hyperphosphorylation of paxillin; binding of FGFR3 to PLCG1 appears to be involved. (PLCG1 = phospholipase C gamma 1; SADDAN = Severe Achondroplasia with Developmental Delay and Acanthosis Nigricans; TDII = Thanatophoric Dysplasia type II)
Here, we present a case with prenatal ultrasonographic findings suggestive of TD, and highlight the patient's postnatal dysmorphic features and typical radiographic findings. The definitive diagnosis of TD type I (TDI) was made postnatally, when molecular genetic analysis revealed the previously described p.R248C mutation in FGFR3. This case is reported due to its relative long life span and the molecular diagnosis.
FGFR3 expression indicated an adverse prognosis for lung adenocarcinoma individuals and promoted metastatic potential of lung adenocarcinoma cells
FGFR1, as well as its downstream regulatory PI3K/AKT kinases, may serve as potential biomarkers for the invasiveness and prognosis of laryngeal cancer.
FGF8 and FGFR3 may therefore play an important role in the onset of deep zone necrosis and pathogenesis in Kashin-Beck disease in adolescent children.
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) 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), FGFR3 (fibroblast growth factor receptor-3), or GHRHR (growth- hormone-releasing-hormone receptor) 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 tumors harbor recurrent chromosomal copy-number changes, including FGFR3 amplification associated with overexpression.
FGFR3-TACC3 is a recurrent resistance mechanism, which can bypass EGFR blockade by all generations of EGFR TKIs in NSCLC.
Mutation in the FGFR3 gene is associated with with Klinefelter syndrome and achondroplasia.
Study explored the transgenic model expressing mouse Fgfr3 containing the achondroplasia (Ach) mutation G380R under the Col2 promoter (Ach). Survival and growth rate of the Ach mice were reduced compared to WT littermates. Axial skeletal defects and abnormalities of the sternebrae and vertebrae were observed in the Ach mice.
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
FGFR3 mutations have very limited urothelial tumorigenicity and that these mutations must collaborate with other genetic events to drive urothelial tumorigenesis.
The findings suggest that the primary role of Fgfr3 and Fgfr4 is to control the orderly formation of elastin fibers. In a normal lung, FGFR3 and FGFR4 restrict the expression of MFAP5, 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 were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH activities.
NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK, SOX9, STAT1, and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chondrocyte models of Achondroplasia.
data suggest that FGF2 levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor expression, an effect that is likely receptor mediated, albeit not by FGFR1, FGFR2, 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)-induced cartilage degeneration. FGFR-3 activation attenuated cartilage degeneration induced by DMM surgery and age.
Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 deletion and treatment with the small molecule HDAC6 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/ERK signaling and upregulation of IHH.
A proliferation-independent and SOX9-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 to regulate skeletal development.
Study revealed spatial and temporal distribution of fgfr3 transcript in chondrocytes of the head cartilages, osteoblasts involved in bone formation, ventricular zone of the brain, undifferentiated mesenchymal cells of the skin, and lens epithelium of the eye.
Leg1 plays a unique role in protecting liver development under different stress conditions by serving as a secreted signaling molecule/modulator.
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 and bFGF 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)