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anti-Human FGFR3 Antibodies:
anti-Mouse (Murine) FGFR3 Antibodies:
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Human Monoclonal FGFR3 Primary Antibody for 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 for 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
Hamster Polyclonal FGFR3 Primary Antibody for IHC (p), IHC - ABIN407668
Lim, Yap, Lim, Goh, Ng: Identification of autocrine growth factors secreted by CHO cells for applications in single-cell cloning media. in Journal of proteome research 2013
Human Polyclonal FGFR3 Primary Antibody for 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 for IHC, WB - ABIN2673406
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 for 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
Results provide evidence that FGFR3 mutations in human papillomavirus positive tonsillar and base of tongue cancer is indicative of worse prognosis.
Increased levels of FGFR3 and PIK3CA (show PIK3CA Antibodies) mutated DNA in urine and plasma are indicative of later progression and metastasis in bladder cancer.
FGFR3 expression increased in classical and neural subtypes of glioma and was associated with differentiated cellular functions. FGFR3 showed very limited correlation with other common receptor tyrosine kinases, and predicted improved survival for glioma patients.
REVIEW. FGFR3 is expressed in chondrocytes and mature osteoblasts where it functions to regulate bone growth. Analysis of the mutations in FGFR3 revealed increased signaling through a combination of mechanisms
Elevated FGFR3 and FGFR1 (show FGFR1 Antibodies) protein expression is common in aggressive ependymomas but likely not driven by genetic alterations. Further studies are warranted to evaluate whether ependymoma patients with high FGFR3 and/or FGFR1 (show FGFR1 Antibodies) expression could benefit from treatment with FGFR (show FGFR2 Antibodies) inhibitor based therapeutic approaches currently under evaluation in clinical trials
There was a lower frequency of mutation in FGFR3, a gene associated with low-risk Bladder Cancer, than reported in the The Cancer Genome Atlas database.
A higher expression of FGFR3, phosphorylated AKT (show AKT1 Antibodies), and ZEB1 (show ZEB1 Antibodies) were observed.
FGFR3 mutation status seems promising to guide decision-making on adjuvant anti-FGFR3 therapy as it appeared homogeneous in RC and lymph nodes +. Based on the results of TUR, the deep part of the tumor needs to be assessed if neoadjuvant anti-FGFR3 treatment is considered
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 Antibodies), TWIST1 (show TWIST1 Antibodies), and FGFR3 mutations were identified in children with tracheal cartilaginous sleeve (TCS). All five children with a W290C mutation in FGFR2 (show FGFR2 Antibodies) had TCS, and most previously reported children with W290C had identification of TCS or early death
The findings suggest that the primary role of Fgfr3 and Fgfr4 (show FGFR4 Antibodies) is to control the orderly formation of elastin (show ELN Antibodies) fibers. In a normal lung, FGFR3 and FGFR4 (show FGFR4 Antibodies) restrict the expression of MFAP5 (show MFAP5 Antibodies), 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 Antibodies) were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH (show PTH Antibodies) activities.
NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK (show MAPK1 Antibodies), SOX9 (show SOX9 Antibodies), STAT1 (show STAT1 Antibodies), and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chondrocyte models of Achondroplasia.
data suggest that FGF2 (show FGF2 Antibodies) levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor (show NR3C1 Antibodies) expression, an effect that is likely receptor mediated, albeit not by FGFR1 (show FGFR1 Antibodies), FGFR2 (show FGFR2 Antibodies), 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 Antibodies))-induced cartilage degeneration. FGFR-3 activation attenuated cartilage degeneration induced by DMM (show COL2A1 Antibodies) surgery and age.
Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 (show HDAC6 Antibodies) deletion and treatment with the small molecule HDAC6 (show HDAC6 Antibodies) 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.
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 Antibodies) and bFGF (show FGF2 Antibodies) 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)