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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
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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
Hamster Polyclonal FGFR3 Primary Antibody für 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 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
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 (zeige ARHGEF16 Antikörper) tumors harbor recurrent chromosomal copy-number changes, including FGFR3 amplification associated with overexpression.
FGFR3-TACC3 (zeige TACC3 Antikörper) is a recurrent resistance mechanism, which can bypass EGFR (zeige EGFR Antikörper) blockade by all generations of EGFR (zeige EGFR Antikörper) 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.
Long-term dovitinib administration was not feasible due to frequent toxicity. Absent clinical activity suggests that patient selection by pFGFR3 IHC alone does not enrich for response to FGFR3 kinase inhibitors in urothelial carcinoma.
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 (zeige PIK3CA Antikörper) 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.
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 (zeige FGFR4 Antikörper) is to control the orderly formation of elastin (zeige ELN Antikörper) fibers. In a normal lung, FGFR3 and FGFR4 (zeige FGFR4 Antikörper) restrict the expression of MFAP5 (zeige MFAP5 Antikörper), 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 (zeige PTH Antikörper) were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH (zeige PTH Antikörper) activities.
NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK (zeige MAPK1 Antikörper), SOX9 (zeige SOX9 Antikörper), STAT1 (zeige STAT1 Antikörper), and PLCgamma, in the growth plates of Fgfr3Y367C/+ mice and in cultured chondrocyte models of Achondroplasia.
data suggest that FGF2 (zeige FGF2 Antikörper) levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor (zeige NR3C1 Antikörper) expression, an effect that is likely receptor mediated, albeit not by FGFR1 (zeige FGFR1 Antikörper), FGFR2 (zeige FGFR2 Antikörper), 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 (zeige VEGFA Antikörper) and bFGF (zeige FGF2 Antikörper) 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)