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anti-Human FGFR3 Antikörper:
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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 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 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
Human Monoclonal FGFR3 Primary Antibody für 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 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
A higher expression of FGFR3, phosphorylated AKT (zeige AKT1 Antikörper), and ZEB1 (zeige ZEB1 Antikörper) 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 (zeige FGFR2 Antikörper), TWIST1 (zeige TWIST1 Antikörper), and FGFR3 mutations were identified in children with tracheal cartilaginous sleeve (TCS). All five children with a W290C mutation in FGFR2 (zeige FGFR2 Antikörper) had TCS, and most previously reported children with W290C had identification of TCS or early death
The Gly380Arg and Asn540Lys are hot spot mutations of the FGFR3 gene among patients with ACH/HCH (zeige DOCK2 Antikörper).
the FGFR3 gene is an infrequent target in the pathogenesis of Han Chinese urothelial cell carcinoma
Our results extend the genetic mutation spectrum of FGFR3.
Study found FGFR3 gene mutation plus GRB10 (zeige GRB10 Antikörper) gene duplication in a patient with achondroplasia plus growth delay with prenatal onset
Our family confirms the consistent and unique phenotype of this condition, and the specificity of the mutation in FGFR3.
no insertions or deletions in FGFR3 have been reported to cause thanatophoric dysplasia types 1 or 2; therefore, this represents the first report to describe such a mutation.
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.
Conditional Fgfr3 deletion in mice aggravated destabilization of medial meniscus (DMM (zeige COL2A1 Antikörper))-induced cartilage degeneration. FGFR-3 activation attenuated cartilage degeneration induced by DMM (zeige COL2A1 Antikörper) surgery and age.
Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 (zeige HDAC6 Antikörper) deletion and treatment with the small molecule HDAC6 (zeige HDAC6 Antikörper) 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 (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)