biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 110-120 kDa (doublet)
species reactivity
human
technique(s)
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:250 using Trypsin-digested, human and animal tissue sections, western blot: 1:1,000 using whole cell extract of transfected 293T cells expressing recombinant human FGFR-3
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... FGFR3(2261)
General description
Fibroblast Growth Factor Receptor-3 (FGFR 3) is a protein that belongs to Tyr protein kinase family and is expressed in various fetal and adult human and animal tissues. It plays a vital role in inducing apoptosis in chondrogenic ATDC5 cells. It also facilitates cell proliferation and differentiation.
Immunogen
synthetic peptide corresponding to amino acids 792-806 of the cytoplasmic region of human FGFR-3 with N-terminal added lysine.
Application
Anti-Fibroblast Growth Factor Receptor-3, cytoplasmic antibody can be used in immunohistochemistry (diluted 1:250) using Trypsin-digested, human and animal tissue sections for identification of FGFR-3. It can also be used in immunoprecipitation.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
Biochem/physiol Actions
Fibroblast Growth Factor Receptor-3 (FGFR-3) plays a vital role in inducing apoptosis in chondrogenic ATDC5 cells. It also facilitates cell proliferation and differentiation. Mutations in the FGFR-3 gene leads to Wolf-Hirshhorn syndrome (growth failure, mental retardation, cardiac and bone malformations) and achondroplasia.
The antibody reacts specifically with FGFR-3 in lysates of transfected cells. No reaction with FGFR-1 and FGFR-2 is detected.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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存储类别
10 - Combustible liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
常规特殊物品
低风险生物材料
此项目有
Multiple congenital malformations of Wolf-Hirschhorn syndrome are recapitulated in Fgfrl1 null mice
Catela C, et al.
Disease models & mechanisms, 2(5-6), 283-294 (2009)
Zhihui Huang et al.
Current protocols in neuroscience, 87(1), e65-e65 (2019-03-13)
Interneurons in the olfactory bulb are generated from neuronal precursor cells migrating from the anterior subventricular zone (SVZa) throughout the embryonic and postnatal life of mammals. This article describes basic methods for in vivo electroporation to label SVZa cells of
Wolfgang Jäger et al.
Oncotarget, 6(25), 21522-21532 (2015-06-05)
Optimal animal models of muscle invasive bladder cancer (MIBC) are necessary to overcome the current lack of novel targeted therapies for this malignancy. Here we report on the establishment and characterization of patient-derived primary xenografts (PDX). Patient tumors were grafted
Yongjun Yin et al.
Disease models & mechanisms, 9(5), 563-571 (2016-04-09)
Activating mutations in fibroblast growth factor receptor 3 (FGFR3) have been identified in multiple types of human cancer and in congenital birth defects. In human lung cancer, fibroblast growth factor 9 (FGF9), a high-affinity ligand for FGFR3, is overexpressed in
Davide Komla-Ebri et al.
The Journal of clinical investigation, 126(5), 1871-1884 (2016-04-12)
Achondroplasia (ACH) is the most frequent form of dwarfism and is caused by gain-of-function mutations in the fibroblast growth factor receptor 3-encoding (FGFR3-encoding) gene. Although potential therapeutic strategies for ACH, which aim to reduce excessive FGFR3 activation, have emerged over
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