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Key Documents

F0425

Sigma-Aldrich

Anti-Fibroblast Growth Factor Receptor-3, Cytoplasmic antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-FGFR-3

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About This Item

MDL number:
UNSPSC Code:
51111800
NACRES:
NA.41

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

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.

Specificity

The antibody reacts specifically with FGFR-3 in lysates of transfected cells. No reaction with FGFR-1 and FGFR-2 is detected.

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)

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.

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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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)
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
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
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
Daisuke Harada et al.
Bone, 41(2), 273-281 (2007-06-15)
The most frequent type of rhizomelic dwarfism, achondroplasia (ACH), is caused by mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. Mutations in FGFR3 result in skeletal dysplasias of variable severity, including mild phenotypic effects in hypochondroplasia (HCH), severe

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