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F0425

Sigma-Aldrich

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

affinity isolated antibody, buffered aqueous solution

Sinônimo(s):

Anti-FGFR-3

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About This Item

Número MDL:
MFCD02096346
Código UNSPSC:
51111800
NACRES:
NA.41

fonte biológica

rabbit

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

forma

buffered aqueous solution

peso molecular

antigen 110-120 kDa (doublet)

reatividade de espécies

human

técnica(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

nº de adesão UniProt

P22607

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... FGFR3(2261)

Descrição geral

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.

Especificidade

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

Imunogênio

synthetic peptide corresponding to amino acids 792-806 of the cytoplasmic region of human FGFR-3 with N-terminal added lysine.

Aplicação

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)

Ações bioquímicas/fisiológicas

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.

forma física

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 15 mM sodium azide.

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 2

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

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

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “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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