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Key Documents

F3922

Sigma-Aldrich

Anti-Fibroblast Growth Factor Receptor-3, Extracellular 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

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~120 kDa

species reactivity

human

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:1,000 using protease-digested, human and animal tissue sections
western blot: 1:500 using extract of FGFR-3 transfected cells

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... FGFR3(2261)

General description

FGFR3 (fibroblast growth factor receptor 3) is widely expressed in many fetal and adult human and animal tissues. It belongs to the fibroblast growth factor receptor (Fgfr) family of proteins. It has 19 exons, an extracellular ligand binding domain, a transmembrane domain and an intracellular tyrosine kinase domain. It is located on human chromosome 4p16.3.

Immunogen

synthetic peptide corresponding to amino acids 359-372 of the extracellular region of human fibroblast growth factor receptor-3.

Application

Anti-Fibroblast Growth Factor Receptor-3, Extracellular antibody produced in rabbit has been used in:
  • immunoblotting
  • immunohistochemistry
  • immunoprecipitation

Biochem/physiol Actions

Fibroblast growth factors (FGFs) are substantially involved in normal development, wound healing and repair, angiogenesis, a variety of neurotrophic activities, and in hematopoiesis as well as in tissue remodeling and maintenance. They have also been implicated in pathological conditions such as tumorigenesis and metastasis. Deletions of chromosome 4p encompassing the FGFR3 (fibroblast growth factor receptor 3) gene cause the Wolf-Hirschhorn syndrome (growth failure, mental retardation, cardiac and bone malformations). Achondroplasia is an inherited disorder in which growth abnormality of bone or cartilage lead to skeletal maldevelopment and dwarfism. It is associated with recurrent mutations of a single amino acid in the transmembrane domain of the FGFR-3 protein.

Physical form

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

Preparation Note

Affinity isolated on a peptide-agarose column.

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 Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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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F R Lamont et al.
British journal of cancer, 104(1), 75-82 (2010-12-02)
Activating mutations of FGFR3 are frequently identified in superficial urothelial carcinoma (UC) and increased expression of FGFR1 and FGFR3 are common in both superficial and invasive UC. The effects of inhibition of receptor activity by three small molecule inhibitors (PD173074
Small molecule FGF receptor inhibitors block FGFR-dependent urothelial carcinoma growth in vitro and in vivo
Lamont FR, et al.
British Journal of Cancer, 104(1), 75-82 (2010)
Fibroblast growth factors: biology, function, and application for tissue regeneration
Yun YR, et al.
Journal of Tissue Engineering, 1(1), 218142-218142 (2010)
Exploring the developmental mechanisms underlying Wolf-Hirschhorn Syndrome: Evidence for defects in neural crest cell migration
Rutherford EL and Lowery LA
Developmental Biology, 420(1), 1-10 (2016)
Loss of heterozygosity at 4p16. 3 and mutation of FGFR3 in transitional cell carcinoma
Sibley K, et al.
Oncogene, 20(6), 686-686 (2001)

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