FGFR3 Antibody (YA3887)(PBS only)
(Synonyms: ACH; CEK2; JTK4; CD333; HSFGFR3EX)FGFR3 Antibody (YA3887) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGFR3.
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Host:
Mouse
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Isotype:
IgG
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Application:
IHC-P, FC, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:200-1:1000 | 1:200-1:400 | 1:10000 |
Product Details
FGFR3 Antibody (YA3887) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGFR3.
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Host Mouse
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 88 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 88 kDa
Purified recombinant fragment of human FGFR3 (AA: 529-694) expressed in E. Coli.
affinity purified.
Non-conjugated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
FGFR3 encodes a receptor tyrosine kinase that acts as a negative regulator of endochondral bone growth by limiting chondrocyte proliferation, hypertrophic differentiation, and osteogenesis in growth plate cartilage[1][2]. Mechanistically, activated FGFR3 signaling inhibits bone growth through MAPK-dependent suppression of chondrocyte differentiation and STAT1-associated suppression of chondrocyte proliferation[3]. In skeletal disease models, activating FGFR3 mutations explain achondroplasia as gain-of-function lesions that intensify this inhibitory growth-control program[1]. In cancer, activating FGFR3 mutations occur in bladder and cervix carcinomas, and FGFR3-TACC3 fusions show oncogenic activity in glioblastoma models[4][5]. Compared with related isoforms, alternative splicing of the FGFR3 IgIII domain generates IIIb/IIIc variants with distinct ligand-binding properties, and FGFR3 IIIb binds only acidic FGF in the reported binding assays[6]. For experimental and translational applications, erdafitinib, an FGFR1-4 tyrosine kinase inhibitor, produced clinical activity in advanced urothelial carcinoma with susceptible FGFR2/3 alterations and later improved overall survival versus chemotherapy after anti-PD-1/PD-L1 treatment[7][8].
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Subcellular Localization
Cell membrane; Single-pass type I membrane protein; Cytoplasmic vesicle; Endoplasmic reticulum; Cell membrane; Single-pass type I membrane protein; Secreted; Cell membrane; Single-pass type I membrane protein
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Expression
Tissue_specificity:Expressed in brain, kidney and testis. Very low or no expression in spleen, heart, and muscle. -
Isoforms & Post-Translational Modification
P22607 has 4 isomers: P22607-1: 87710 Da (predicted); P22607-2: 88157 Da (predicted); P22607-3: 75696 Da (predicted); P22607-4: 85083 Da (predicted).
Autophosphorylated. Binding of FGF family members together with heparan sulfate proteoglycan or heparin promotes receptor dimerization and autophosphorylation on tyrosine residues. Autophosphorylation occurs in trans between the two FGFR molecules present in the dimer. Phosphorylation at Tyr-724 is essential for stimulation of cell proliferation and activation of PIK3R1, STAT1 and MAP kinase signaling. Phosphorylation at Tyr-760 is required for interaction with PIK3R1 and PLCG1;Ubiquitinated. Is rapidly ubiquitinated after ligand binding and autophosphorylation, leading to receptor internalization and degradation. Subject to both proteasomal and lysosomal degradation;N-glycosylated in the endoplasmic reticulum. The N-glycan chains undergo further maturation to an Endo H-resistant form in the Golgi apparatus -
Subunit
Monomer. Homodimer after ligand binding. Interacts with FGF1, FGF2, FGF4, FGF6; FGF8, FGF9, FGF10, FGF17, FGF18, FGF19, FGF20 and FGF23 (in vitro). Interacts with KLB. Affinity for fibroblast growth factors (FGFs) is increased by heparan sulfate glycosaminoglycans that function as coreceptors. Likewise, KLB increases the affinity for FGF19 and FGF21. Interacts with PIK3R1, PLCG1, SOCS1 and SOCS3. Isoform 3 forms disulfide-linked dimers
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SwissProt ID
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Synonyms
ACH; CEK2; JTK4; CD333; HSFGFR3EX
Documentation
References
[2]. Wang Q, Green RP, Zhao G, Ornitz DM. Differential regulation of endochondral bone growth and joint development by FGFR1 and FGFR3 tyrosine kinase domains. Development. 2001 Oct;128(19):3867-76. [Content Brief]
[3]. Murakami S, et al. Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype. Genes Dev. 2004 Feb 1;18(3):290-305. [Content Brief]
[4]. Cappellen D, et al. Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas. Nat Genet. 1999 Sep;23(1):18-20. [Content Brief]
[5]. Singh D, et al. Transforming fusions of FGFR and TACC genes in human glioblastoma. Science. 2012 Sep 7;337(6099):1231-5. [Content Brief]
[6]. Chellaiah AT, et al. Fibroblast growth factor receptor (FGFR) 3. Alternative splicing in immunoglobulin-like domain III creates a receptor highly specific for acidic FGF/FGF-1. J Biol Chem. 1994 Apr 15;269(15):11620-7. [Content Brief]
[7]. Loriot Y, et al. Erdafitinib in Locally Advanced or Metastatic Urothelial Carcinoma. N Engl J Med. 2019 Jul 25;381(4):338-348. [Content Brief]
[8]. Loriot Y, et al. Erdafitinib or Chemotherapy in Advanced or Metastatic Urothelial Carcinoma. N Engl J Med. 2023 Nov 23;389(21):1961-1971. [Content Brief]
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