FGFR4 Antibody (YA3886)
(Synonyms: FGFR4; TKF; JTK2)FGFR4 Antibody (YA3886) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGFR4.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, FC, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS with 0.05% sodium azide
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:400 | 1:10000 |
Product Details
FGFR4 Antibody (YA3886) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGFR4.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 88 kDaNote: 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 CD334 (AA: extra 22-369) expressed in E. Coli.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% sodium azide
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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
FGFR4 is a receptor tyrosine kinase within the FGFR1-4 family, and normal adult tissues show differential FGFR expression patterns that support receptor-specific functional diversity[1]. Mechanistically, βKlotho (KLB) combines with selected FGFR isoforms to determine endocrine FGF19/FGF21 metabolic activity, while FGF19 requires KLB for FGFR4 binding, intracellular signaling, and downstream gene modulation[2][3]. In hepatocyte models, bile acid-activated FXR induces FGF19, and the hepatic FGF19-FGFR4-ERK1/2 pathway inhibits CYP7A1 expression, linking FGFR4 to bile acid synthesis control[4]. In mouse models, FGFR4 activation mediates FGF19-induced hepatocyte proliferation and suppression of bile acid biosynthesis, but it is not essential for FGF19 effects on glucose and lipid metabolism[5]. Compared with related isoforms, FGF19 shows unique specificity for FGFR4, and this ligand-receptor selectivity distinguishes FGFR4-centered signaling from broader FGFR1-3 biology[6]. For experimental applications, fisogatinib/BLU-554 and BLU9931 provide selective FGFR4 inhibition tools for studying FGF19-driven hepatocellular carcinoma models and activated FGFR4 signaling[7][8].
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Subcellular Localization
Cell membrane; Single-pass type I membrane protein; Endosome; Endoplasmic reticulum; Secreted
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Expression
Tissue_specificity:It is expressed in gastrointestinal epithelial cells, pancreas, and gastric and pancreatic cancer cell lines. -
Isoforms & Post-Translational Modification
P22455 has 2 isomers: P22455-1: 87954 Da (predicted); P22455-2: 83452 Da (predicted).
N-glycosylated. Full maturation of the glycan chains in the Golgi is essential for high affinity interaction with FGF19;Ubiquitinated. Subject to proteasomal degradation when not fully glycosylated;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 -
Subunit
Monomer. Homodimer after ligand binding. Interacts with FGF1, FGF2, FGF4, FGF6, FGF8, FGF9, FGF16, FGF17, FGF18, FGF19, FGF21 and FGF23 (in vitro). Binding affinity for FGF family members is enhanced by interactions between FGFs and heparan sulfate proteoglycans. Interacts with KLB; this strongly increases the affinity for FGF19 and FGF23. Affinity for FGF19 is strongly increased by KLB and sulfated glycosaminoglycans. KLB and KL both interact with the core-glycosylated FGFR4 in the endoplasmic reticulum and promote its degradation, so that only FGFR4 with fully mature N-glycans is expressed at the cell surface. Identified in a complex with NCAM1, CDH2, PLCG1, FRS2, SRC, SHC1, GAP43 and CTTN. Interacts with MMP14 and HIP1 (PubMed:11433297, PubMed:16597617, PubMed:17623664, PubMed:18670643, PubMed:20683963, PubMed:20798051, PubMed:21653700, PubMed:7518429, PubMed:8663044). Interacts with STAT3 (PubMed:26675719)
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SwissProt ID
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Synonyms
FGFR4; TKF; JTK2
Documentation
[1]. Hughes SE. Differential expression of the fibroblast growth factor receptor (FGFR) multigene family in normal human adult tissues. J Histochem Cytochem. 1997 Jul;45(7):1005-19. doi: 10.1177/002215549704500710. PMID: 9212826. et al. Differential expression of the fibroblast growth factor receptor (FGFR) multigene family in normal human adult tissues. J Histochem Cytochem. 1997 Jul;45(7):1005-19. [Content Brief]
[2]. Kurosu H, et al. Tissue-specific expression of betaKlotho and fibroblast growth factor (FGF) receptor isoforms determines metabolic activity of FGF19 and FGF21. J Biol Chem. 2007 Sep 14;282(37):26687-26695. [Content Brief]
[3]. Lin BC, et al. Liver-specific activities of FGF19 require Klotho beta. J Biol Chem. 2007 Sep 14;282(37):27277-27284. [Content Brief]
[4]. Song KH, et al. Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7alpha-hydroxylase gene expression. Hepatology. 2009 Jan;49(1):297-305. [Content Brief]
[5]. Wu AL, et al. FGF19 regulates cell proliferation, glucose and bile acid metabolism via FGFR4-dependent and independent pathways. PLoS One. 2011 Mar 18;6(3):e17868. [Content Brief]
[6]. Xie MH, et al. FGF-19, a novel fibroblast growth factor with unique specificity for FGFR4. Cytokine. 1999 Oct;11(10):729-35. [Content Brief]
[7]. Kim RD, et al. First-in-Human Phase I Study of Fisogatinib (BLU-554) Validates Aberrant FGF19 Signaling as a Driver Event in Hepatocellular Carcinoma. Cancer Discov. 2019 Dec;9(12):1696-1707. [Content Brief]
[8]. Hagel M, et al. First Selective Small Molecule Inhibitor of FGFR4 for the Treatment of Hepatocellular Carcinomas with an Activated FGFR4 Signaling Pathway. Cancer Discov. 2015 Apr;5(4):424-37. [Content Brief]