research use only

FGFR3 Antibody [G21B24]

Cat.No.: F0728

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:50
    1:50
    1:200
    Application
    WB, IP, IHC, IF
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    125,145,165 kDa
    Positive Control Small cell lung carcinoma; Human FGFR-3 cytoplasmic fragment proteins; KMS-11 cells
    Negative Control RPMI-8226 cells

    Datasheet & SDS

    Biological Description

    Specificity
    FGFR3 Antibody [G21B24] detects endogenous levels of total FGFR3 protein.
    Clone
    G21B24
    Synonym(s)
    Fibroblast growth factor receptor 3; FGFR-3; CD333; FGFR3; JTK4
    Background
    Fibroblast Growth Factor Receptor 3, a member of the FGFR1-4 receptor tyrosine kinase family, is composed of three extracellular immunoglobulin-like domains, with the D2 and D3 domains binding fibroblast growth factors and heparan sulfates, a single transmembrane helix featuring a heptad motif and N-terminal GG4-like motifs that enable dimer switching, a juxtamembrane region, and a cytoplasmic tyrosine kinase domain. Upon ligand binding, FGFR3 undergoes conformational changes that promote asymmetric dimerization and autophosphorylation of key tyrosines in its kinase domain, sites analogous to those in FGFR1 important for catalytic activity and for docking of proteins such as PLCγ and Crk. FGFR3 mediates FGF signaling and regulates chondrocyte proliferation and differentiation, bone growth, and tissue homeostasis. This is achieved through transmembrane helix rotation, kinase activation, and stimulation of downstream pathways, including MAPK/ERK for cell proliferation, PI3K/AKT for survival, and PLCγ, which collectively restrain excessive cartilage growth and support angiogenesis. Gain-of-function mutations in FGFR3, such as the achondroplasia G380R mutation that stabilizes the active transmembrane dimer or mutations causing thanatophoric dysplasia, lead to skeletal dysplasias, while somatic alterations and overexpression drive oncogenesis in bladder carcinoma, multiple myeloma, and cervical cancer by promoting hyperproliferative signaling.
    References
    • https://pubmed.ncbi.nlm.nih.gov/24120763/
    • https://pubmed.ncbi.nlm.nih.gov/21487019/

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