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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GFRα1 (F7R3F) Rabbit mAb #50650

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  • WB
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 65, 60
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 1:400 - 1:1600

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    GFRα1 (F7R3F) Rabbit mAb recognizes endogenous levels of total GFRα1 protein. Non-specific nuclear staining was observed in human esophagus by immunohistochemistry.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala381 of human GFRα1 protein.

    Background

    Glial cell-derived neurotrophic factor (GDNF) plays an important role in the development and maintenance of the central and peripheral nervous system, renal morphogenesis, and spermatogenesis (1). GDNF and the related GDNF family of ligands (GFLs) neurturin, persephin, and artemin bind to the GDNF family receptor alpha (GFRα) proteins, which signal through the rearranged during transfection (RET) receptor tyrosine kinase (2,3). GDNF binds GFRα1, activating signaling cascades that promote neuronal differentiation, plasticity, and survival. In particular, the pro-survival effect of GDNF/GFRα1/RET signaling in dopaminergic neurons has garnered attention in Parkinson’s disease (PD) therapeutic research (4,5). GFRα1 can also function in a RET-independent manner, binding and signaling through the neural cell adhesion molecule (NCAM). This interaction has reported roles in neurogenesis, cell migration, and axon regeneration following nerve injury (6-8). GFRα1 expression has been reported to be upregulated in activated astrocytes under pathological conditions as well, suggesting that it may play a role in modulating neuroinflammation (4). In addition, GFRα1 has been implicated in cancer cell progression, metastasis, and treatment resistance. Its potential as a therapeutic target for cancer is under investigation (9-13).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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