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Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit Monoclonal Antibody #4168

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  • WB

    Product Specifications

    REACTIVITY H
    SENSITIVITY Transfected Only
    MW (kDa) 140
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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

    Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit Monoclonal Antibody detects transfected levels of TrkA and TrkB when phosphorylated at Tyr785 of TrkA or Tyr816 of TrkB. This antibody may cross-react with other tyrosine-phosphorylated proteins.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr785 of human TrkA protein.

    Background

    The family of Trk receptor tyrosine kinases consists of TrkA, TrkB, and TrkC. While the sequence of these family members is highly conserved, they are activated by different neurotrophins: TrkA by NGF, TrkB by BDNF or NT4, and TrkC by NT3 (1). Neurotrophin signaling through these receptors regulates a number of physiological processes, such as cell survival, proliferation, neural development, and axon and dendrite growth and patterning (1). In the adult nervous system, the Trk receptors regulate synaptic strength and plasticity. TrkA regulates proliferation and is important for development and maturation of the nervous system (2). Phosphorylation at Tyr490 is required for Shc association and activation of the Ras-MAP kinase cascade (3,4). Residues Tyr674/675 lie within the catalytic domain, and phosphorylation at these sites reflects TrkA kinase activity (3-6). Point mutations, deletions, and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA (7-10). TrkA is activated in many malignancies including breast, ovarian, prostate, and thyroid carcinomas (8-13). Research studies suggest that expression of TrkA in neuroblastomas may be a good prognostic marker as TrkA signals growth arrest and differentiation of cells originating from the neural crest (10).
    Phosphorylation at Tyr785 is required for activation of phospholipase Cγ and subsequent activation of the Ras-MAP kinase cascade. The phosphorylation site is conserved between TrkA and TrkB, as Tyr785 of TrkA corresponds to Tyr816 in TrkB of the human sequence (5,14).

    Alternate Names

    BDNF-tropomyosine receptor kinase B; BDNF/NT-3 growth factors receptor; DKFZp781I14186; EIEE58; gp140trk; GP145-TrkB; High affinity nerve growth factor receptor; MTC; neurotrophic receptor tyrosine kinase 1; neurotrophic receptor tyrosine kinase 2; Neurotrophic tyrosine kinase receptor type 1; Neurotrophic tyrosine kinase receptor type 2; neurotrophic tyrosine kinase, receptor, type 1; neurotrophic tyrosine kinase, receptor, type 2; NTRK1; NTRK2; OBHD; Oncogene TRK; p140-TrkA; TRK; Trk-A; Trk-B; TRK1; TRK1-transforming tyrosine kinase protein; TRKA; TRKB; TrkB tyrosine kinase; Tropomyosin-related kinase A; Tropomyosin-related kinase B; Tyrosine kinase receptor; tyrosine kinase receptor A; tyrosine kinase receptor B

    For Research Use Only. Not for Use in Diagnostic Procedures.
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    U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.
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