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Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-08-01 15:32:49.513
Product last modified at: 2024-07-13T07:01:09.365Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464
  1. Products /
  2. Primary Antibodies /
  3. TrkB Antibody

TrkB Antibody #4606

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Product Name

4603 TrkB (80E3) Rabbit mAb
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Inquiry Info. # 4606

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    Supporting Data

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

    Product Information

    Storage

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

    Protocol

    Specificity / Sensitivity

    TrkB Antibody detects transfected levels of total TrkB protein.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human TrkB. Antibodies are purified by protein A and peptide affinity chromatography.

    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).

    The phosphorylation sites are conserved between TrkA and TrkB: Tyr490 of TrkA corresponds to Tyr512 in TrkB, and Tyr674/675 of TrkA to Tyr706/707 in TrkB of the human sequence (14). TrkB is overexpressed in tumors, such as neuroblastoma, prostate adenocarcinoma, and pancreatic ductal adenocarcinoma (15). Research studies have shown that in neuroblastomas, overexpression of TrkB correlates with an unfavorable disease outcome when autocrine loops signaling tumor survival are potentiated by additional overexpression of brain-derived neurotrophic factor (BDNF) (16-18). An alternatively spliced truncated TrkB isoform lacking the kinase domain is overexpressed in Wilms’ tumors and this isoform may act as a dominant-negative regulator of TrkB signaling (17).
    1. Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
    2. Segal, R.A. and Greenberg, M.E. (1996) Annu Rev Neurosci 19, 463-89.
    3. Stephens, R.M. et al. (1994) Neuron 12, 691-705.
    4. Marsh, H.N. et al. (2003) J Cell Biol 163, 999-1010.
    5. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
    6. Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
    7. Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.
    8. Reuther, G.W. et al. (2000) Mol Cell Biol 20, 8655-66.
    9. Greco, A. et al. (1997) Genes Chromosomes Cancer 19, 112-23.
    10. Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
    11. Lagadec, C. et al. (2009) Oncogene 28, 1960-70.
    12. Greco, A. et al. (2010) Mol Cell Endocrinol 321, 44-9.
    13. Ødegaard, E. et al. (2007) Hum Pathol 38, 140-6.
    14. Pierotti, M.A. and Greco, A. (2006) Cancer Lett. 232, 90-98.
    15. Geiger, T.R. and Peeper, D.S. (2005) Cancer Res 65, 7033-6.
    16. Han, L. et al. (2007) Med Hypotheses 68, 407-9.
    17. Aoyama, M. et al. (2001) Cancer Lett 164, 51-60.
    18. Desmet, C.J. and Peeper, D.S. (2006) Cell Mol Life Sci 63, 755-9.

    Database Links

    UniProt ID: Q16620


    Entrez-Gene Id: 4915


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