Cell Signaling Technology

Product Pathways - Neuroscience

TrkA (14G6) Rabbit mAb #2508

Applications Reactivity Sensitivity MW (kDa) Isotype
W IHC-P H Endogenous 140 Rabbit IgG

Applications Key:  W=Western Blotting  IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

TrkA (14G6) Rabbit mAb detects endogenous levels of total TrkA protein. This antibody does not cross-react with TrkB.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide surrounding Arg220 of human TrkA.

Western Blotting

Western Blotting

Western blot analysis of extracts from NIH/3T3, NIH/3T3-TrkA, NIH/3T3-TrkB and NIH/3T3-TrkC and K562 cells using TrkA (14G6) Rabbit mAb (upper) TrkB (80G2) Rabbit mAb Antibody #4607 (middle) and PLCγ1 Antibody #2822 (lower).

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast using TrkA (14G6) Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma using Trk A (14G6) Rabbit mAb #2508 in the presence of control peptide (left) or Trk A Blocking Peptide #1435 (right).


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).

  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.

Application References

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Companion Products

Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.

For Research Use Only. Not For Use In Diagnostic Procedures.

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