Product Pathways - Neuroscience
Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb #4168
| Applications | Reactivity | Sensitivity | MW (kDa) | Isotype |
|---|---|---|---|---|
| W | R (H) (M) | Endogenous | 140 | Rabbit IgG |
Applications Key:
W=Western Blotting
Reactivity Key:
H=Human
M=Mouse
R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
- 4168:
- Western Blotting
Specificity / Sensitivity
Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb detects endogenous 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.
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).
- Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
- Segal, R.A. and Greenberg, M.E. (1996) Annu Rev Neurosci 19, 463-89.
- Stephens, R.M. et al. (1994) Neuron 12, 691-705.
- Marsh, H.N. et al. (2003) J Cell Biol 163, 999-1010.
- Obermeier, A. et al. (1993) EMBO J 12, 933-41.
- Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
- Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.
- Reuther, G.W. et al. (2000) Mol Cell Biol 20, 8655-66.
- Greco, A. et al. (1997) Genes Chromosomes Cancer 19, 112-23.
- Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
- Lagadec, C. et al. (2009) Oncogene 28, 1960-70.
- Greco, A. et al. (2010) Mol Cell Endocrinol 321, 44-9.
- Ødegaard, E. et al. (2007) Hum Pathol 38, 140-6.
- Chou, T.T. et al. (2000) J Biol Chem 275, 565-70.
Application References
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Rabbit monoclonal antibody is produced under license (granting certain rights including those under U. S. Patent No. 5,675,063) from Epitomics, Inc.
For Research Use Only. Not For Use In Diagnostic Procedures.