Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAbProduct information
Product Pathways - Neuroscience
Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb #4168
|4168S||100 µl (10 western blots)||---||In Stock||---|
|4168P||40 µl (4 western blots)||---||In Stock||---|
|4168||carrier free and custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Species predicted to react based on 100% sequence homology: Human, Mouse.
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.
Western blot analysis of extracts from NIH/3T3 cells transfected with TrkB, untreated or treated with hBDNF #3897, using Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb (upper) and Trk (pan) (C17F1) Rabbit mAb #4609 (lower).
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.
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This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.
U.S. Patent No. 5,675,063.
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