PathScan® Phospho-TrkB (panTyr) Chemiluminescent Sandwich ELISA Kit #7087
Supporting Data
| REACTIVITY | H |
Application Key:
- ELISA-ELISA
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Description
*Antibodies in this kit are custom formulations specific to kit.
Protocol
Specificity / Sensitivity
Species Reactivity:
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).
Many tyrosine 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).
- 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.
- Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
- Geiger, T.R. and Peeper, D.S. (2005) Cancer Res 65, 7033-6.
- Han, L. et al. (2007) Med Hypotheses 68, 407-9.
- Aoyama, M. et al. (2001) Cancer Lett 164, 51-60.
- Desmet, C.J. and Peeper, D.S. (2006) Cell Mol Life Sci 63, 755-9.
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