Product Pathways - Neuroscience
Phospho-TrkA (Tyr490) Antibody #9141
|W IP||R (H) (M)||Endogenous||140||Rabbit|
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.
Specificity / Sensitivity
Phospho-TrkA (Tyr490) Antibody detects endogenous levels of Trk only when phosphorylated at tyrosine 490. This antibody also detects TrkB and TrkC when phosphorylated at the corresponding residues.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr490 of human TrkA. Antibodies are purified by protein A and peptide affinity chromatography.
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).
- 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.
- Anneren, C. et al. (2000) GTK, a Src-related tyrosine kinase, induces nerve growth factor-independent neurite outgrowth in PC12 cells through activation of the Rap1 pathway. J. Biol. Chem. 275, 29153-29161. Applications: Western Blotting
- Binder, D. K. et al. (1999) Immunohistochemical evidence of seizure-induced activation of trk receptors in the mossy fiber pathway of adult rat hippocampus. J. Neurosci. 19, 4616-4626. Applications: Western Blotting
- Gil, C. et al. (2000) Activation of signal transduction pathways involving trkA, PLCgamma-1, PKC isoforms and ERK-1/2 by tetanus toxin. FEBS Lett. 481, 177-182. Applications: Western Blotting
- Reuther, G. W. et al. (2000) Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia. Mol. Cell. Biol. 20, 8655-8666. Applications: Western Blotting
- Binder, D. K. et al. (1999) Selective inhibition of kindling development by intraventricular administration of TrkB receptor body. J. Neurosci. 19, 1424-1436. Applications: Western Blotting
- Xu, B. et al. (2002) Neuroscience 115, 1295-308. Applications: Western Blotting
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