Neuroscience

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. TrkA regulates proliferation and is important for development and maturation of the nervous system (1). Phosphorylation at Tyr490 is required for Shc association and activation of the Ras-MAP kinase cascade. Residues Tyr674/675 lie within the catalytic domain, and phosphorylation at this site reflects TrkA kinase activity (2-6). Point mutations, deletions and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA. Many malignancies including breast, colon, prostate and thyroid carcinomas and acute myeloid leukemia have activated TrkA. Expression of TrkA in neuroblastomas is a good prognostic marker because it signals growth arrest and differentiation of cells originating from the neural crest (1).

1. Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
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. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
5. Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
6. Yao, R. and Cooper, G.M. (1995) Science 267, 2003-6.

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TrkA Blocking Peptide

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