TrkB Antibody

4606:

Western Blotting

TrkB Antibody detects transfected levels of total TrkB protein.

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human TrkB. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western blot analysis of extracts from NIH/3T3, NIH/3T3-TrkA, NIH/3T3-TrkB and NIH/3T3-TrkC cells, using TrkB Antibody (upper), TrkA Antibody #2505 (middle) and PLCγ1 Antibody #2822 (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. 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).

The 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 (7). TrkB is overexpressed in tumors such as neuroblastoma, prostate adenocarcinoma and pancreatic ductal adenocarcinoma. In neuroblastomas overexpression of TrkB correlates with unfavorable disease outcome when autocrine loops signaling tumor survival are potentiated by additional overexpression of brain-derived neurotrophic factor (BDNF). An alternatively spliced truncated TrkB isoform lacking the kinase domain is overexpressed in Wilms’s tumors and this isoform may act as a dominant-negative to TrkB signaling (8).

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.
7. Pierotti, M.A. and Greco, A. (2006) Cancer Lett. 232, 90-98.
8. Huang, E.J. and Reichardt, L.F. (2003) Annu. Rev. Biochem. 72, 609-42.
9. Desmet, C.J. and Peeper, D.S. (2006) Cell Mol. Life Sci. 63, 755-759.

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• 2431 Phospho-Shc (Tyr317) Antibody
• 2432 Shc Antibody
• 3965 Ras Antibody
• 9141 Phospho-TrkA (Tyr490) Antibody
• 2505 TrkA Antibody
• 7071 Phototope^® -HRP Western Blot Detection System, Anti-rabbit IgG, HRP-linked Antibody
• 7074 Anti-rabbit IgG, HRP-linked Antibody
• 7720 Prestained Protein Marker, Broad Range (Premixed Format)
• 7727 Biotinylated Protein Ladder Detection Pack
• 7003 20X LumiGLO^® Reagent and 20X Peroxide

For Research Use Only. Not For Use In Diagnostic Procedures.