Cell Signaling Technology

Product Pathways - Neuroscience

TrkB (80E3) Rabbit mAb #4603

Applications Reactivity Sensitivity MW (kDa) Isotype
W H M R Endogenous 90, 140 Rabbit IgG

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

TrkB (80E3) Rabbit mAb detects endogenous levels of total TrkB protein. The antibody does not cross-react with TrkA.

Source / Purification

Monoclonal antibody is produced by immunizing rabbits with a synthetic peptide (KLH-coupled) surrounding Pro50 of human TrkB.

Western Blotting

Western Blotting

Western blot analysis of extracts from neonatal mouse brain, rat brain and NIH/3T3/TrkB cells using TrkB (80E3) Rabbit mAb.

Background

The family of Trk receptor tyrosine kinases consists of TrkA, TrkB and TrkC. While the sequence of these family members is highly conserved, these family members 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 (chimera) cause ligand-independent receptor dimerization and activation of TrkA. Many malignancies (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’ 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, 90-98.
  2. Segal, R.A. and Greenberg, M.E. (1996) Annu. Rev. Neurosci. 19, 463-489.
  3. Stephens, R.M. et al. (1994) Neuron 12, 691-705.
  4. Obermeier, A. et al. (1993) EMBO J. 12, 933-941.
  5. Obermeier, A. et al. (1994) EMBO J. 13, 1585-1590.
  6. Yao, R. and Cooper, G.M. (1995) Science 267, 2003-2006.
  7. Huang, E.J. and Reichardt, L.F. (2003) Annu. Rev. Biochem, 72, 609-642.
  8. Desmet, C.J. and Peeper, D.S. (2006) Cell Mol. Life Sci. 63, 755-759.

Application References

Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!

Companion Products

Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.

This product is for in vitro research use only and is not intended for use in humans or animals. This product is not intended for use as therapeutic or in diagnostic procedures.

Product Pathways

Drug Discovery Tools

Featured Technologies

Protein Classes