Cell Signaling Technology

Product Pathways - Neuroscience

TrkB (80G2) Rabbit mAb #4607

Applications Reactivity MW (kDa) Source Isotype
IHC-P IF-IC F H (M) (R) 140 Rabbit IgG

Applications Key:  IHC-P=Immunohistochemistry (Paraffin)  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

TrkB (80G2) 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.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma using TrkB (80G2) Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded NIH/3T3/TrkB (left) or NIH/3T3/TrkA (right) cell pellets using TrkB (80G2) Rabbit mAb.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of NIH/3T3 cells, untransfected (red) or TrkB transfected (blue), using TrkB (80G2) Rabbit mAb.


IF-IC

IF-IC

Confocal immunofluorescent analysis of dissociated NIH/3T3 cells, wild-type (upper left), NIH/3T3/TrkA (upper right), NIH/3T3/TrkB (lower left), or NIH/3T3/TrkC (lower right), using TrkB (80G2) Rabbit mAb (green). Blue pseudocolor = DRAQ5™ (fluorescent DNA dye).

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’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, 90-98.
  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

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Companion Products

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

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