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Neuroscience

Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb #4168

Item # Description List Price Web Price QTY Buy
4168P Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb - 40ul $165.00 $148.50
4168S Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb - 100ul $377.00 $339.30
Applications Reactivity Sensitivity MW (kDa) Source
W H M R Transfected Only 140 Rabbit

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

Protocols

Specificity / Sensitivity

Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb detects transfected levels of TrkA and TrkB when phosphorylated at Tyr785 of TrkA or Tyr816 of TrkB. This antibody may cross-react with other tyrosine-phosphorylated proteins.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr785 of human TrkA protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from NIH/3T3 cells transfected with TrkB, untreated or treated with hBDNF #3897, using Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb (upper) and Trk (pan) (C17F1) Rabbit mAb #4609 (lower).

Western Blotting

Western Blotting

Western blot analysis of extracts from NIH/3T3 cells transfected with TrkA, untreated or treated with NGF, using Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit mAb (upper) and TrkA (14G6) Rabbit mAb #2508 (lower).

Background

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. et al. (2006) Cancer Lett232, 90 - 8.
  2. Segal, R.A. and Greenberg, M.E. et al. (1996) Annu Rev Neurosci19, 463 - 89.
  3. Stephens, R.M. et al. (1994) Neuron12, 691 - 705.
  4. Obermeier, A. et al. (1993) EMBO J12, 933 - 41.
  5. Obermeier, A. et al. (1994) EMBO J13, 1585 - 90.
  6. Yao, R. and Cooper, G.M. et al. (1995) Science267, 2003 - 6.

Application References

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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.