Cell Signaling Technology

Product Pathways - Neuroscience

Phospho-TrkA (Tyr490) Antibody #9141

NGF Receptor   NGFR   p140 (trk)   trk a   trkb   Trkl  

No. Size Price
9141L 300 µl ( 30 western blots ) ¥8,792.00 现货查询 购买询价
9141S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
9141 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Rat, Endogenous 140 Rabbit
IP 1:100

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,


Species predicted to react based on 100% sequence homology: Human, Mouse,

Specificity / Sensitivity

Phospho-TrkA (Tyr490) Antibody detects endogenous levels of Trk only when phosphorylated at tyrosine 490. This antibody also detects TrkB and TrkC when phosphorylated at the corresponding residues.

Phospho-TrkA(Tyr490) Antibody 兔多抗识别内源性的Tyr490磷酸化的Trk蛋白。它也可以识别对应氨基酸残基磷酸化的TrkB和TrkC蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr490 of human TrkA. Antibodies are purified by protein A and peptide affinity chromatography.


Western Blotting

Western Blotting

Western blot analysis of extracts from PC12 cells, untreated or NGF-treated (100 ng/ml), using Phospho-TrkA (Tyr490) Antibody.

Western blot分析PC12细胞,未处理或经NGF(100 ng/ml)处理,使用的抗体是Phospho-TrkA (Tyr490)Antibody 兔多抗。


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. Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
  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. Marsh, H.N. et al. (2003) J Cell Biol 163, 999-1010.
  5. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
  6. Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
  7. Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.
  8. Reuther, G.W. et al. (2000) Mol Cell Biol 20, 8655-66.
  9. Greco, A. et al. (1997) Genes Chromosomes Cancer 19, 112-23.
  10. Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
  11. Lagadec, C. et al. (2009) Oncogene 28, 1960-70.
  12. Greco, A. et al. (2010) Mol Cell Endocrinol 321, 44-9.
  13. Ødegaard, E. et al. (2007) Hum Pathol 38, 140-6.

Application References

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Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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