Cell Signaling Technology

Product Pathways - Neuroscience

Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb #4619

EC   Neurotrophic tyrosine kinase receptor type   NTRK   p140-Trk   sc-8058   Trk   TRK transforming tyrosine kinase protein  

No. Size Price
4619S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
4619T 20 µl ( 2 western blots ) ¥1,500.00 现货查询 购买询价
4619 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Rat, Endogenous 140 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

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


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

Specificity / Sensitivity

Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb detects endogenous levels of TrkA and TrkB only when phosphorylated at Tyr490 and Tyr516, respectively. This antibody may cross-react with Bcr-Abl phosphorylated at an unkown tyrosine residue.

Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb 兔单抗可识别内源性的Tyr490/Tyr516磷酸化的TrkA/TrkB。此抗体可能与某未知酪氨酸残基磷酸化的Bcr-Abl蛋白有交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr490 of human TrkA.


Western Blotting

Western Blotting

Western blot analysis of extracts from untreated or NGF-treated 3T3/TrkA and PC12 cells using Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb.

Western blot分析未处理或经NGF处理的3T3/TrkA和PC12细胞提取物,使用的抗体是Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9)Rabbit mAb 兔单抗。

Western Blotting

Western Blotting

Western blot analysis of extracts from NIH/3T3 cells stably transfected with either TrkA or TrkB, left untreated or treated with NGF or BDNF, respectively, using Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb (upper) and pooled TrkA/TrkB antibodies (lower).

Western blot分析稳定转染了TrkA或TrkB的NIH/3T3细胞,未处理或分别使用NGF或BDNF处理,使用的抗体是Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9)Rabbit mAb 兔单抗(上图)和pooled TrkA/TrkB Antibody 兔多抗(下图)。


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).


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  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.
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  5. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
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  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.
  14. Huang, E.J. and Reichardt, L.F. (2003) Annu. Rev. Biochem. 72, 609-42.
  15. Geiger, T.R. and Peeper, D.S. (2005) Cancer Res 65, 7033-6.
  16. Han, L. et al. (2007) Med Hypotheses 68, 407-9.
  17. Aoyama, M. et al. (2001) Cancer Lett 164, 51-60.
  18. Desmet, C.J. and Peeper, D.S. (2006) Cell Mol Life Sci 63, 755-9.

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