antibody

TrkA, TrkB, phosphorylated, TrkA (Tyr490), TrkB (Tyr516) (Tyrosine Kinase Receptor A,B)

T8663-15B

100 ul

monoclonal

domestic rabbit

nonconjugated

phosphorylated

9j154(C35G9)

TrkA, TrkB, phosphorylated, TrkA (Tyr490), TrkB (Tyr516) (Tyrosine Kinase Receptor A,B)

rabbit

Mab

Phosphorylated

Antibodies

100 ul

9j154(C35G9)

IgG

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). Applications: Suitable for use in Western Blot and Immunoprecipitation. Other applications not tested. Recommended Dilution: Western Blot: 1:1000. For Western blot, incubate membrane with diluted antibody in 5% w/v BSA, 1X TBS, 0.1% Tween-20 at 4°C with gentle shaking overnight. Immunoprecipitation: 1:50 Optimal dilutions to be determined by the researcher. Storage and Stability: May be stored at 4°C for short-term only. For long-term storage, aliquot and store at -20°C. Aliquots are stable for 12 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

Hu Rt

Synthetic phosphopeptide corresponding to residues surrounding Tyr490 of human TrkA. Species sequence homology: mouse.

Recognizes endogenous levels of human TrkA and TrkB at 140kD only when phosphorylated at Tyr490 and Tyr516, respectively. This antibody may cross-react with Bcr-Abl phosphorylated at an unkown tyrosine residue. Species Crossreactivity: rat.

Supernatant

Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, 0.1mg/ml BSA, 50% glycerol.

Not determined

Product Type: Mab Isotype: IgG Clone No: 9j154(C35G9) Host: rabbit Source: human Concentration: Not determined. Form: Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, 0.1mg/ml BSA, 50% glycerol. Purity: Supernatant Immunogen: Synthetic phosphopeptide corresponding to residues surrounding Tyr490 of human TrkA. Species sequence homology: mouse. Specificity: Recognizes endogenous levels of human TrkA and TrkB at 140kD only when phosphorylated at Tyr490 and Tyr516, respectively. This antibody may cross-react with Bcr-Abl phosphorylated at an unkown tyrosine residue. Species Crossreactivity: rat. Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.

IP WB

-20°C

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.

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