Upstream / Downstream

Explore pathways related to this product.

Important Ordering Details

Custom Ordering Details: Product is assembled upon order to ensure maximum activity. United States: Please allow up to two weeks for your order to be processed and shipped. Outside of the United States: Please allow up to three weeks, depending on the country, for your order to be processed and shipped. When ordering five or more kits, please contact us for processing time and pricing at sales@cellsignal.com.

Antibody Guarantee

CST Antibody Performance Guarantee

LEARN MORE  

Questions?

Find answers on our FAQs page.

ANSWERS  

Visit PhosphoSitePlus®

PTM information and tools available.

LEARN MORE

REACTIVITY
Product Includes Volume Solution Color
TrkB Ab Coated Microwells 96 tests
TrkB Detection Ab 11 ml Green
Anti-mouse IgG, HRP-linked Antibody 11 ml Red
TMB Substrate 7004 11 ml Colorless
STOP Solution 7002 11 ml Colorless
Sealing Tape 2 sheets
ELISA Wash Buffer (20X) 25 ml Colorless
Sample Diluent 25 ml Blue
Cell Lysis Buffer (10X) 9803 15 ml Yellowish

Product Description

The PathScan® Total TrkB Sandwich ELISA Kit is a solid phase sandwich enzyme-linked immunosorbent assay (ELISA) that detects transfected levels of total TrkB protein. A TrkB Mouse Antibody has been coated onto the microwells. After incubation with cell lysates, TrkB (phospho and nonphospho) is captured by the coated antibody. Following extensive washing, a TrkB Rabbit Detection Antibody is added to detect tyrosine phosphorylation of the captured TrkB protein. Anti-rabbit IgG HRP-Linked Antibody is then used to recognize the bound detection antibody. HRP substrate, TMB, is added to develop color. The magnitude of the absorbance for this developed color is proportional to the quantity of TrkB protein.


Specificity / Sensitivity

CST's PathScan® Total TrkB Sandwich ELISA Kit #7106 detects transfected levels of total TrkB protein. The kit sensitivity is shown in figure 2. This kit detects proteins from the indicated species, as determined through in-house testing, but may also detect homologous proteins from other species.


Species Reactivity: Human

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 (1). Neurotrophin signaling through these receptors regulates a number of physiological processes, such as cell survival, proliferation, neural development, and axon and dendrite growth and patterning (1). In the adult nervous system, the Trk receptors regulate synaptic strength and plasticity. TrkA regulates proliferation and is important for development and maturation of the nervous system (2). Phosphorylation at Tyr490 is required for Shc association and activation of the Ras-MAP kinase cascade (3,4). Residues Tyr674/675 lie within the catalytic domain, and phosphorylation at these sites reflects TrkA kinase activity (3-6). Point mutations, deletions, and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA (7-10). TrkA is activated in many malignancies including breast, ovarian, prostate, and thyroid carcinomas (8-13). Research studies suggest that expression of TrkA in neuroblastomas may be a good prognostic marker as TrkA signals growth arrest and differentiation of cells originating from the neural crest (10).


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 (14). TrkB is overexpressed in tumors, such as neuroblastoma, prostate adenocarcinoma, and pancreatic ductal adenocarcinoma (15). Research studies have shown that in neuroblastomas, overexpression of TrkB correlates with an unfavorable disease outcome when autocrine loops signaling tumor survival are potentiated by additional overexpression of brain-derived neurotrophic factor (BDNF) (16-18). An alternatively spliced truncated TrkB isoform lacking the kinase domain is overexpressed in Wilms’ tumors and this isoform may act as a dominant-negative regulator of TrkB signaling (17).


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.  Reuther, G. W. et al. (2000) Mol. Cell. Biol. 20, 8655-8666.

6.  Obermeier, A. et al. (1993) EMBO J 12, 933-41.

7.  Obermeier, A. et al. (1994) EMBO J 13, 1585-90.

8.  Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.

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.


Entrez-Gene Id 4915
Swiss-Prot Acc. Q16620


For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
PathScan® is a trademark of Cell Signaling Technology, Inc.