Cat. # | Size | Price | Inventory |
---|---|---|---|
7087C | 1 Kit (96 assays) |
When ordering five or more kits, please contact us for processing time and pricing.
Looking for this ELISA kit in a 384-well format? Inquire for availability, processing time, and pricing.
REACTIVITY | H |
Product Includes | Volume | Solution Color | |||
---|---|---|---|---|---|
TrkB Mouse mAb Coated Microwells | 96 tests | ||||
Phospho-Tyrosine Mouse Detection mAb (Biotinylated) | 1 ea | Green (Lyophilized) | |||
HRP-Linked Streptavidin (ELISA Formulated) | 1 ea | Red (Lyophilized) | |||
Detection Antibody Diluent | 5.5 ml | Green | |||
HRP Diluent | 5.5 ml | Red | |||
Luminol/Enhancer Solution | 3 ml | ||||
Stable Peroxide Buffer | 3 ml | ||||
Sealing Tape | 2 ea | ||||
ELISA Wash Buffer (20X) 9801 | 25 ml | ||||
ELISA Sample Diluent | 25 ml | Blue | |||
Cell Lysis Buffer (10X) 9803 | 15 ml |
Product Information
NOTE: Refer to product-specific datasheets for assay incubation temperature. This chemiluminescent ELISA is offered in low volume microplates. Only 50 µl of samples or reagents are required in each microwell.
NOTE: Prepare solutions with purified water.
*NOTE: Some PathScan® ELISA Kits may include HRP-Linked Streptavidin in place of HRP-Linked Antibody.
posted November 2013
revised July 2024
Protocol Id: 66
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).
Many tyrosine 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).
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