Neurotrophic Tyrosine Kinase, Receptor, Type 2 (NTRK2)
Clone
polyclonal
Host Species
Rabbit
Reactive Species
mouse, rat, human
Isotype
n/a
Format
affinity purified
Size
50 μg
Concentration
n/a
Applications
Western Blotting (WB),Immunohistochemistry (IHC)
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Description
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 . 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 . 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 . 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 these sites reflects TrkA kinase activity . Point mutations, deletions, and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA . TrkA is activated in many malignancies including breast, ovarian, prostate, and thyroid carcinomas . 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 . 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 . TrkB is overexpressed in tumors, such as neuroblastoma, prostate adenocarcinoma, and pancreatic ductal adenocarcinoma . 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) . 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 . Synonyms: GP145-TrkB, TRKB,