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).
Immunoprecipitation of mouse neonatal brain extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is Trk (pan) (A7H6R) Rabbit mAb. Western blot analysis was performed using Trk (pan) (A7H6R) Rabbit mAb.
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 analysis of extracts from mouse neonatal and rat fetal brain using Trk (pan) (A7H6R) Rabbit mAb.
Western blot analysis of extracts from M0-91, KM12 cells and mouse neonatal brain using Trk (pan) (A7H6R) Rabbit mAb.
|Phospho-TrkA (Tyr490)/TrkB (Tyr516) (C35G9) Rabbit mAb 4619||100 µl||H R||140||Rabbit IgG|
|Trk (pan) (A7H6R) Rabbit mAb 92991||100 µl||H M R||120-140||Rabbit IgG|
PhosphoPlus® Duets from Cell Signaling Technology (CST) provide a means to assess protein activation status. Each Duet contains an activation-state and total protein antibody to your target of interest. These antibodies have been selected from CST's product offering based upon superior performance in specified applications.
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).
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U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.