CST, 4603S, TrkB (80E3) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying TrkB. Validated for Western Blotting,Simple Western™. Available in 2 sizes. Highly specific and rigorously validated in-house, TrkB (80E3) Rabbit Monoclonal Antibody (CST #4603) is ready to ship. Product Usage Information Western Blotting: 1:1000 Simple Western™: 1:10 - 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting Specificity / Sensitivity TrkB (80E3) Rabbit Monoclonal Antibody detects endogenous levels of total TrkB protein. This antibody does not cross-react with TrkA. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide surrounding Pro50 of human TrkB. Background 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). Alternate Names BDNF-tropomyosine receptor kinase B; BDNF/NT-3 growth factors receptor; EIEE58; GP145-TrkB; neurotrophic receptor tyrosine kinase 2; Neurotrophic tyrosine kinase receptor type 2; neurotrophic tyrosine kinase, receptor, type 2; NTRK2; OBHD; Trk-B; TRKB; TrkB tyrosine kinase; Tropomyosin-related kinase B; tyrosine kinase receptor B Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 90, 140 Source/Isotype: Rabbit IgG