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BRAND / VENDOR: CST

CST, 4168T, Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit Monoclonal Antibody

CATALOG NUMBER: 4168T
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Product Description
Monoclonal Antibody for studying TrkA (Tyr791) phosphate/TrkB (Tyr817) phosphate. Validated for Western Blotting. Available in 2 sizes. Highly specific and rigorously validated in-house, Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit Monoclonal Antibody (CST #4168) is ready to ship. Product Usage Information Western Blotting: 1:1000 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 Phospho-TrkA (Tyr785)/TrkB (Tyr816) (C67C8) Rabbit Monoclonal Antibody detects transfected levels of TrkA and TrkB when phosphorylated at Tyr785 of TrkA or Tyr816 of TrkB. This antibody may cross-react with other tyrosine-phosphorylated proteins. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr785 of human TrkA protein. 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). Phosphorylation at Tyr785 is required for activation of phospholipase Cγ and subsequent activation of the Ras-MAP kinase cascade. The phosphorylation site is conserved between TrkA and TrkB, as Tyr785 of TrkA corresponds to Tyr816 in TrkB of the human sequence (5,14). Alternate Names BDNF-tropomyosine receptor kinase B; BDNF/NT-3 growth factors receptor; DKFZp781I14186; EIEE58; gp140trk; GP145-TrkB; High affinity nerve growth factor receptor; MTC; neurotrophic receptor tyrosine kinase 1; neurotrophic receptor tyrosine kinase 2; Neurotrophic tyrosine kinase receptor type 1; Neurotrophic tyrosine kinase receptor type 2; neurotrophic tyrosine kinase, receptor, type 1; neurotrophic tyrosine kinase, receptor, type 2; NTRK1; NTRK2; OBHD; Oncogene TRK; p140-TrkA; TRK; Trk-A; Trk-B; TRK1; TRK1-transforming tyrosine kinase protein; TRKA; TRKB; TrkB tyrosine kinase; Tropomyosin-related kinase A; Tropomyosin-related kinase B; Tyrosine kinase receptor; tyrosine kinase receptor A; tyrosine kinase receptor B Specification REACTIVITY: H SENSITIVITY: Transfected Only MW (kDa): 140 Source/Isotype: Rabbit IgG

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Collaboration

Tony Tang

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