|Other Names||NT-3 growth factor receptor, GP145-TrkC, Trk-C, Neurotrophic tyrosine kinase receptor type 3, TrkC tyrosine kinase, NTRK3, TRKC|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7688a was selected from the N-term region of human TRKC . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Receptor tyrosine kinase involved in nervous system and probably heart development. Upon binding of its ligand NTF3/neurotrophin-3, NTRK3 autophosphorylates and activates different signaling pathways, including the phosphatidylinositol 3-kinase/AKT and the MAPK pathways, that control cell survival and differentiation.|
|Cellular Location||Membrane; Single-pass type I membrane protein|
|Tissue Location||Widely expressed but mainly in nervous tissue. Isoform 2 is expressed at higher levels in adult brain than in fetal brain|
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Provided below are standard protocols that you may find useful for product applications.
TRKC, a member of the insuline receptor subfamily of Tyr protein kinases, is a receptor for neurotrophin-3 (NT-3). Known substrates for the TRK receptors are SHC, PI-3 kinase, and PLCG1. The different isoforms do not have identical signaling properties. The protein is widely expressed, mainly in the nervous tissue. The isoform B is expressed in a relatively large amount in the adult brain comparatively to fetal brain. TRKC is subject to ligand-mediated auto-phosphorylation. The protein structure contains 2 immunoglobulin-like C2-type domains and 2 leucine-rich (LRR) repeats.
McGregor, L.M., et al., Genomics 22(2):267-272 (1994).Shelton, D.L., et al., J. Neurosci. 15 (1 Pt 2), 477-491 (1995).
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