Human TrkC Alexa Fluor® 488-conjugated Antibody Summary
Cys32-Asp428
Accession # Q16288
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
Background: TrkC
The neurotrophins, including NGF, BDNF, NT-3 and NT-4/5, constitute a group of structurally related, secreted proteins that play an important role in the development and function of the nervous system. The biological activities of the neurotrophins are mediated by binding to and activating two unrelated receptor types: the p75 neurotrophin receptor (p75NTR) and the Trk family of receptor tyrosine kinases (1, 2). P75NTR is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and has been designated TNFRSF16. It binds all neurotrophins with low-affinity to transduce cellular signaling pathways that synergize or antagonize those activated by the Trk receptors. Three Trk family proteins, TrkA, TrkB and TrkC, exhibiting different ligand specificities, have been identified. TrkA binds NGF and NT‑3, TrkB binds BDNF, NT-3 and NT-4/5, and TrkC only binds NT-3 (1, 2). All Trk family proteins share a conserved, complex subdomain organization consisting of a signal peptide, two cysteine-rich domains, a cluster of three leucine-rich motifs, and two immunoglobulin-like domains in the extracellular region, as well as an intracellular region that contains the tyrosine kinase domain (3). Natural splice variants of the different Trks, lacking the first cysteine-rich domain, the first and second or all three of the leucine-rich motifs, or the tyrosine kinase domain, have been described (4). At the protein sequence level, Trks are highly conserved between species with the extracellular domains of human and mouse TrkC's showing 94% amino acid sequence identity (5). The proteins also exhibit cross-species activity. The primary location of TrkC expression is in the nervous system and, specifically, in regions of the CNS. Low level TrkC expression has also been observed in a wide variety of tissues outside the nervous system (6).
- Huang, E.J. and L.F. Reichardt. (2003) Annu. Rev. Biochem. 72:(epub ahead of print).
- Dechant, G. (2001) Cell Tissue Res. 305:229.
- Schneider, R. and M. Schweiger (1991) Oncogene 6:1807.
- Ninkina, N. et al. (1997) J. Biol. Chem. 272:13019.
- Menn, B. et al. (1998) J. Comp. Neurol. 401:47.
- Shelton, D. et al. (1995) J. Neurosci. 15:477.
Product Datasheets
Product Specific Notices
This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.
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