|Calculated MW||91999 Da|
|Other Names||BDNF/NT-3 growth factors receptor, GP145-TrkB, Trk-B, Neurotrophic tyrosine kinase receptor type 2, TrkB tyrosine kinase, Tropomyosin-related kinase B, NTRK2, TRKB|
|Target/Specificity||A phospho specific peptide corresponding to residues surrounding Tyrosine 817 of human TrkB was used as an immunogen. This antibody detects TrkB phosphorylated at Y817.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Trk B Antibody Phospho (pY817) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor tyrosine kinase involved in the development and the maturation of the central and the peripheral nervous systems through regulation of neuron survival, proliferation, migration, differentiation, and synapse formation and plasticity. Receptor for BDNF/brain-derived neurotrophic factor and NTF4/neurotrophin- 4. Alternatively can also bind NTF3/neurotrophin-3 which is less efficient in activating the receptor but regulates neuron survival through NTRK2. Upon ligand-binding, undergoes homodimerization, autophosphorylation and activation. Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades. Through SHC1, FRS2, SH2B1, SH2B2 activates the GRB2-Ras-MAPK cascade that regulates for instance neuronal differentiation including neurite outgrowth. Through the same effectors controls the Ras-PI3 kinase-AKT1 signaling cascade that mainly regulates growth and survival. Through PLCG1 and the downstream protein kinase C-regulated pathways controls synaptic plasticity. Thereby, plays a role in learning and memory by regulating both short term synaptic function and long-term potentiation. PLCG1 also leads to NF-Kappa-B activation and the transcription of genes involved in cell survival. Hence, it is able to suppress anoikis, the apoptosis resulting from loss of cell-matrix interactions. May also play a role in neutrophin- dependent calcium signaling in glial cells and mediate communication between neurons and glia.|
|Cellular Location||Cell membrane; Single-pass type I membrane protein. Endosome membrane; Single-pass type I membrane protein. Note=Internalized to endosomes upon ligand-binding.|
|Tissue Location||Isoform TrkB is expressed in the central and peripheral nervous system. In the central nervous system (CNS), expression is observed in the cerebral cortex, hippocampus, thalamus, choroid plexus, granular layer of the cerebellum, brain stem, and spinal cord. In the peripheral nervous system, it is expressed in many cranial ganglia, the ophthalmic nerve, the vestibular system, multiple facial structures, the submaxillary glands, and dorsal root ganglia. Isoform TrkB-T1 is mainly expressed in the brain but also detected in other tissues including pancreas, kidney and heart. Isoform TrkB-T-Shc is predominantly expressed in the brain|
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Provided below are standard protocols that you may find useful for product applications.
There is increasing evidence that neurotrophins and their receptors play an important role in regulating development of both the central and the peripheral nervous systems (1). The binding of neurotrophin ligands to their respective Trk cellular receptors initiates intracellular signals essential for the growth and survival of neurons. The site of neurotrophin binding has been located to the fifth extracellular domain of the Trk receptor, with this region regulating both the affinity and specificity of Trk receptor:neurotrophin interaction (2). The TrkB receptor tyrosine kinase and its ligand, BDNF, have an essential role in certain forms of synaptic plasticity. Results provide evidence that TrkB mediates hippocampal plasticity via recruitment of PLCgamma, and by subsequent phosphorylation of CaMKIV (3). Also, TrkB has been found to be essential to the development of GABAergic neurons and regulates synapse formation in addition to its role in the development of axon terminals (4).
1. Nakagawara A, et al. Genomics 25(2):538-46, 1995
2. Banfield MJ, et al. Structure 9(12):1191-9, 2001
3. Minichiello L, et al. Neuron 36(1):121-37, 2002
4. Rico B, et al. Nat Neurosci 5(3):225-33, 2002
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