T8694
TrkB/Fc Chimera human
>90% (SDS-PAGE), recombinant, expressed in NSO cells, lyophilized powder
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biological source
human
Quality Level
recombinant
expressed in NSO cells
Assay
>90% (SDS-PAGE)
form
lyophilized powder
potency
0.1-0.4 μg/mL ED50
mol wt
120-130 kDa by SDS-PAGE (reducing)
calculated mol wt 71 kDa
packaging
pkg of 100 μg
storage condition
avoid repeated freeze/thaw cycles
technique(s)
western blot: suitable
impurities
endotoxin, tested
UniProt accession no.
storage temp.
−20°C
Gene Information
human ... NTRK2(4915)
Related Categories
Application
TrkB/Fc Chimera human can be used in synaptoneurosome preparation and western blot analysis. Intracerebroventricular administeration of TrkB/Fc chimera human blocks TrkB ligand signaling and was used to study the role of BDNF in ATN response augmentation.
Biochem/physiol Actions
Member of the Trk family tyrosine kinase receptors. Binds specifically to mediate neurotrophins BDNF and NT-4/5.
TrkB/Fc Chimera human consist of extracellular domain of human TrkB1 fused to histidine-tagged Fc region of human IgG1 by using a polypeptide linker. TrkB belongs to tyrosine kinase receptors family and facilitates the hippocampal development as well as regulating the synaptic plasticity that underlies long-term potentiation and learning. Brain derived neurotrophic factor (BDNF) and Neurotrophin 4 or 5 are preferred ligands for TrkB. Nevertheless it can also bind to NTF3/neurotrophin-3 that is less efficient in activating the receptor but regulates neuron survival through NTRK2.
Other Notes
Extracellular domain of human TrkB fused to the C-terminal histidine-tagged Fc region of human IgG1.
Physical form
Lyophilized from 0.2 μm filtered solution in phosphate buffered saline.
Reconstitution
Reconstitute to 100 μg/mL in phosphate buffered saline.
Analysis Note
Inhibits BDNF-induced proliferation of TrkB transfected cells, BaF-TrkB-BD.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Marian Tsanov et al.
Hippocampus, 21(1), 1-8 (2010-01-01)
The hippocampus projects to the anterior thalamic nuclei both directly and indirectly via the mammillary bodies, but little is known about the electrophysiological properties of these convergent pathways. Here we demonstrate, for the first time, the presence of long-term plasticity
Di Liu et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 45(9), 1557-1566 (2020-05-20)
Lithium has been used to treat major depressive disorder, yet the neural circuit mechanisms underlying this therapeutic effect remain unknown. Here, we demonstrated that the ventral tegmental area (VTA) dopamine (DA) neurons that project to the medial prefrontal cortex (mPFC)
Giles S H Yeo et al.
Nature neuroscience, 7(11), 1187-1189 (2004-10-21)
An 8-year-old male with a complex developmental syndrome and severe obesity was heterozygous for a de novo missense mutation resulting in a Y722C substitution in the neurotrophin receptor TrkB. This mutation markedly impaired receptor autophosphorylation and signaling to MAP kinase.
N Ninkina et al.
The Journal of biological chemistry, 272(20), 13019-13025 (1997-05-16)
We have isolated two novel variants involving the extracellular domain of TrkB from developing sensory neurons. These variants are generated by alternative splicing and lack two or all three of the leucine-rich motifs. Each of these variants is expressed as
Ana-Clara Bobadilla et al.
Addiction biology, 24(5), 860-873 (2018-06-12)
Brain-derived neurotrophic factor (BDNF) regulates a variety of physiological processes, and several studies have explored the role of BDNF in addiction-related brain regions like the nucleus accumbens core (NAcore). We sought to understand the rapid effects of endogenous BDNF on
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