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Merck

T8694

TrkB/Fc Chimera human

>90% (SDS-PAGE), recombinant, expressed in NSO cells, lyophilized powder

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A propos de cet article

UNSPSC Code:
51111800
NACRES:
NA.32
MDL number:
Form:
lyophilized powder
Assay:
>90% (SDS-PAGE)
Biological source:
human
Recombinant:
expressed in NSO cells
Mol wt:
120-130 kDa by SDS-PAGE (reducing), calculated mol wt 71 kDa
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biological source

human

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

Quality Level

Gene Information

human ... NTRK2(4915)

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

Binds specifically to mediate neurotrophins BDNF and NT-4/5.
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.

Physical form

Lyophilized from 0.2 μm filtered solution in phosphate buffered saline.

Preparation Note

Reconstitute to 100 μg/mL in phosphate buffered saline.

Analysis Note

Inhibits BDNF-induced proliferation of TrkB transfected cells, BaF-TrkB-BD.

Other Notes

Extracellular domain of human TrkB fused to the C-terminal histidine-tagged Fc region of human IgG1.

Classe de stockage

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Consulter la Bibliothèque de documents

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)
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
Yun-yue Ju et al.
Acta pharmacologica Sinica, 36(12), 1437-1443 (2015-11-17)
Brain-derived neurotrophic factor (BDNF) plays an important role in learning and memory in multiple brain areas. In the present study, we investigated the roles of BDNF in aversive memories associated with conditioned drug withdrawal in acute morphine-dependent rats. Conditioned place
BDNF-TrkB signaling through Erk1/2 MAPK phosphorylation mediates the enhancement of fear memory induced by glucocorticoids.
Revest JM, Le Roux A, Roullot-Lacarriere V, et al.
Molecular Psychiatry, 19(9), 1001-1009 (2014)

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