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Key Documents

T8694

Sigma-Aldrich

TrkB/Fc Chimera human

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

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About This Item

Numéro MDL:
Code UNSPSC :
51111800
Nomenclature NACRES :
NA.32

Source biologique

human

Niveau de qualité

Produit recombinant

expressed in NSO cells

Pureté

>90% (SDS-PAGE)

Forme

lyophilized powder

Puissance

0.1-0.4 μg/mL ED50

Poids mol.

120-130 kDa by SDS-PAGE (reducing)
calculated mol wt 71 kDa

Conditionnement

pkg of 100 μg

Conditions de stockage

avoid repeated freeze/thaw cycles

Technique(s)

western blot: suitable

Impuretés

endotoxin, tested

Numéro d'accès UniProt

Température de stockage

−20°C

Informations sur le gène

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.

Actions biochimiques/physiologiques

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.

Autres remarques

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

Forme physique

Lyophilized from 0.2 μm filtered solution in phosphate buffered saline.

Reconstitution

Reconstitute to 100 μg/mL in phosphate buffered saline.

Remarque sur l'analyse

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

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°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
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.

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