Human TrkB-Fc Chimera

Proteins

Israel

Storage as Solution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles. - Storage before Reconstitution: The product is shipped as a lyophilized powder at room temperature. Upon receipt, store the product at -20°C. Protect from moisture. - Storage after Reconstitution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.

Lyophilized

An Inhibitor of BDNF Activity

An Inhibitor of BDNF Activity

12352202

0.1 - 0.4 µg/ml in the presence of 10 ng/ml of human BDNF.

Centrifuge the vial before adding solvent (10, 000 x g for 5 minutes) to spin down all the powder to the bottom of the vial. The lyophilized product may be difficult to visualize. Add solvent directly to the centrifuged vial. Tap the vial to aid in dissolving the lyophilized product. Tilt and gently roll the liquid over the walls of the vial. Avoid vigorous vortexing. Light vortexing for up to 3 seconds is acceptable if needed. For long-term storage in solution, we recommend preparing a stock solution by dissolving the product in sterile water at a concentration of at least 0.1 mg/mL. Divide the stock solution into small aliquots and store at -20°C. Before use, thaw the relevant vial(s) and dilute to the desired working concentration in your working buffer. It is recommended to prepare fresh solutions in working buffers just before use. Repeat freeze-thawing may result in loss of activity.

yes

TrkB is a receptor tyrosine kinase of the Trk family. It is activated by brain-derived neurotrophic factor (BDNF), neurotrophin-3, -4 and -5 and is involved in the development and maintenance of the nervous system1. TrkB-Fc is a fusion protein combining the extracellular binding domain of TrkB and the Fc domain of human IgG. TrkB-Fc is a tool for studying the biological actions of BDNF 2.A large number of in vitro studies support the notion that TrkB-Fc inhibits BDNF activity3. Addition of TrkB-Fc to hippocampal and cortical slices and cultured cortical, striatal, and dentate granule cells either abolishes or opposes the effect of BDNF. The TrkB-Fc fusion protein, a specific inhibitor of Trk kinase activity, K252, and a TrkB neutralizing antibody all have similar BDNF-blocking effects. In addition, administration of TrkB-Fc in vivo has consequences that are in accordance with decreased BDNF activity. Systemic nerve growth factor treatment, which leads to a condition resembling peripheral inflammation, raises BDNF levels in sensory neurons and increases nociceptive spinal reflex excitability. This increased central excitability is reduced by TrkB-Fc4. Moreover, intraventricular delivery of TrkB-Fc suppresses epileptogenesis, similar to what has been observed in heterozygous BDNF knockout mice and in transgenic mice overexpressing truncated TrkB receptors and with decreased endogenous BDNF levels5. In contrast to these data, Croll et al.2 reported that TrkB-Fc can potentiate BDNF-induced TrkB phosphorylation. However, this effect was observed only when TrkB-Fc and BDNF were coinfused intracerebrally in equimolar concentrations.