This product is freeze dried. All water molecules have been removed.
Every lot is tried & tested in a relevant biological assay.
0.1 EU per 1 µg of the protein by the LAL method & lyophilized from a 0.2 µm filtered solution.
- Quadrato, G. et al. (2012) Proc. Natl. Acad. Sci. U.S.A. 109, E1499.
- Boulle, F. et al. (2012) Prog. Neurobiol. 98, 197.
- Duclot, F. and Kabbaj, M. (2013) J. Neurosci. 33, 11048.
- Cabelli, R.J. et al. (1997) Neuron 19, 63.
- Kang, H. et al. (1997) Neuron 19, 653.
- McAllister, A.K. et al. (1997) Neuron 18, 767.
- Croll, S.D. et al. (1998) Exp. Neurol. 152, 20.
- Zhang, X. et al. (2012) J. Neural. Transm. 119, 329.
- Alomone Labs Human TrkB-Fc Chimera inhibits BDNF-induced ERK1/2 MAPK phosphorylation in TrkB stably expressed in HEK 293 cells.TrkB-stably transfected HEK 293 cells were serum deprived for 2 hrs followed by a 10 min stimulation with 10 ng/ml Recombinant human BDNF protein (#B-250) (lane 2), 0.3 µg/ml Human TrkB-Fc Chimera (#RPC-001) preincubated with 10 ng/ml Recombinant human BDNF protein for 10 min (lane 3). Control cells incubated without Recombinant human BDNF protein are shown in lane 1. Cell proteins were resolved by SDS-PAGE and detected with anti-phospho-ERK1/2.
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.
Human TrkB-Fc Chimera (#RPC-001) is a highly pure, recombinant, and biologically active protein.