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trkB Receptor

A protein-tyrosine kinase receptor that is specific for BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; neurotrophin 4 and neurotrophin 5. It is widely expressed in nervous tissue and plays a role in mediating the effects of neurotrophins on growth and differentiation of neuronal cells.
Also Known As:
Receptor, trkB; Brain Derived Neurotrophic Factor Receptor; Neurotrophic Tyrosine Kinase Receptor Type 2; Receptor, Neurotrophic Tyrosine Kinase Type 2; trkB(gp145) Protein; Receptor, BDNF; Receptor, NTRK2; BDNF Receptor; NTRK2 Receptor; Neurotrophic Factor, Brain-Derived, Receptor
Networked: 282 relevant articles (9 outcomes, 29 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1. Ye, Keqiang: 6 articles (01/2022 - 03/2012)
2. Xu, Baoji: 6 articles (01/2020 - 07/2003)
3. Castrén, Eero: 4 articles (01/2021 - 06/2004)
4. Dorsey, Susan G: 4 articles (11/2020 - 07/2006)
5. Renn, Cynthia L: 4 articles (11/2020 - 07/2006)
6. Roesler, Rafael: 4 articles (01/2019 - 01/2010)
7. McNamara, James O: 4 articles (11/2015 - 01/2004)
8. Yang, Tao: 3 articles (01/2022 - 12/2018)
9. Liu, Xia: 3 articles (01/2021 - 06/2013)
10. Faden, Alan I: 3 articles (11/2020 - 07/2013)

Related Diseases

1. Inflammation (Inflammations)
2. Stroke (Strokes)
3. Hypoxia (Hypoxemia)
4. Morphine Dependence
5. Infarction (Infarctions)
12/01/2016 - "The decreased infarct volumes of sEH-/- mice were diminished by intracerebroventricular injection of a blocker of BDNF receptor. "
01/12/2009 - "In addition, we studied whether the outcome of motor function was associated with the expression of BDNF (brain derived neurotrophic factor), trkB (receptor, trkB) and infarct volume. "
03/01/2001 - "In this model, we found: (1) a permanent reduction of brain-derived neurotrophic factor (BDNF) and its full-length receptor, TrkB, in the infarcted core; (2) a transient increase in BDNF immunoreactivity in the internal region of the border of the infarct (penumbra area) at 12 h after MCA occlusion; (3) increased truncated TrkB immunoreactivity in astrocytes surrounding the area of the infarction; and (4) increased full-length TrkB immunoreactivity in scattered neurons, distant from the infarct, in ipsilateral and contralateral cortices at 24 and 48 h after MCA occlusion. "
01/01/2011 - "In the acute intervention study, T and T+R, but not R alone, improved NO, reduced infarct volume, inflammation (TNFα), and induced TrkB receptor and neuronal survival in comparison to V. T, R or T+R had similar beneficial effects on stroke incidence and NO in hypertensive rats, confirming BP reduction as determinant factor in stroke prevention. "
01/01/2019 - "The effects of catalpol on behavior, neurogenesis surrounding the infarction ipsilateral to pMCAO, and the expression of brain-derived neurotrophic factor (BDNF) and its receptor (TrkB) were evaluated. "

Related Drugs and Biologics

1. Brain-Derived Neurotrophic Factor (BDNF)
2. trkB Receptor
3. Proteins (Proteins, Gene)
4. Neuroprotective Agents
5. Retinaldehyde (Retinal)
6. Nitric Oxide Synthase (NO Synthase)
7. Conditioned Culture Media
8. Nitric Oxide (Nitrogen Monoxide)
9. Monoclonal Antibodies
10. baicalin

Related Therapies and Procedures

1. Therapeutics
2. Drug Therapy (Chemotherapy)
3. Immunomodulation