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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Neurotrophic tyrosine kinase, receptor, type 2

receptor for brain-derived neurotrophic factor (BDNF) [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Brain-derived neurotrophic factor, TM3, V1a, CAN, trkA
Papers using TrkB antibodies
The effects of acute and long-term lithium treatments on trkB neurotrophin receptor activation in the mouse hippocampus and anterior cingulate cortex.
Gaetani Silvana, In PLoS ONE, 2005
... Moses Chao, Skirball Institute, NY, USA), sc-11-R (1∶2000, Santa Cruz Biotechnology), anti-TrkB (1∶2000, BD Biosciences) or anti-BDNF (N-20/sc-546, Santa ...
Mutation of PTB binding sites causes misregulation of alternative 3′ splice site selection in vivo.
Maas Stefan, In PLoS ONE, 1996
... The mouse TrkB 5′ leaders (Fig 1a), with the exception of L1, were cloned from a mouse brain cDNA library (Clontech) with EcoRI and NcoI ...
Papers on TrkB
BDNF - a key transducer of antidepressant effects.
Monteggia et al., Stockholm, Sweden. In Neuropharmacology, Mar 2016
The antidepressant-like response of ketamine is abolished in BDNF and TrkB conditional knockout mice, eEF2 kinase knockout mice, in mice carrying the BDNF met/met allele, and by intra-cortical infusions of BDNF-neutralizing antibodies.
Environmental enrichment delays limbic epileptogenesis and restricts pathologic synaptic plasticity.
Jones et al., Melbourne, Australia. In Epilepsia, Feb 2016
Timm's staining revealed significant reductions in aberrant mossy fiber sprouting in EE rats (p < 0.05), and these effects of EE were accompanied by reduced expression of TrkB and CRH genes.
Brain-derived neurotrophic factor (BDNF) - TrkB signaling in inflammation-related depression and potential therapeutic targets.
Hashimoto et al., Chiba, Japan. In Curr Neuropharmacol, Feb 2016
Signaling via brain-derived neurotrophic factor (BDNF) and its receptor, tropomycin receptor kinase B (TrkB) plays a key role in the pathophysiology of depression and in the therapeutic mechanisms of antidepressants.
Increased Olfactory Bulb BDNF Expression Does Not Rescue Deficits in Olfactory Neurogenesis in the Huntington's Disease R6/2 Mouse.
Guthrie et al., Boca Raton, United States. In Chem Senses, Feb 2016
Newly maturing cells express the BDNF receptor TrkB, suggesting that mhtt may interfere with normal BDNF trophic activity, increasing their loss.
Caffeine exposure during rat brain development causes memory impairment in a sex selective manner that is offset by caffeine consumption throughout life.
Porciúncula et al., Porto Alegre, Brazil. In Behav Brain Res, Feb 2016
TrkB receptor was decreased in the hippocampus from both sexes and treatment regimens.
Normal Molecular Specification and Neurodegenerative Disease-Like Death of Spinal Neurons Lacking the SNARE-Associated Synaptic Protein Munc18-1.
Kania et al., Montréal, Canada. In J Neurosci, Feb 2016
Consistent with cell-autonomous degeneration, we demonstrate defects in the trafficking of the synaptic proteins Syntaxin1a and PSD-95 and the TrkB and DCC receptors in Munc18-1(-/-) neurons; these defects do not appear to cause ER stress, suggesting other mechanisms for degeneration.
Brain-derived neurotrophic factor and its clinical implications.
Das et al., Vishākhapatnam, India. In Arch Med Sci, Jan 2016
BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates signal transduction cascades (IRS1/2, PI3K, Akt), crucial for CREB and CBP production, that encode proteins involved in β cell survival.
7,8-dihydroxyflavone, a small molecular TrkB agonist, is useful for treating various BDNF-implicated human disorders.
Ye et al., Wuhan, China. In Transl Neurodegener, Dec 2015
Brain-derived neurotrophic factor (BDNF) regulates a variety of biological processes predominantly via binding to the transmembrane receptor tyrosine kinase TrkB.
The paraventricular thalamus controls a central amygdala fear circuit.
Li et al., New York City, United States. In Nature, Apr 2015
Notably, PVT modulation of SOM(+) CeL neurons was mediated by activation of the brain-derived neurotrophic factor (BDNF) receptor tropomysin-related kinase B (TrkB).
The cellular and molecular basis of direction selectivity of Aδ-LTMRs.
Ginty et al., Baltimore, United States. In Cell, 2015
The neurotrophic factor BDNF is synthesized in epithelial cells on the caudal, but not rostral, side of hair follicles, in close proximity to Aδ-LTMR lanceolate endings, which express TrkB.
Early Life Stress Effects on Glucocorticoid-BDNF Interplay in the Hippocampus.
Kranz et al., New York City, United States. In Front Mol Neurosci, 2014
The neurotrophin and GC-signaling pathways co-exist throughout the central nervous system (CNS), particularly in the hippocampus, which has high expression levels of glucocorticoid-receptors (GR) and mineralocorticoid-receptors (MR) as well as brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase receptor B (TrkB).
α-Linolenic Acid, A Nutraceutical with Pleiotropic Properties That Targets Endogenous Neuroprotective Pathways to Protect against Organophosphate Nerve Agent-Induced Neuropathology.
Marini et al., Bethesda, United States. In Molecules, 2014
The pleiotropic properties of ALA target endogenous neuroprotective and neurorestorative pathways in brain and involve the transcription factor nuclear factor kappa B (NF-κB), brain-derived neurotrophic factor (BDNF), a major neuroprotective protein in brain, and downstream signaling pathways likely mediated via activation of TrkB, the cognate receptor of BDNF.
Small-molecule modulation of neurotrophin receptors: a strategy for the treatment of neurological disease.
Massa et al., Stanford, United States. In Nat Rev Drug Discov, 2013
One strategy to overcome these limitations is to target individual neurotrophin receptors — such as tropomyosin receptor kinase A (TRKA), TRKB, TRKC, the p75 neurotrophin receptor or sortilin — with small-molecule ligands.
Sexually dimorphic BDNF signaling directs sensory innervation of the mammary gland.
Ginty et al., Baltimore, United States. In Science, 2013
Brain-derived neurotrophic factor (BDNF), emanating from mammary mesenchyme and signaling through its receptor TrkB on sensory axons, is required for establishing mammary gland sensory innervation of both sexes at early developmental stages.
Intrinsically determined cell death of developing cortical interneurons.
Alvarez-Buylla et al., San Francisco, United States. In Nature, 2012
The death of transplanted neurons was not affected by the cell-autonomous disruption of TrkB (tropomyosin kinase receptor B), the main neurotrophin receptor expressed by neurons of the central nervous system.
Shp-2 regulates the TrkB receptor activity in the retinal ganglion cells under glaucomatous stress.
Graham et al., Port Macquarie, Australia. In Biochim Biophys Acta, 2012
these findings implicate a molecular basis of Shp2 mediated TrkB deactivation leading to retinal ganglion cells (RGC) degeneration observed in glaucoma
Age-dependent decline of motor neocortex but not hippocampal performance in heterozygous BDNF mice correlates with a decrease of cortical PSD-95 but an increase of hippocampal TrkB levels.
Alberch et al., Barcelona, Spain. In Exp Neurol, 2012
30-week-old BDNF/ mice displayed increased TrkB levels in the hippocampus but not in the motor neocortex
Suppression of hydatidiform molar growth by inhibiting endogenous brain-derived neurotrophic factor/tyrosine kinase B signaling.
Terada et al., Akita, Japan. In Endocrinology, 2012
Findings demonstrate the importance of paracrine signaling by the BDNF/TrkB system in the proliferation and survival of molar trophoblast.
Increased expression of TrkB and Capzb2 accompanies preserved cognitive status in early Alzheimer disease pathology.
Delalle et al., Boston, United States. In J Neuropathol Exp Neurol, 2012
This study suggested that increased expression of TrkB and Capzb2 accompanies adequate brain reserve in the initial stages of AD pathology.
Vagal nerve stimulation rapidly activates brain-derived neurotrophic factor receptor TrkB in rat brain.
Frazer et al., San Antonio, United States. In Plos One, 2011
Data show that vagal nerve stimulation (VNS) rapidly activates TrkB phosphorylation and this effect persists over time.
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