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1 lls still begin to develop in the absence of neurotrophin 3.
2 eurotrophic factor, nerve growth factor, and neurotrophin 3.
3 M1 activates TrkC by inducing the release of neurotrophin-3.
4 252a did not prevent GM1-mediated release of neurotrophin-3.
5 rs for brain-derived neurotrophic factor and neurotrophin-3.
6 utants, but were less severe in mice lacking neurotrophin-3.
7 factor, brain-derived neurotrophic factor or neurotrophin-3.
8 phosphorylated ERK5 with MEF2 in response to neurotrophin-3.
9 Taken together, these results suggest that neurotrophin 3 activation of TrkC induces Schwann cell m
13 ligands, brain-derived neurotrophic factor, neurotrophin 3 and neurotrophin 4, are survival factors
14 mbination of basic fibroblast growth factor, neurotrophin-3 and brain derived growth factor delivered
15 ession of GDNF by glia and overexpression of neurotrophin-3 and neurotrophin-4 in muscle did not caus
20 oreactive brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 were detected in 22
21 TrkC, ie, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5, showed that immuno
23 FGF-2/Adts), nerve growth factor (NGF/Adts), neurotrophin-3, and the cell adhesion molecules N-cadher
24 enteric nervous system suggest that trkC and neurotrophin-3 are a major neurotrophin system in the ga
25 t that brain-derived neurotrophic factor and neurotrophin-3 are anterogradely transported from midbra
26 NGF, brain-derived neurotrophic factor, and neurotrophin-3 are likely to be sorted similarly and rel
28 tor receptors, namely, the trkC receptor for neurotrophin 3, as well as receptors for neurturin and g
30 associated viral vector (AAV) encoding human Neurotrophin-3 at a clinically-feasible time-point after
31 embryonic spinal cord tissue and delivery of neurotrophin-3 at the injury site further increased spin
33 inding of NGF equivalent to TrkA, maintained neurotrophin-3 binding equivalent to TrkC, and also boun
35 r survival were unaffected by the absence of neurotrophin-3 but neuronal survival was compromised so
37 sciatic nerves, is significantly enhanced by neurotrophin 3, but not by nerve growth factor or brain-
41 ial treatment with embryonic transplants and neurotrophin-3 can potentiate the effects of enriched ho
42 this possibility, we compared neuron loss in neurotrophin-3-deficient mice with that in nerve growth
44 abilized chABC in combination with sustained neurotrophin-3 delivery showed significant improvement i
46 ise in brain-derived neurotrophic factor and neurotrophin 3 during exercise, the increased growth pot
47 ic nerves of p75NTR-/- mice, indicating that neurotrophin 3 enhances cell migration through TrkC.
48 ons in brain-derived neurotrophic factor and neurotrophin 3 expression in muscle without appreciably
50 imulation with either nerve growth factor or neurotrophin-3 failed to evoke any changes in Kv1.3 func
52 nglion in vivo, and found that expression of neurotrophin-3 from the vector protected peripheral sens
53 rneal expressions of nerve growth factor and neurotrophin-3 genes were unchanged; receptor gene expre
54 e with a targeted disruption of the gene for neurotrophin-3 have 50% fewer neurons than those of wild
55 GF) and those in TrkC involved in binding to neurotrophin-3 have been mapped in this domain, the Trk
56 nervous system cells, fibroblasts expressing neurotrophin-3, hybridoma cells expressing inhibitory pr
58 ired availability of nerve growth factor and neurotrophin 3 in the sciatic nerve and significant prev
61 neurotrophic factor, nerve growth factor and neurotrophin-3 in the supernatant and increased intracel
63 The trkC locus encodes several receptors for neurotrophin-3, including the well studied full-length t
68 tide exchange factor (RhoGEF) that regulates neurotrophin-3-induced cell migration in Schwann cells.
71 nfusion also increased hippocampal levels of neurotrophin 3, insulin-like growth factor 1, and nerve
72 y expressed on all the follicle cells, while neurotrophin 3 is transiently expressed only in the cell
73 Taken together these results suggest that neurotrophin-3 is required for survival of some sympathe
79 ed brain-derived neurotrophic factor (BDNF), neurotrophin-3, neurotrophin-4, ciliary neurotrophic fac
80 eurons by brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-4, or glial-cell-line-deriv
83 e percentage of hSK1-positive cells, whereas neurotrophin 3 (NT-3) and glial cell line-derived neurot
84 ), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3) and neurotrophin 5 (NT-5) and basi
85 mice that overexpress neurotrophins NGF and neurotrophin 3 (NT-3) at high levels in skin have shown
87 suggested qualitatively different effects of neurotrophin 3 (NT-3) in cochlear innervation patterning
93 tional and structural synaptic regulation by neurotrophin 3 (NT-3), using the neuromuscular synapse a
96 r activity is composed of two neurotrophins, neurotrophin-3 (NT-3) and Brain-Derived Neurotrophic Fac
97 esence of fibroblast growth factor (FGF) and neurotrophin-3 (NT-3) and differentiate in the presence
100 have evaluated changes in the expression of neurotrophin-3 (NT-3) and its tyrosine kinase C (TrkC) r
105 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their receptors trkB and trkC,
106 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their respective high-affinity
108 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are hypothesized to play an import
109 neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) are potent chemotactic agents for
112 to synaptic plasticity, we examined whether neurotrophin-3 (NT-3) changed the number, size, vesicle
113 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) contribute to those trophic effect
114 he present investigation, we studied whether neurotrophin-3 (NT-3) contributes to the rescue of axoto
116 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) differ among rat strains exhibitin
117 se and transfer of anterogradely transported neurotrophin-3 (NT-3) from a presynaptic to a postsynapt
119 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have been localized to the sensory
121 een identified, the biological functions for neurotrophin-3 (NT-3) in early retinal development remai
124 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in the development of synaptic tra
127 To obtain insights into the expression of neurotrophin-3 (NT-3) in the mouse, we have utilized mic
128 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) into C7 lesion sites, we found bot
129 roinjection of nerve growth factor (NGF) and neurotrophin-3 (NT-3) into the rostral pontine tegmentum
136 actor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3) mRNA expression patterns in the at
138 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) mRNAs were revealed in OLGs in viv
139 neuron loss in nerve growth factor (NGF) and neurotrophin-3 (NT-3) null mutant mice have supported th
141 e effects of transgenic cellular delivery of neurotrophin-3 (NT-3) on morphological and functional di
143 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) on the dendritic complexity of lay
144 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) on the intraspinal regeneration of
145 neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) on trigeminal axon growth patterns
147 tral tegmental area (VTA) microinjections of neurotrophin-3 (NT-3) or brain-derived neurotrophic fact
148 Concurrently, lentiviral vectors expressing neurotrophin-3 (NT-3) or green fluorescent protein (GFP)
150 th was prevented by co-treatment with either neurotrophin-3 (NT-3) or nerve growth factor (NGF).
151 ecause neither nerve growth factor (NGF) nor neurotrophin-3 (NT-3) prevented NO-induced growth cone c
152 ent receptor potential channel M5 (TrpM5) or neurotrophin-3 (NT-3) project to defined clusters of glo
156 rlier work in our laboratory showed that the neurotrophin-3 (NT-3) receptor TrkC is activated by T. c
158 n the perirhinal cortex, although endogenous neurotrophin-3 (NT-3) regulates the expression of VGF in
163 ophins brain-derived neurotrophin (BDNF) and neurotrophin-3 (NT-3) synergistically enhance survival o
165 were treated with either saline or exogenous neurotrophin-3 (NT-3) to promote the survival of proprio
166 he present study, we evaluate the ability of neurotrophin-3 (NT-3) to protect neurons against the tox
168 in noise-exposed mice that local delivery of neurotrophin-3 (NT-3) to the round window niche, 24 hour
169 al perfusion technique for local delivery of neurotrophin-3 (NT-3) to various regions of developing X
170 y of NGF leads to axonal elongation, whereas neurotrophin-3 (NT-3) treatment leads to short branching
173 ascular endothelial growth factor (VEGF) and neurotrophin-3 (NT-3) were significantly elevated in fem
176 e injured axon was administered by injecting neurotrophin-3 (NT-3) within and beyond a cervical spina
177 sustained release of the neurotrophic factor neurotrophin-3 (NT-3) would support axonal plasticity in
178 erent neurons retrogradely transported [125I]neurotrophin-3 (NT-3), [125I]nerve growth factor (NGF),
179 neurons and thereby induces transcription of neurotrophin-3 (NT-3), a novel gene target of MEF2.
181 or brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derived neuro
182 Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4) activat
183 ns brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5) upo
184 ly brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5), co
188 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), are able to produce a long-lastin
189 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), are believed to be genuine molecu
190 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), are critical for the maintenance
191 phins, such as nerve growth factor (NGF) and neurotrophin-3 (NT-3), are essential for development, fu
192 that the endogenous neurotrophins, BDNF and neurotrophin-3 (NT-3), are transported anterogradely by
193 ntitative PCR (qPCR) to assay NTF expression-neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, a
196 brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3), but not nerve growth factor (NGF)
197 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), but not proinflammatory molecules
200 ic factor (BDNF), nerve-growth factor (NGF), neurotrophin-3 (NT-3), fibroblast growth factor-2 (FGF-2
201 Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), glial cell line-derived neurotrop
202 from the brain metastatic protein signature, neurotrophin-3 (NT-3), has a dual function of regulating
204 tors expressing nerve growth factor (NGF) or neurotrophin-3 (NT-3), neurons in the DRG were transduce
205 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and glial
206 ell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and their
207 1: brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), ciliary ne
208 F, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), tyrosine k
210 ophins, including nerve growth factor (NGF), neurotrophin-3 (NT-3), NT-4/5 and brain-derived neurotro
211 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4) results
212 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4), each at
213 , particularly nerve growth factor (NGF) and neurotrophin-3 (NT-3), play a role in the regulation of
214 to platelet-derived growth factor (PDGF) and neurotrophin-3 (NT-3), primary cultures of cortical olig
216 ure to brain-derived neurotrophic factor and neurotrophin-3 (NT-3), suggesting that the electrophysio
217 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), the cognate ligands for TrkA, Trk
218 se expression of the analogous neurotrophin, neurotrophin-3 (NT-3), was unaltered in the same irises.
219 by evidence that neurotrophins, particularly neurotrophin-3 (NT-3), which has been shown to promote s
220 , many of which are muscle afferents and are neurotrophin-3 (NT-3)-responsive, were severely decrease
229 t not acute, forms of synaptic modulation by neurotrophin-3 (NT-3): endocytosis of NT-3-receptor comp
230 coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5-20 mg . kg-1 . d-1, s.c.) during
232 roliferation and survival in the presence of neurotrophin 3 (NT3) and brain-derived neurotrophin fact
233 ides 1315-1412 show ligand responsiveness to neurotrophin 3 (NT3) and myelin-associated glycoprotein
235 on neurotrophins, however, has revealed that neurotrophin 3 (NT3) is critically involved in several a
238 ), platelet-derived growth factor (PDGF), or neurotrophin 3 (NT3) to clonal density cultures of corti
239 ), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4), is impli
240 ), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5).
243 We previously demonstrated that endogenous neurotrophin-3 (NT3) acting through the TrkC tyrosine ki
244 s, treatment with nerve growth factor (NGF), neurotrophin-3 (NT3) and glial-cell-line-derived neurotr
245 fication to probe cDNA arrays, we found that neurotrophin-3 (NT3) and trkB mRNA expression were reduc
246 , we report that embryonic overexpression of neurotrophin-3 (NT3) in muscles disrupts the development
247 s a specific downregulation in expression of neurotrophin-3 (NT3) in the transgenic cochleas before t
250 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) were identified in Schwann cell/dor
251 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3), act to enhance cell growth and bra
252 or (NGF), brain-derived neurotrophin (BDNF), neurotrophin-3 (NT3), and neurotrophin-4 (NT4)-and their
254 RT-PCR analyses, that TrkC, the receptor for neurotrophin-3 (NT3), is expressed by mouse perisynaptic
255 rophic factors nerve growth factor (NGF) and neurotrophin-3 (NT3), the actions of which must be execu
256 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3), to the tyrosine-kinase (Trk) recep
257 the neuromuscular junction (NMJ) induced by neurotrophin-3 (NT3), using Xenopus nerve-muscle co-cult
260 We show here that intramuscular delivery of neurotrophin-3 (NT3, encoded by NTF3) can induce sensori
261 rs (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT3; neurotrophin 4/5, NT4/5; or glial-d
263 ts of enriched environment, transplants, and neurotrophin-3 on the plasticity of synaptic structures
266 ed neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could pro
267 eric neurons along with recent evidence that neurotrophin-3 plays a role in the development of the en
268 neurotrophic factor, nerve growth factor, or neurotrophin-3 provided no protection of striatal output
271 cers, we identified in ACC expression of the neurotrophin-3 receptor TrkC/NTRK3, neural crest marker
272 y nerve growth factor receptor, or TrkC, the neurotrophin-3 receptor, and immunoreactive mPTPRO and T
273 mas, mouse tumors with reduced levels of the neurotrophin-3 receptor, trkC/Ntrk3, display decreased a
275 in growth factor-1, nerve growth factor, and neurotrophin 3 receptors in dorsal root ganglion cells.
276 ctor, brain-derived neurotrophic factor, and neurotrophin-3) regulate axonal mRNA levels and use dist
278 demonstrate that axonal growth triggered by neurotrophin-3 remotely inhibits neurite outgrowth throu
279 rs for brain-derived neurotrophic factor and neurotrophin-3, respectively) displayed a widespread dis
280 ically significant increase in cell death of neurotrophin-3-responsive and nonresponsive medulloblast
281 Brain-derived neurotrophic factor, but not neurotrophin-3, selectively regulated immunoglobulin dom
284 tin filaments, nerve growth factor (NGF) and neurotrophin-3 still induced growth cone protrusion and
286 ed higher brain-derived neurotrophic factor, neurotrophin 3, synapsin I, and GAP43 mRNA levels than t
289 ed vector containing the coding sequence for neurotrophin-3 to transduce sensory neurons of the rat d
295 s target myocyte enhancer factor 2 (MEF2) to neurotrophin-3/TrkC-induced medulloblastoma cell death.
297 microm), and large-(> 40 microm), neurones, neurotrophin-3 was seen in medium and small neurones, wh
298 -derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3
299 nnel, brain-derived neurotrophic factor, and neurotrophin 3) were also abnormal, in parallel with the
300 ons of brain-derived neurotrophic factor and neurotrophin 3, which stimulated neurite outgrowth from
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