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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 trations correlated with higher retention of neurotrophin-3.
9 phosphorylated ERK5 with MEF2 in response to neurotrophin-3.
10   Taken together, these results suggest that neurotrophin 3 activation of TrkC induces Schwann cell m
11             Previously, we demonstrated that neurotrophin 3 activation of TrkC inhibits Schwann cell
12                      Eliminating one or both neurotrophin-3 alleles in mice that lack nerve growth fa
13                                              Neurotrophin-3 also enhanced locomotor recovery.
14  ligands, brain-derived neurotrophic factor, neurotrophin 3 and neurotrophin 4, are survival factors
15 mbination of basic fibroblast growth factor, neurotrophin-3 and brain derived growth factor delivered
16 ession of GDNF by glia and overexpression of neurotrophin-3 and neurotrophin-4 in muscle did not caus
17 ition to modulate intracellular responses to neurotrophin-3 and/or nerve growth factor.
18 rain-derived neurotrophic factor (BDNF), and neurotrophins 3 and 4 (NT3 and NT4).
19 (NGF, brain-derived neurotrophic factor, and neurotrophin 3) and secrete NGF.
20 or (NGF), brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4.
21 FGF-2/Adts), nerve growth factor (NGF/Adts), neurotrophin-3, and the cell adhesion molecules N-cadher
22 enteric nervous system suggest that trkC and neurotrophin-3 are a major neurotrophin system in the ga
23 t that brain-derived neurotrophic factor and neurotrophin-3 are anterogradely transported from midbra
24                Our findings pave the way for Neurotrophin-3 as a therapy that treats the underlying c
25 tor receptors, namely, the trkC receptor for neurotrophin 3, as well as receptors for neurturin and g
26 nd brain-derived neurotrophic factor but not neurotrophin-3, as measured by ELISA.
27 associated viral vector (AAV) encoding human Neurotrophin-3 at a clinically-feasible time-point after
28 embryonic spinal cord tissue and delivery of neurotrophin-3 at the injury site further increased spin
29                                    In vitro, neurotrophin 3 binding to p75NTR increases neurite lengt
30 inding of NGF equivalent to TrkA, maintained neurotrophin-3 binding equivalent to TrkC, and also boun
31                       GM1 failed to displace neurotrophin-3 binding, suggesting that this ganglioside
32 r survival were unaffected by the absence of neurotrophin-3 but neuronal survival was compromised so
33                                  GM1 induced neurotrophin-3 (but not brain-derived neurotrophic facto
34 sciatic nerves, is significantly enhanced by neurotrophin 3, but not by nerve growth factor or brain-
35                   Furthermore, expression of neurotrophin-3, but not nerve growth factor, brain-deriv
36 id and significant increase in the amount of neurotrophin-3, but not other neurotrophins.
37                               Application of neurotrophin-3, but not related neurotrophins, prevented
38 ial treatment with embryonic transplants and neurotrophin-3 can potentiate the effects of enriched ho
39 this possibility, we compared neuron loss in neurotrophin-3-deficient mice with that in nerve growth
40 us, closely relating this mouse model to the neurotrophin-3-deficient one.
41 abilized chABC in combination with sustained neurotrophin-3 delivery showed significant improvement i
42  Excess brain-derived neurotrophic factor or neurotrophin-3 did not inhibit neurite outgrowth.
43 ise in brain-derived neurotrophic factor and neurotrophin 3 during exercise, the increased growth pot
44 ic nerves of p75NTR-/- mice, indicating that neurotrophin 3 enhances cell migration through TrkC.
45 ons in brain-derived neurotrophic factor and neurotrophin 3 expression in muscle without appreciably
46                  At the time of neuron loss, neurotrophin-3 expression, assayed with a lacZ reporter,
47 imulation with either nerve growth factor or neurotrophin-3 failed to evoke any changes in Kv1.3 func
48 C-expressing neurons and their dependence on neurotrophin-3 for survival.
49           The time constant for clearance of neurotrophin-3 from cochlear tissues was 38 h but neurot
50         We verified the sustained release of neurotrophin-3 from peptide-conjugated PEG hydrogels res
51 nglion in vivo, and found that expression of neurotrophin-3 from the vector protected peripheral sens
52   Based on the results, we overexpressed the neurotrophin-3 gene, NTF3, in the dorsal amygdala using
53 rneal expressions of nerve growth factor and neurotrophin-3 genes were unchanged; receptor gene expre
54                                              Neurotrophin-3 growth factor can improve cochlear neuron
55 e with a targeted disruption of the gene for neurotrophin-3 have 50% fewer neurons than those of wild
56 GF) and those in TrkC involved in binding to neurotrophin-3 have been mapped in this domain, the Trk
57 nervous system cells, fibroblasts expressing neurotrophin-3, hybridoma cells expressing inhibitory pr
58 thelial growth factor A, angiopoietin 1, and neurotrophin 3 in the ischemic muscle.
59 ired availability of nerve growth factor and neurotrophin 3 in the sciatic nerve and significant prev
60 y system that can allow localized release of neurotrophin-3 in a controlled and sustained manner.
61         Here, we demonstrate a novel role of neurotrophin-3 in synaptic assembly and function as a po
62 th factor (NGF), or antibody inactivation of neurotrophin-3 in the presence of NGF.
63 neurotrophic factor, nerve growth factor and neurotrophin-3 in the supernatant and increased intracel
64 on of neurotrophins (nerve growth factor and neurotrophin-3) in FAP nerves.
65 The trkC locus encodes several receptors for neurotrophin-3, including the well studied full-length t
66                                  In culture, neurotrophin-3 increases the survival of proliferating s
67 n, and brain-derived neurotrophic factor and neurotrophin-3 induced cellular maturation.
68 RK5 activator, MEK5, significantly inhibited neurotrophin-3-induced cell death.
69                            Additionally, the neurotrophin-3-induced cell migration depended on Rho GT
70 tide exchange factor (RhoGEF) that regulates neurotrophin-3-induced cell migration in Schwann cells.
71                                          The neurotrophin-3-induced cell migration was also observed
72 , whereas TrkC receptors are responsible for neurotrophin-3 inhibition.
73 nfusion also increased hippocampal levels of neurotrophin 3, insulin-like growth factor 1, and nerve
74 y expressed on all the follicle cells, while neurotrophin 3 is transiently expressed only in the cell
75    Taken together these results suggest that neurotrophin-3 is required for survival of some sympathe
76                                In transgenic neurotrophin-3 lacZ-neo (NT-3(lacZneo)) mice, in which t
77 richia coli lacZ gene is integrated into the neurotrophin-3 locus (NT-3(lacZneo)).
78                                              Neurotrophin-3 mRNA levels decrease in the hippocampus f
79 hippocampal neurons inversely correlate with neurotrophin-3 mRNA levels.
80 ts in an increase in miR21 and a decrease in neurotrophin-3 mRNA.
81 ed brain-derived neurotrophic factor (BDNF), neurotrophin-3, neurotrophin-4, ciliary neurotrophic fac
82 eurons by brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-4, or glial-cell-line-deriv
83                                              Neurotrophin-3 normalized the short latency Hoffmann ref
84                                              Neurotrophin-3 not only enhanced ERK5 phosphorylation bu
85 e percentage of hSK1-positive cells, whereas neurotrophin 3 (NT-3) and glial cell line-derived neurot
86  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
88                       Essential functions of neurotrophin 3 (NT-3) in regulating afferent and efferen
89  Tie2 also exhibit a chemotactic response to neurotrophin 3 (NT-3), a specific ligand for TrkC.
90                     ADNF causes secretion of neurotrophin 3 (NT-3), and both proteins regulate NMDA r
91 nd neonatal mice with mutations in the BDNF, neurotrophin 3 (NT-3), and TrkC genes.
92 tional and structural synaptic regulation by neurotrophin 3 (NT-3), using the neuromuscular synapse a
93 mpounds have been identified that potentiate neurotrophin 3 (NT-3)-mediated activation of trk A.
94  also be activated by high concentrations of neurotrophin 3 (NT-3).
95 r activity is composed of two neurotrophins, neurotrophin-3 (NT-3) and Brain-Derived Neurotrophic Fac
96 esence of fibroblast growth factor (FGF) and neurotrophin-3 (NT-3) and differentiate in the presence
97                            Administration of neurotrophin-3 (NT-3) and insulin-like growth factor-I (
98                                              Neurotrophin-3 (NT-3) and its high-affinity receptor Trk
99  have evaluated changes in the expression of neurotrophin-3 (NT-3) and its tyrosine kinase C (TrkC) r
100                         The binding sites of neurotrophin-3 (NT-3) and nerve growth factor (NGF) to t
101                               The effects of neurotrophin-3 (NT-3) and NT-4/5 on the function of axot
102 metics 1 were designed to mimic hot spots of neurotrophin-3 (NT-3) and others.
103 d to p75NTR and the 2:2 symmetric complex of neurotrophin-3 (NT-3) and p75NTR.
104 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their receptors trkB and trkC,
105 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their respective high-affinity
106                              Animals lacking neurotrophin-3 (NT-3) are born with deficits in almost a
107 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are hypothesized to play an import
108  neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) are potent chemotactic agents for
109                Nerve growth factor (NGF) and neurotrophin-3 (NT-3) are target-derived proteins that r
110           Similar effects were observed with neurotrophin-3 (NT-3) but not nerve growth factor.
111  to synaptic plasticity, we examined whether neurotrophin-3 (NT-3) changed the number, size, vesicle
112 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) contribute to those trophic effect
113 he present investigation, we studied whether neurotrophin-3 (NT-3) contributes to the rescue of axoto
114 brain-derived neurotrophin factor (BDNF) and neurotrophin-3 (NT-3) did not induce cell death.
115 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) differ among rat strains exhibitin
116 se and transfer of anterogradely transported neurotrophin-3 (NT-3) from a presynaptic to a postsynapt
117                   Removal of the TrkC ligand neurotrophin-3 (NT-3) from cerebellar granule cells, whi
118 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have been localized to the sensory
119 een identified, the biological functions for neurotrophin-3 (NT-3) in early retinal development remai
120 ld-type and transgenic mice that overexpress neurotrophin-3 (NT-3) in muscle (myo/NT-3 mice).
121        To clarify the role of muscle-derived neurotrophin-3 (NT-3) in the development of sensory neur
122 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in the development of synaptic tra
123       Here, we report that overexpression of neurotrophin-3 (NT-3) in the eye accelerates RGC laminar
124             We show that genetic ablation of neurotrophin-3 (NT-3) in the mouse neocortex results in
125    To obtain insights into the expression of neurotrophin-3 (NT-3) in the mouse, we have utilized mic
126 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) into C7 lesion sites, we found bot
127 roinjection of nerve growth factor (NGF) and neurotrophin-3 (NT-3) into the rostral pontine tegmentum
128                                              Neurotrophin-3 (NT-3) is a cystine knot growth factor th
129                                              Neurotrophin-3 (NT-3) is a member of the neurotrophin fa
130                                              Neurotrophin-3 (NT-3) is expressed specifically in cells
131                                        Since neurotrophin-3 (NT-3) is highly expressed in non-neural
132                                              Neurotrophin-3 (NT-3) is known to promote enteric neuron
133                               Interestingly, neurotrophin-3 (NT-3) is upregulated in the brains of wi
134 edicted to target (and thus inhibit) NGF and neurotrophin-3 (NT-3) mRNA.
135 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) mRNAs were revealed in OLGs in viv
136  (STZ)-diabetic rats and examined effects of neurotrophin-3 (NT-3) on diabetes-induced events.
137 e effects of transgenic cellular delivery of neurotrophin-3 (NT-3) on morphological and functional di
138                To investigate the effects of neurotrophin-3 (NT-3) on postnatal proprioceptive neuron
139 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) on the dendritic complexity of lay
140 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) on the intraspinal regeneration of
141  neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) on trigeminal axon growth patterns
142                           Addition of either neurotrophin-3 (NT-3) or BDNF increases axon growth and
143 tral tegmental area (VTA) microinjections of neurotrophin-3 (NT-3) or brain-derived neurotrophic fact
144  Concurrently, lentiviral vectors expressing neurotrophin-3 (NT-3) or green fluorescent protein (GFP)
145                                 Mice lacking neurotrophin-3 (NT-3) or its receptor, TrkC, lose many s
146 th was prevented by co-treatment with either neurotrophin-3 (NT-3) or nerve growth factor (NGF).
147 ecause neither nerve growth factor (NGF) nor neurotrophin-3 (NT-3) prevented NO-induced growth cone c
148 ent receptor potential channel M5 (TrpM5) or neurotrophin-3 (NT-3) project to defined clusters of glo
149                                              Neurotrophin-3 (NT-3) promotes enteric neuronal developm
150                                   Endogenous neurotrophin-3 (NT-3) protein is present in the ganglion
151                   Elevated expression of the neurotrophin-3 (NT-3) receptor TrkC by childhood medullo
152 rlier work in our laboratory showed that the neurotrophin-3 (NT-3) receptor TrkC is activated by T. c
153                     Here, we investigate how neurotrophin-3 (NT-3) regulates DA cell density in the m
154 n the perirhinal cortex, although endogenous neurotrophin-3 (NT-3) regulates the expression of VGF in
155 on site if axons are guided by a gradient of neurotrophin-3 (NT-3) rostral to the lesion.
156                                              Neurotrophin-3 (NT-3) signaling has been shown to be req
157                                              Neurotrophin-3 (NT-3) supported striking terminal arbori
158                                              Neurotrophin-3 (NT-3) supports the survival and differen
159 ophins brain-derived neurotrophin (BDNF) and neurotrophin-3 (NT-3) synergistically enhance survival o
160 ously reported that retrogradely transported neurotrophin-3 (NT-3) to lumbar MNs attenuated SCI-induc
161                               The ability of neurotrophin-3 (NT-3) to prevent abnormalities in neurof
162 were treated with either saline or exogenous neurotrophin-3 (NT-3) to promote the survival of proprio
163 he present study, we evaluate the ability of neurotrophin-3 (NT-3) to protect neurons against the tox
164                                  Addition of neurotrophin-3 (NT-3) to the culture medium rescued some
165 in noise-exposed mice that local delivery of neurotrophin-3 (NT-3) to the round window niche, 24 hour
166 al perfusion technique for local delivery of neurotrophin-3 (NT-3) to various regions of developing X
167 y of NGF leads to axonal elongation, whereas neurotrophin-3 (NT-3) treatment leads to short branching
168  and neurotrophin-4/5 (NT-4/5) via TrkB, and neurotrophin-3 (NT-3) via TrkC.
169                     Finally, potentiation by neurotrophin-3 (NT-3) was also target specific.
170 ascular endothelial growth factor (VEGF) and neurotrophin-3 (NT-3) were significantly elevated in fem
171                Lentiviral vectors expressing neurotrophin-3 (NT-3) were then injected into an appropr
172 e injured axon was administered by injecting neurotrophin-3 (NT-3) within and beyond a cervical spina
173 sustained release of the neurotrophic factor neurotrophin-3 (NT-3) would support axonal plasticity in
174 erent neurons retrogradely transported [125I]neurotrophin-3 (NT-3), [125I]nerve growth factor (NGF),
175 neurons and thereby induces transcription of neurotrophin-3 (NT-3), a novel gene target of MEF2.
176 effect of this s-ODN on subsequent Fos, NGF, neurotrophin-3 (NT-3), and actin expression.
177 or brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derived neuro
178 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial cell line-derived neuro
179    Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4) activat
180 ns brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5) upo
181 ly brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5), co
182 retion of brain-derived neurotrophic factor, neurotrophin-3 (NT-3), and neurotrophin-4/5.
183         IYIY-I2-BODIPY binds TrkC similar to neurotrophin-3 (NT-3), and NT-3 has been reported to mod
184 ng brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4.
185 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), are believed to be genuine molecu
186 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), are critical for the maintenance
187 phins, such as nerve growth factor (NGF) and neurotrophin-3 (NT-3), are essential for development, fu
188  that the endogenous neurotrophins, BDNF and neurotrophin-3 (NT-3), are transported anterogradely by
189 ntitative PCR (qPCR) to assay NTF expression-neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, a
190         In this study, fibroblasts producing neurotrophin-3 (NT-3), brain-derived neurotrophic factor
191  brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3), but not nerve growth factor (NGF)
192 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), but not proinflammatory molecules
193          We have shown previously that BDNF, neurotrophin-3 (NT-3), chlorphenylthio-cAMP (cpt-cAMP) (
194                               We report that neurotrophin-3 (NT-3), delivered chronically via fibrobl
195 ic factor (BDNF), nerve-growth factor (NGF), neurotrophin-3 (NT-3), fibroblast growth factor-2 (FGF-2
196    Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), glial cell line-derived neurotrop
197 from the brain metastatic protein signature, neurotrophin-3 (NT-3), has a dual function of regulating
198           Neurotrophic factors, particularly neurotrophin-3 (NT-3), may increase the regenerative cap
199 tors expressing nerve growth factor (NGF) or neurotrophin-3 (NT-3), neurons in the DRG were transduce
200 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and glial
201 ell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and their
202 1: brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), ciliary ne
203 F, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), tyrosine k
204 ic neurotrophins [nerve growth factor (NGF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4)].
205 ophins, including nerve growth factor (NGF), neurotrophin-3 (NT-3), NT-4/5 and brain-derived neurotro
206 ), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4) results
207 to platelet-derived growth factor (PDGF) and neurotrophin-3 (NT-3), primary cultures of cortical olig
208 nar release of nerve growth factor (NGF) and neurotrophin-3 (NT-3), respectively.
209 ure to brain-derived neurotrophic factor and neurotrophin-3 (NT-3), suggesting that the electrophysio
210 rain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), the cognate ligands for TrkA, Trk
211 se expression of the analogous neurotrophin, neurotrophin-3 (NT-3), was unaltered in the same irises.
212 by evidence that neurotrophins, particularly neurotrophin-3 (NT-3), which has been shown to promote s
213  signals in response to two ligands, NGF and neurotrophin-3 (NT-3), with very different functional co
214 , many of which are muscle afferents and are neurotrophin-3 (NT-3)-responsive, were severely decrease
215 es of podocytes treated with the TrkC ligand neurotrophin-3 (Nt-3).
216  cones of forebrain neurons is stimulated by neurotrophin-3 (NT-3).
217  gradient of collapsin-1/semaphorin III/D or neurotrophin-3 (NT-3).
218 ons in p75NTR, nerve growth factor (NGF) and neurotrophin-3 (NT-3).
219 lcholine, but not for the turning induced by neurotrophin-3 (NT-3).
220 in resting membrane potential (RMP) or added neurotrophin-3 (NT-3).
221 ophins such as nerve growth factor (NGF) and neurotrophin-3 (NT-3).
222 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3).
223 ions as an active protein tyrosine kinase by neurotrophin-3 (NT-3).
224 t not acute, forms of synaptic modulation by neurotrophin-3 (NT-3): endocytosis of NT-3-receptor comp
225  coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5-20 mg . kg-1 . d-1, s.c.) during
226                                              Neurotrophin 3 (NT3) ablation in mice causes a more seve
227 roliferation and survival in the presence of neurotrophin 3 (NT3) and brain-derived neurotrophin fact
228 ides 1315-1412 show ligand responsiveness to neurotrophin 3 (NT3) and myelin-associated glycoprotein
229                 The selective elimination of neurotrophin 3 (NT3) from muscle spindles had no effect
230 on neurotrophins, however, has revealed that neurotrophin 3 (NT3) is critically involved in several a
231                 Recent studies indicate that neurotrophin 3 (NT3) may be important for the maintenanc
232 ), platelet-derived growth factor (PDGF), or neurotrophin 3 (NT3) to clonal density cultures of corti
233 ), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4), is impli
234 ), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4).
235 ), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5).
236 ey also express neurotrophins NGF, BDNF, and neurotrophin 3 (NT3).
237                                              Neurotrophin-3 (NT3) acting through the TrkC receptor ty
238   We previously demonstrated that endogenous neurotrophin-3 (NT3) acting through the TrkC tyrosine ki
239 s, treatment with nerve growth factor (NGF), neurotrophin-3 (NT3) and glial-cell-line-derived neurotr
240 fication to probe cDNA arrays, we found that neurotrophin-3 (NT3) and trkB mRNA expression were reduc
241 , we report that embryonic overexpression of neurotrophin-3 (NT3) in muscles disrupts the development
242 s a specific downregulation in expression of neurotrophin-3 (NT3) in the transgenic cochleas before t
243               In the chick embryo, exogenous neurotrophin-3 (NT3) is sufficient to promote the differ
244                                              Neurotrophin-3 (NT3) plays a key role in the development
245                             We show that the neurotrophin-3 (NT3) TrkCT1-truncated receptor binds to
246 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) were identified in Schwann cell/dor
247 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3), act to enhance cell growth and bra
248 or (NGF), brain-derived neurotrophin (BDNF), neurotrophin-3 (NT3), and neurotrophin-4 (NT4)-and their
249                                 We expressed neurotrophin-3 (NT3), deoxyribonuclease (DNase), or vasc
250 RT-PCR analyses, that TrkC, the receptor for neurotrophin-3 (NT3), is expressed by mouse perisynaptic
251 rophic factors nerve growth factor (NGF) and neurotrophin-3 (NT3), the actions of which must be execu
252 brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3), to the tyrosine-kinase (Trk) recep
253  the neuromuscular junction (NMJ) induced by neurotrophin-3 (NT3), using Xenopus nerve-muscle co-cult
254                            Here we show that neurotrophin-3 (NT3)-induced potentiation of synaptic tr
255    One necessary factor for these neurons is neurotrophin-3 (NT3).
256  We show here that intramuscular delivery of neurotrophin-3 (NT3, encoded by NTF3) can induce sensori
257                                              Neurotrophin-3 (Ntf3) and brain derived neurotrophic fac
258               Together, these data implicate neurotrophin-3/NTRK3 signaling in the dorsal amygdala in
259 ts of enriched environment, transplants, and neurotrophin-3 on the plasticity of synaptic structures
260 th BDNF during activity blockade, but not by neurotrophin 3 or nerve growth factor.
261 sponse to brain-derived neurotrophic factor, neurotrophin 3, or neurotrophin 4/5.
262 ed neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could pro
263 eric neurons along with recent evidence that neurotrophin-3 plays a role in the development of the en
264 hydrogels with affinity peptides specific to neurotrophin-3 proteins.
265 GFbetaR), TEL/Janus kinase 2 (JAK2), and TEL/neurotrophin-3 receptor (TRKC).
266  PTK (protein-tyrosine kinase) domain of the neurotrophin-3 receptor NTRK3.
267 cers, we identified in ACC expression of the neurotrophin-3 receptor TrkC/NTRK3, neural crest marker
268 y nerve growth factor receptor, or TrkC, the neurotrophin-3 receptor, and immunoreactive mPTPRO and T
269 mas, mouse tumors with reduced levels of the neurotrophin-3 receptor, trkC/Ntrk3, display decreased a
270                            Expression of the neurotrophin-3 receptor, tyrosine kinase C (TrkC), is as
271 in growth factor-1, nerve growth factor, and neurotrophin 3 receptors in dorsal root ganglion cells.
272 ctor, brain-derived neurotrophic factor, and neurotrophin-3) regulate axonal mRNA levels and use dist
273                                     Finally, neurotrophin 3 released from muscle spindles regulates t
274 trophin-3 from cochlear tissues was 38 h but neurotrophin-3 remained detectable for at least 2 weeks.
275  demonstrate that axonal growth triggered by neurotrophin-3 remotely inhibits neurite outgrowth throu
276 ically significant increase in cell death of neurotrophin-3-responsive and nonresponsive medulloblast
277 e a radioactive tracer was used to determine neurotrophin-3 retention, distribution and clearance aft
278   Brain-derived neurotrophic factor, but not neurotrophin-3, selectively regulated immunoglobulin dom
279                Nerve growth factor (NGF) and neurotrophin-3 serve as attractive cues for chick embryo
280          MiR21 is a candidate for regulating neurotrophin-3 signaling in the hippocampus following st
281 tin filaments, nerve growth factor (NGF) and neurotrophin-3 still induced growth cone protrusion and
282                  Additionally, human NGF and neurotrophin-3 stimulated c-Yes in brain-metastatic 70W
283 ed higher brain-derived neurotrophic factor, neurotrophin 3, synapsin I, and GAP43 mRNA levels than t
284 ified a miR21 binding site, in the 3' UTR of neurotrophin-3 that inhibits translation.
285 hat the binding is specifically inhibited by neurotrophin-3, the natural TrkC ligand.
286 ed vector containing the coding sequence for neurotrophin-3 to transduce sensory neurons of the rat d
287  had no effect on TrkB or TrkC activation in neurotrophin 3 treatment.
288 phic factor and neurotrophin-4/5 (trkB), and neurotrophin-3 (trkC).
289 NA encoding the receptor tyrosine kinase for neurotrophin-3, TrkC, were unchanged.
290        Our investigation of the mechanism of neurotrophin-3/TrkC-induced apoptosis has identified a n
291                                              Neurotrophin-3/TrkC-induced apoptosis is inhibited by th
292 s target myocyte enhancer factor 2 (MEF2) to neurotrophin-3/TrkC-induced medulloblastoma cell death.
293                                              Neurotrophin-3 was evident in the semi-circular canals w
294                                       (125)I-neurotrophin-3 was injected into guinea pig cochleae usi
295 rograde transport of nerve growth factor and neurotrophin-3 was not evident.
296  microm), and large-(> 40 microm), neurones, neurotrophin-3 was seen in medium and small neurones, wh
297                              Distribution of neurotrophin-3 was widespread throughout the cochlear ti
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
301 drogel formulation for localized delivery of neurotrophin-3, which provides affinity-controlled relea

 
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