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1 -term enhancement of presynaptic function by neurotrophin.
2 in the biological responses induced by this neurotrophin.
3 neuronal differentiation in response to this neurotrophin.
4 s to release anti-inflammatory cytokines and neurotrophins.
5 ithelia are the key endogenous source of the neurotrophins.
6 ear factor-kappaB (NF-kappaB) pathway by the neurotrophins.
7 DCVs for future release of neuropeptides and neurotrophins.
9 ), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4), is impli
13 nfusion also increased hippocampal levels of neurotrophin 3, insulin-like growth factor 1, and nerve
14 ons of brain-derived neurotrophic factor and neurotrophin 3, which stimulated neurite outgrowth from
19 ent receptor potential channel M5 (TrpM5) or neurotrophin-3 (NT-3) project to defined clusters of glo
20 in noise-exposed mice that local delivery of neurotrophin-3 (NT-3) to the round window niche, 24 hour
22 ntitative PCR (qPCR) to assay NTF expression-neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, a
23 from the brain metastatic protein signature, neurotrophin-3 (NT-3), has a dual function of regulating
26 We show here that intramuscular delivery of neurotrophin-3 (NT3, encoded by NTF3) can induce sensori
29 t that brain-derived neurotrophic factor and neurotrophin-3 are anterogradely transported from midbra
31 associated viral vector (AAV) encoding human Neurotrophin-3 at a clinically-feasible time-point after
35 cers, we identified in ACC expression of the neurotrophin-3 receptor TrkC/NTRK3, neural crest marker
36 demonstrate that axonal growth triggered by neurotrophin-3 remotely inhibits neurite outgrowth throu
38 hic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4), is implicated in the physiology of
39 roblast growth factor-4, CX3CL1/fractalkine, neurotrophin 4 oncostatin-M, pulmonary and activation-re
40 ration of the endogenous TrkB agonist ligand neurotrophin-4 (NT-4) profoundly decreases food intake a
41 brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4) have different developmental roles
42 ived neurotrophic factor (BDNF) is an active neurotrophin abundantly expressed throughout the nervous
44 Huh7 human hepatocyte cells showed that the neurotrophins activate the sterol regulatory element-bin
46 roteasome activator IU1, suggesting that the neurotrophin acts by decreasing proteasome activity.
47 roles, how BDNF, or more generally speaking, neurotrophins affect synapses, particularly nerve termin
49 , long-term potentiation and depression, and neurotrophin and retrograde endocannabinoid signaling.
52 hese findings reveal a non-neuronal role for neurotrophins and identify a new regulatory pathway in i
53 used by altered expression of genes encoding neurotrophins and ion channels, and altered activity of
54 serum markers of inflammation, and levels of neurotrophins and neurotransmitters, but the BL group ha
55 ittermates, notably in the downregulation of neurotrophins and their cognate neurotrophin receptors a
58 f HNE were not associated with production of neurotrophins and were unaffected by pretreatment with a
59 found that a few hours of treatment with the neurotrophin (and to a lower extent with basic FGF and E
60 t in Drosophila melanogaster pro- and mature neurotrophins are capable of inducing death and survival
62 e kinase on mouse neuroblastoma cells by the neurotrophin artemin (ART) is quantitatively coupled to
64 or a given reward and that expression of the neurotrophin BDNF in the mOFC is both necessary and suff
67 -Pep5) and in mice lacking the extracellular neurotrophin binding site of p75 neurotrophin receptor.
71 , we silenced the neuroplasticity-associated neurotrophin brain-derived neurotrophic factor (BDNF).
74 s ideal for examining this issue because the neurotrophins brain-derived neurotrophic factor (BDNF) a
75 on's disease (HD), controls transport of the neurotrophin, brain-derived neurotrophic factor (BDNF),
76 ic ligands (i.e., proneurotrophins or mature neurotrophins), but several of the intracellular adaptor
77 Neurons release neuropeptides, enzymes, and neurotrophins by exocytosis of dense-core vesicles (DCVs
82 ologic inhibition of Trk signaling decreases neurotrophin-dependent ERK activation and BTIC growth.
85 ivating insults ranging from nerve injury to neurotrophin deprivation result in both c-Jun N-terminal
88 or tissue-based stem cells, cell fusion, and neurotrophin elaboration--offer renewed hope for develop
89 ion efficacy was improved when combined with neurotrophins, elevation of cyclic AMP levels, olfactory
91 oreceptor apoptosis, gliosis, and changes in neurotrophin expression, and it preserved the photorespo
92 nstroke mice did not alter motor behavior or neurotrophin expression, suggesting that the prorecovery
93 A for neurotrophins, including brain-derived neurotrophin factor (BNDF), was decreased following ION
95 ived neurotrophic factor) is a member of the neurotrophin family and it is implicated in regulating b
96 brain-derived neurotrophic factor (BDNF), a neurotrophin family member which is known to promote tum
98 neurotrophic factor (BDNF), a member of the neurotrophin family, regulates both survival and differe
101 fects of adeno-associated virus vectors with neurotrophin gene inserts, AAV.BDNF and AAV.Ntf3, on gui
102 th in healthy immature brains by unbalancing neurotrophin homeostasis via p75 neurotrophin receptor s
104 evidence supporting a critical role for this neurotrophin in physiological mechanisms regulating nutr
105 d provide evidence for a global role of this neurotrophin in the homeostasis of the organism by signa
106 ions per year attests to the significance of neurotrophins in biomedical sciences and underlines thei
108 property of NaPB that may be used to augment neurotrophins in the CNS and improve synaptic function i
109 s increased expression of activity-dependent neurotrophins in the contralesional cortex, including br
110 vailability make exogenous administration of neurotrophins in vivo problematic; therefore, alternativ
114 a feedforward loop, whereby upregulation of neurotrophins increases sympathetic innervation and loca
115 rally occurring death period, neurons become neurotrophin-independent and, further, that this develop
116 etary salt can affect blood pressure through neurotrophin-induced plasticity in a central homeostatic
117 for limiting neurotrophic support, and local neurotrophin insufficiency triggers caspase-dependent ax
119 However, pharmacological modulation of this neurotrophin is challenging because BDNF is generated by
121 el a new role for BDNF, suggesting that this neurotrophin is necessary and sufficient to maintain the
125 ts demonstrate that a transient elevation in neurotrophin levels can sustain the cochlear neural subs
129 accharides exhibited increased activation of neurotrophin-mediated signaling pathways and enhanced ax
134 ast in part to a reduction in the endogenous neurotrophin (NT) supply, normally provided by hair cell
135 ound that postnatal ASM innervation required neurotrophin (NT)-4 signaling through the TrkB receptor
139 mental insight into the effects of exogenous neurotrophins on a degenerating neural system, and for t
142 s amyloid-beta (Abeta) and the precursors of neurotrophins, outbalance neurotrophic signals, causing
143 at supporting cells influence the outcome of neurotrophin over-expression aimed at enhancing the coch
146 These results indicate that glial-derived neurotrophins play critical roles in inner ear synapse d
147 ntial loss of cochlear hair cells, exogenous neurotrophins prevent degeneration of the auditory nerve
148 lausible therapeutic target because neuronal neurotrophin production is aberrant in AD and other neur
150 r regions that include genes associated with neurotrophins, programmed cell death, synaptic function,
151 gulated intramembrane proteolysis of the p75 neurotrophin receptor (also known as p75 cleavage).
152 is and recent evidence suggests that the p75 neurotrophin receptor (NTR) contributes significantly to
153 while down-regulating the expression of p75 neurotrophin receptor (NTR), phospho-JNK, and Bcl-2-asso
155 TAp73 is a transcriptional activator of p75 neurotrophin receptor (p75(NTR)) and that p75(NTR) mRNA
156 trophic factor (BDNF)-activated TrkB and p75 neurotrophin receptor (p75(NTR)) by disrupting the endos
161 rve growth factor (NGF) signaling by the p75 neurotrophin receptor (p75(NTR)) is critical for neurona
162 distinct structural determinants in the p75 neurotrophin receptor (p75(NTR)) is crucial for the iden
167 uctures of complexes formed by the DD of p75 neurotrophin receptor (p75(NTR)) with RhoGDI, for activa
168 This produced a substantial loss of both p75 neurotrophin receptor (p75(NTR))-positive and choline ac
172 ur goal was to determine the role of the p75 neurotrophin receptor (p75NTR) in the loss of islet symp
173 myelin-associated glycoprotein recruited p75 neurotrophin receptor (p75NTR) into a complex with LRP1
175 Plasticity was rescued by inhibiting p75 neurotrophin receptor (p75NTR) signaling or its downstre
176 drinking produces a mobilization of DLS p75 neurotrophin receptor (p75NTR), whose activities oppose
180 ed a mouse model with a mutation in the TrkA neurotrophin receptor (P782S) that results in reduced ub
181 hibition of the cell death domain of the p75 neurotrophin receptor (TAT-Pep5) and in mice lacking the
182 udies provide a new reagent for altering p75 neurotrophin receptor actions after injury and suggest t
185 growth factor (NGF) in complex with the p75 neurotrophin receptor but is distinct from that of micro
186 lus propofol applications at the peak of p75 neurotrophin receptor expression after experimental trau
187 ricted to the developing nervous system when neurotrophin receptor expression peaks, indicate that BI
189 developmental-like programs and increase p75 neurotrophin receptor expression, probably to foster rep
190 S-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40
195 aline residue at position 264 in the rat p75 neurotrophin receptor is necessary for the ability of p7
197 compound, EVT901, which interferes with p75 neurotrophin receptor oligomerization through direct int
204 kinase TrkA (also called NTRK1), the common neurotrophin receptor p75(NTR), and the proneurotrophin
205 ability of SorCS2 to form complexes with the neurotrophin receptor p75(NTR), required for pro-brain-d
208 same set of transcription factors from a p75 neurotrophin receptor peptide (p75NTRp)-tagged adenoviru
209 indicate that the ubiquitination of the TrkA neurotrophin receptor plays a critical role in NGF-media
211 sults revealed new functions for proBDNF-p75 neurotrophin receptor signaling pathway in the control o
213 re, we demonstrate that EVT901 abrogates p75 neurotrophin receptor signalling by other ligands, such
216 cate that UCH-L1 is important for regulating neurotrophin receptor sorting to signaling endosomes and
217 that LRP1 activation could phosphorylate the neurotrophin receptor TrkA in PC12 cells and increase ne
218 rs of the neural crest and expression of the neurotrophin receptor TrkB and its ligand, brain-derived
219 -ERK-CREB-BDNF pathway as pre-treatment with neurotrophin receptor TrkB inhibitor ANA-12 and MEK inhi
224 e, nicotinic acetylcholine receptor, and p75 neurotrophin receptor), thus demonstrating that pseudoty
226 or induced apoptosis in cells expressing p75 neurotrophin receptor, and enhances neurite outgrowth in
227 es binding of pro-nerve growth factor to p75 neurotrophin receptor, blocks pro-nerve growth factor in
228 ceptor B (trkB) and a truncated form of this neurotrophin receptor, favoring the inactive form throug
230 rats by the recruitment of the low-affinity neurotrophin receptor, p75NTR, whose activities opposes
233 assays with cysteine-rich domains-fused p75 neurotrophin receptor, we confirmed that EVT901 interfer
234 library for genes affecting the dynamics of neurotrophin receptor-containing endosomes in motor neur
239 ng cells (BTICs) and show that BTICs express neurotrophin receptors (p75NTR, TrkA, TrkB, and TrkC) an
240 egulation of neurotrophins and their cognate neurotrophin receptors among other classes of transcript
244 hat Toll paralogs unrelated to the mammalian neurotrophin receptors function as neurotrophin receptor
246 dings indicate that intracellular sorting of neurotrophin receptors is critical for postnatal neuroge
247 ss sensory neuron-associated markers such as neurotrophin receptors TrkA, TrkB, TrkC, and RET and the
249 om fresh human malignant gliomas express the neurotrophin receptors TrkB and TrkC, not TrkA, and they
250 and increasing the co-localisation of these neurotrophin receptors with retromer-associated sorting
253 t control transcription are coordinated with neurotrophin-regulated actions that transpire in the axo
254 e neuroD1 differentiation marker and BDNF, a neurotrophin required for the terminal differentiation o
255 theless, the poor pharmacokinetic profile of neurotrophins severely restricts their clinical use.
256 s an essential scaffold protein coordinating neurotrophin signal pathways in neurites and is spatiall
258 s provide new insight into synaptic roles of neurotrophin signaling and mechanisms controlling synapt
259 iguing link between Abeta catabolism and pro-neurotrophin signaling converging on this receptor.
260 rneurons is disrupted due to a deficiency in neurotrophin signaling during early development in FXS.
263 ns: instead, SAD-A/B functions downstream of neurotrophin signaling in sensory neurons to mediate a l
264 provides new insight into the involvement of neurotrophin signaling in synapse development and plasti
265 by activation of neurotrophin signaling, and neurotrophin signaling is sufficient for long term BTIC
267 n ACC a previously unrecognized pro-survival neurotrophin signaling pathway and link it with cancer p
268 results demonstrate the existence of a novel neurotrophin signaling pathway that is required for syna
270 cules of the transcriptional program linking neurotrophin signaling to sensory neuronal differentiati
271 f neuronal IL-4 receptors, which potentiated neurotrophin signaling via the AKT and MAPK pathways.
272 neurotrophic factor (BDNF) levels, impaired neurotrophin signaling, and compromised mitochondrial fu
273 nhibitors could be overcome by activation of neurotrophin signaling, and neurotrophin signaling is su
274 ing of Trk-family receptor tyrosine kinases, neurotrophin signaling, and possibly neuronal differenti
277 ression peaks, indicate that BICD1 regulates neurotrophin signalling by modulating the endosomal sort
279 Genetic interactions also revealed that the neurotrophin Spatzle3 (Spz3) is a likely Tollo ligand.
281 ation provides a mechanism whereby sustained neurotrophin stimulation can be integrated over time, so
284 to elevate cAMP is pretreating neurons with neurotrophins, such as brain-derived neurotrophic factor
285 hese findings suggest a target organ-derived neurotrophin suppresses development of that organ's sens
288 Neuregulin 1 (NRG1) is a multifunctional neurotrophin that mediates neurodevelopment and schizoph
289 rain-derived neurotrophic factor (BDNF) is a neurotrophin that promotes neuronal proliferation, survi
290 rain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates synaptic function and plasti
291 genetically re-engineers neurons to produce neurotrophins that are neuroprotective to vulnerable dop
293 phic action in the nervous system by linking neurotrophins to the survival of immature neurons at the
295 ink between calcineurin signalling, impaired neurotrophin trafficking and neurodevelopmental deficits
296 onclusion, clinically practicable short-term neurotrophin treatment is sufficient for long-term survi
297 owed that variation in the expression of the neurotrophin tyrosine kinase receptor type 3 (NTRK3) in
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