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1 ronal pathologies, in which it may influence neuronal survival.
2 of axonal transport, a critical function for neuronal survival.
3 ng mutations in genes encoding regulators of neuronal survival.
4 e by neurons, and had the ability to enhance neuronal survival.
5 ibited extensive spinal damage and decreased neuronal survival.
6 d morphology, motor control, and age-related neuronal survival.
7 s a key component in synaptic plasticity and neuronal survival.
8 p600/calmodulin interaction is required for neuronal survival.
9 naling, compromising synaptic plasticity and neuronal survival.
10 In addition, CART is a regulator of neuronal survival.
11 egulate locomotion, motor axon targeting and neuronal survival.
12 biquitin/proteasome pathway is essential for neuronal survival.
13 cultured neurons and examined how it affects neuronal survival.
14 d protein p600 (also known as UBR4) promotes neuronal survival.
15 g through gp130 in photoreceptors to promote neuronal survival.
16 th tau variants on subcellular transport and neuronal survival.
17 ion of Akt signaling, resulting in augmented neuronal survival.
18 d inhibiting the UPR and thus contributes to neuronal survival.
19 toplasmic dynein is necessary for axonal and neuronal survival.
20 me of the main aSyn hallmarks are related to neuronal survival.
21 antly and concentration-dependently enhanced neuronal survival.
22 bolism of acidic substrates is essential for neuronal survival.
23 o suppress oxidative damage and thus promote neuronal survival.
24 e intracellular signaling pathways mediating neuronal survival.
25 and axonal development, synaptogenesis, and neuronal survival.
26 crease or increase the RNase activity affect neuronal survival.
27 ocal microenvironment that is deleterious to neuronal survival.
28 o hypoxic conditions plays a pivotal role in neuronal survival.
29 tasis more conducive to brain resiliency and neuronal survival.
30 onal cells such that it results in increased neuronal survival.
31 of hypertonic saline hydroxyethyl starch on neuronal survival.
32 hat TLE1 is necessary for the maintenance of neuronal survival.
33 ement responsible for mTOR-dependent retinal neuronal survival.
34 the quality control mechanisms required for neuronal survival.
35 nd this response was important in prolonging neuronal survival.
36 ablished roles in muscle differentiation and neuronal survival.
37 ignaling proteins regulating cell growth and neuronal survival.
38 ntal toxins, and other stimuli that threaten neuronal survival.
39 h integrin receptor signaling, that controls neuronal survival.
40 grade transport of TrkA endosomes to support neuronal survival.
41 urite outgrowth and dendritic elaboration to neuronal survival.
42 brain development including neurogenesis and neuronal survival.
43 e, while intermediate doses had no effect on neuronal survival.
44 ulate neuronal plasticity, neurogenesis, and neuronal survival.
45 l nervous system (CNS), ultimately affecting neuronal survival.
46 s, documenting the role of the Grx system in neuronal survival.
47 e, normalized clearance of ROS, and improved neuronal survival.
48 ns in the regulation of memory formation and neuronal survival.
49 hancement of antioxidant defenses to promote neuronal survival.
50 is a trophic factor essential for long-term neuronal survival.
51 itical for the control of synaptogenesis and neuronal survival.
52 for synaptic function, memory formation, and neuronal survival.
53 ion of mutant huntingtin protein (mtHtt) and neuronal survival.
54 (MEF2D), a transcription factor required for neuronal survival.
55 crease or increase the RNase activity affect neuronal survival.
56 1 and the interplay between inflammation and neuronal survival.
57 C expression, unlike NR2A and NR2B, supports neuronal survival.
58 eath, whereas cell cycle inhibition elevates neuronal survival.
59 er factor 2D activity, which is required for neuronal survival.
60 d in synaptic plasticity, axonal growth, and neuronal survival.
61 or presenilin-dependent memory formation and neuronal survival.
62 lement-binding protein (CREB) and to promote neuronal survival.
63 llular signals driven by dynein is vital for neuronal survival.
64 that is essential for neurotransmission and neuronal survival.
65 shut-off aerobic glycolysis is essential for neuronal survival.
66 , including regulating neuroinflammation and neuronal survival.
67 s, essential for learning and memory and for neuronal survival.
68 ffects cellular iron homeostasis and DAergic neuronal survival.
69 despite full recovery of vesicle docking and neuronal survival.
70 ion in neuronal progenitors and post-mitotic neuronal survival.
71 bute to defects in synaptic transmission and neuronal survival.
72 role of mitochondrial dynamics in regulating neuronal survival.
73 nti-neoplastic drug, significantly decreased neuronal survival.
74 lling in striatal pathways, and in promoting neuronal survival.
75 excitatory synaptic connectivity and enhance neuronal survival.
76 ulation of striatal output, and in promoting neuronal survival.
77 al survival, whereas increased PS1 increases neuronal survival.
78 ng synapse formation, neurite outgrowth, and neuronal survival.
79 d little effect on global RNA processing and neuronal survival.
80 diate neurite outgrowth, synaptogenesis, and neuronal survival.
81 , but not from IL-4-deficient mice, enhanced neuronal survival.
82 ctional perturbation of proteins critical to neuronal survival.
83 ic reticulum chaperone that is implicated in neuronal survival.
84 in memory formation, synaptic function, and neuronal survival.
85 pment and function, neuronal metabolism, and neuronal survival.
86 dicating that (1) IHCs are not necessary for neuronal survival, (2) neuronal loss in the other hearin
87 In addition, in vivo, 1) We examined CA1 neuronal survival 7 days after global forebrain ischemia
88 c response in the neonatal cochlea preserves neuronal survival, afferent innervation, and hearing sen
89 ical neurons in culture with IL-10 increased neuronal survival after exposure to oxygen-glucose depri
91 release, two processes that would compromise neuronal survival after ischemic/excitotoxic insults.
92 and intracellular pathways that can promote neuronal survival after retinal injury, but the intrinsi
94 dox effector factor-1 correlate closely with neuronal survival against ischemic insults, depending on
95 (HDAC) inhibitors have been used to promote neuronal survival and ameliorate neurological dysfunctio
99 sms that create a supportive environment for neuronal survival and axon regeneration after spinal cor
100 urthermore, Armcx1 knockdown undermines both neuronal survival and axon regeneration in the high rege
101 t impacts neuronal injury responses, such as neuronal survival and axon regeneration, remain largely
103 in receptors, it is also thought to regulate neuronal survival and blood vessel development through U
105 he HDAC proteins have been shown to regulate neuronal survival and death, whether HDAC7 has a similar
109 shed the critical role of PIKE in regulating neuronal survival and development by substantiating the
111 that have recently emerged as regulators of neuronal survival and developmental neuroplasticity.
112 e four MEF2 isoforms play important roles in neuronal survival and differentiation and in synapse for
113 neurotrophic factor (BDNF) is essential for neuronal survival and differentiation during development
114 es diverse biological functions ranging from neuronal survival and differentiation during development
120 ate supplies of cellular Ub is essential for neuronal survival and establish that decreased Ub availa
122 role for PS and tau in axonal transport and neuronal survival and function and implicate their misre
123 ophic factor (BDNF) has been shown to impact neuronal survival and function and improve synaptic plas
129 derived neurotrophic factor (BDNF) regulates neuronal survival and growth and promotes synaptic plast
131 harmacological treatments, which can promote neuronal survival and improve outcome in Huntington's di
132 termine structure-activity relationships for neuronal survival and in parallel characterized the enzy
134 g both SAG directional neurite outgrowth and neuronal survival and is expressed in both the developin
136 To better understand the role of LRRK2 in DA neuronal survival and its role in the susceptibility of
137 rate that PDGF-CC is critically required for neuronal survival and may potentially be used to treat n
138 enesis, glial differentiation and migration, neuronal survival and metabolism, neuronal morphogenesis
139 to cellular homeostasis might contribute to neuronal survival and modulate the pathogenic process in
140 ial role in learning and memory by promoting neuronal survival and modulating synaptic connectivity.
143 in multiple physiological actions including neuronal survival and neurite outgrowth during developme
144 1, two transcription factors associated with neuronal survival and neurite outgrowth, and increased L
146 ing and memory, and plays a critical role in neuronal survival and neuroinflammation in pathological
148 e beneficial effects of hypertonic saline on neuronal survival and on cerebral blood flow have been s
149 trophic factor (BDNF) is closely linked with neuronal survival and plasticity in psychiatric disorder
150 ide range of biological responses, including neuronal survival and plasticity, cardiac stress respons
152 ed in animal and in vitro studies to enhance neuronal survival and programmed cell death depending on
153 , miR-210 inhibition significantly increased neuronal survival and protected the activity of mitochon
154 elicits a rapid immune response that affects neuronal survival and recovery, but the role of meningea
155 fibrillary tangles, TIA1 reduction increased neuronal survival and rescued behavioral deficits and li
156 tion of both Hdac1 and Hdac2 in mice impacts neuronal survival and results in an excessive grooming p
157 Finally, we show that the VEGF164-mediated neuronal survival and SEMA3A-mediated axon guidance coop
159 s substantially overlap with those promoting neuronal survival and synapse integrity and with those a
160 derived astrocytes were capable of promoting neuronal survival and synaptogenesis when co-cultured wi
161 ate the structural changes to the effects on neuronal survival and the ability to induce stress granu
162 ted the structural changes to the effects on neuronal survival and the ability to induce stress granu
163 nation to a demyelinated state that supports neuronal survival and ultimately remyelination of axons.
164 rthermore, RGMa blocking antibodies promoted neuronal survival, and enhanced the plasticity of descen
165 racellular signaling pathway responsible for neuronal survival, and lay the foundation for future neu
166 he collapse of the laminB2 meshwork, impairs neuronal survival, and markedly reduces the cellularity
167 athways, including reducing edema, improving neuronal survival, and modulating inflammation and apopt
168 gulating neuronal differentiation, promoting neuronal survival, and modulating synaptic efficacy and
172 understand how Kv3.3 mutations are linked to neuronal survival, and to develop strategies for treatme
176 s (NMDARs), moderate NMDAR activity supports neuronal survival at least in part by regulating gene tr
177 ted proteins, were shown to be essential for neuronal survival, because siRNA knockdown resulted in d
178 The strong association of LCB levels with neuronal survival both in vivo and in vitro suggests hig
179 hat both Cav1.2 and Cav1.3 are necessary for neuronal survival but are differentially required for th
180 evidence for the role of endogenous Pink1 in neuronal survival, but also supports a role of DJ-1 and
181 Neurotrophins are widely thought to regulate neuronal survival, but this role has not been clearly de
182 DNTs) bind Toll receptors instead to promote neuronal survival, but whether they can also regulate ce
183 tinuous cerebral blood flow is essential for neuronal survival, but whether vascular tone influences
184 h IGF-1, a neurotrophic factor that promotes neuronal survival by activating Akt, prevents the apopto
186 affects epigenetic histone modification and neuronal survival by facilitating HDAC3 activity and reg
187 ines may contribute to in vivo regulation of neuronal survival by modulating microglial neurotoxic pr
188 t diabetes-induced peroxynitrite impairs NGF neuronal survival by nitrating TrkA receptor and enhanci
190 e biological functions in mammals, including neuronal survival, cholesterol metabolism, cell differen
191 week postinjury, a time point when increased neuronal survival correlated with reduced apoptosis.
192 stitutive, whereas after the critical period neuronal survival could be actively promoted by both con
193 target-derived proneurotrophins might affect neuronal survival/death decisions through a retrograde t
194 pposite functions in synaptic plasticity and neuronal survival/death, which may be related to their d
195 es mouse and chick SAG neurite outgrowth and neuronal survival, demonstrating key instructional roles
198 , VEGF-B treatment at the dose effective for neuronal survival did not cause retinal neovascularizati
199 c factor (GDNF), which is known to influence neuronal survival, differentiation, and neurite morphoge
200 with high potency and specificity, promoting neuronal survival, differentiation, and synaptic functio
201 kinase receptor B (TrkB) receptor, mediates neuronal survival, differentiation, synaptic plasticity,
204 onditions, whereas exogenous PEA15 increases neuronal survival even in the absence of PS1, which indi
205 ically stabilizes activated Ret and enhances neuronal survival, even though Cbl-family E3 ligases nor
209 ovel neuroprotective agent that may increase neuronal survival following injury by reducing surface e
210 annel can be selectively targeted to improve neuronal survival following injury in vivo The experimen
212 that when expressed on the surface, promotes neuronal survival following NMDA-induced excitotoxicity.
215 wth factor (bFGF or FGF2), are necessary for neuronal survival, growth, and differentiation, and may
218 eractions and enhances neurite outgrowth and neuronal survival homophilically, i.e. by self binding.
219 s that TLE1 cooperates with FoxG1 to promote neuronal survival in a CK2- and PI3K-Akt-dependent manne
223 sion molecule promotes neurite outgrowth and neuronal survival in homophilic and heterophilic interac
227 OXR1) has emerged as a critical regulator of neuronal survival in response to oxidative stress, and i
229 strategy to improve penumbral blood flow and neuronal survival in stroke or other ischemic conditions
233 f learning and memory and the maintenance of neuronal survival in the brain and suggest that presenil
234 tau aggregates was associated with improved neuronal survival in the cerebral cortex and the brainst
236 st the hypotheses that DRG11 is required for neuronal survival in the V pathway and that PrV cell dea
237 gamma-Protocadherins (PCDH-gamma) regulate neuronal survival in the vertebrate central nervous syst
239 linked to neurodegenerative disease hindered neuronal survival in this model; of these mutations, the
241 we identify OMA1 as a critical regulator of neuronal survival in vivo and demonstrate that stress-in
242 tion of p75NTR can also significantly affect neuronal survival in vivo by changing the intracellular
243 schaemic brain tissue, reflected by enhanced neuronal survival, increased angiogenesis and decreased
245 of neurodegeneration by virtue of promoting neuronal survival independently of early disease-specifi
246 r to those of murine astrocytes in promoting neuronal survival, inducing functional synapse formation
251 e that the role of the Pcdhg gene cluster in neuronal survival is primarily, if not specifically, med
252 uclear transcription factor known to promote neuronal survival, is directly phosphorylated by GSK3bet
254 ular link between activation of GSK3beta and neuronal survival machinery which may underlie in part G
255 , chaperone-mediated autophagy modulates the neuronal survival machinery, and dysregulation of this p
256 n primary neurons, suggesting that decreased neuronal survival might be a consequence of an impaired
257 ed in neurons and glia that is implicated in neuronal survival on the basis that mutations in the GRN
260 odulin knockdown did not significantly alter neuronal survival or synapse formation but depressed spo
262 A1 astrocytes lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocy
264 rly stages of neuronal development involving neuronal survival, polarization, and neuritic growth and
265 te axon regeneration, alone they can promote neuronal survival possibly by regulating the retrograde
266 its high-affinity receptor TrkB and promotes neuronal survival; restoring BDNF signaling is thus of p
268 ation of the signaling pathways that mediate neuronal survival signaling could lead to new therapeuti
269 as effects on mitochondrial permeability and neuronal survival similar to those caused by PARP1 activ
271 oxG1 blocks the ability of IGF-1 to maintain neuronal survival suggesting that FoxG1 is a downstream
272 the dendritic network, memory formation, and neuronal survival, suggesting that pharmacological inhib
274 e results show that C1q can directly promote neuronal survival, thereby demonstrating new interaction
275 hic factor (BDNF) plays an important role in neuronal survival through activation of TrkB receptors.
276 increased the level of laminin and promoted neuronal survival through an integrin-dependent mechanis
277 microtubule associated protein tau promotes neuronal survival through binding and stabilization of M
278 Nna1 is a monomeric enzyme essential for neuronal survival through hydrolysis of polyglutamate-co
279 irst to report a role for MMP9 in regulating neuronal survival through the developmental process that
280 ts the balance between neurodegeneration and neuronal survival toward the stimulation of pro-survival
281 mulation of autophagosomes is detrimental to neuronal survival under certain neurodegenerative condit
282 Inhibition of gamma-secretase also decreases neuronal survival under GD conditions, which suggests th
284 mber of the globin superfamily, may regulate neuronal survival under hypoxia or oxidative stress.
285 thermore, down-regulation of PEA15 decreases neuronal survival under reduced glucose conditions, wher
286 ated animals demonstrated significantly more neuronal survival upstream of the lesion site, with some
288 gest that presenilin functions in memory and neuronal survival via its role as a gamma-secretase subu
291 flammation was decreased and hippocampal CA3 neuronal survival was increased, although hemorrhage vol
296 n of presenilin 1 (PS1) results in decreased neuronal survival, whereas increased PS1 increases neuro
298 provement in motor deficits and dopaminergic neuronal survival with non-invasive intranasal delivery,
300 eature of CNS injury that heavily influences neuronal survival, yet the signals that initiate and con
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