ライフサイエンスコーパス: axonal regeneration

1 t facial motoneurons, Srf deletion inhibited axonal regeneration.

2 xpression of Smad2 also blocked SLPI-induced axonal regeneration.

3 sm, suggesting a cytoplasmic SRF function in axonal regeneration.

4 expressed in neural stem cells and controls axonal regeneration.

5 egenerative disease models, it also inhibits axonal regeneration.

6 on at later time points, but no evidence for axonal regeneration.

7 e need for additional control and shaping of axonal regeneration.

8 ce but also provides compelling evidence for axonal regeneration.

9 Schwann cells may suggest the potential for axonal regeneration.

10 plore factors that may differentially affect axonal regeneration.

11 ment of blood vessel growth might facilitate axonal regeneration.

12 peroxidasins as extracellular inhibitors of axonal regeneration.

13 dent synaptic plasticity, and injury-induced axonal regeneration.

14 ons caudal to the injury site as evidence of axonal regeneration.

15 s-induced neurodegeneration and insufficient axonal regeneration.

16 ium levels in a range that is permissive for axonal regeneration.

17 nd associated neurological disorders and for axonal regeneration.

18 l scar forms and becomes a major obstacle to axonal regeneration.

19 l functions, including neurite outgrowth and axonal regeneration.

20 t options for motor neuron disease and motor axonal regeneration.

21 reports on the extent to which they support axonal regeneration.

22 bitor of oligodendrocyte differentiation and axonal regeneration.

23 glycoprotein (MAG) is a potent inhibitor of axonal regeneration.

24 NgR signaling limits functional recovery and axonal regeneration.

25 ant step for understanding the regulation of axonal regeneration.

26 that NFs may play a role in the mechanism of axonal regeneration.

27 ays a role in glial-neuronal interaction and axonal regeneration.

28 or manipulating its expression in studies of axonal regeneration.

29 insights and a few surprises in the field of axonal regeneration.

30 les after CNS injury is believed to restrict axonal regeneration.

31 suppressive environment to one that promotes axonal regeneration.

32 ent activation of these pathways and promote axonal regeneration.

33 its induction in spinal motor neurons during axonal regeneration.

34 se to CNS injury and limits the capacity for axonal regeneration.

35 s expressed at sites of SCI and may restrict axonal regeneration.

36 l cord of the immunosuppressed rat to induce axonal regeneration.

37 permissive nature of the adult CNS to induce axonal regeneration.

38 ins from Reticulon 1, 2 and 3 do not inhibit axonal regeneration.

39 microglia, which appear to be important for axonal regeneration.

40 sal columns of the rat spinal cord to induce axonal regeneration.

41 venting axonal degeneration and/or promoting axonal regeneration.

42 cological interventions aiming to accelerate axonal regeneration.

43 overexpressing neurotrophic factors enhance axonal regeneration.

44 ractions between them that lead to increased axonal regeneration.

45 NS), also support a modest degree of central axonal regeneration.

46 s (Muller and Mauthner cells) are capable of axonal regeneration.

47 MAG is a potent inhibitor of axonal regeneration.

48 for treatment of CNS conditions that require axonal regeneration.

49 generation without cell death is followed by axonal regeneration.

50 ebris, in Schwann cell proliferation, and in axonal regeneration.

51 well as a role for macrophages in promoting axonal regeneration.

52 st-injury period and during later peripheral axonal regeneration.

53 vation could have important consequences for axonal regeneration.

54 of mammalian glia and neurons and stimulates axonal regeneration.

55 cable formation, Schwann cell migration, and axonal regeneration.

56 ated' Schwann cells, which are essential for axonal regeneration.

57 th-cone guidance during both development and axonal regeneration.

58 dorsal root axotomy led to extensive central axonal regeneration.

59 morphological repair phenotype that promotes axonal regeneration.

60 Thus, the level of LOTUS function titrates axonal regeneration.

61 ssential preparatory stage to the process of axonal regeneration.

62 erotonergic pathways and corticospinal tract axonal regeneration.

63 nd we identify Collagen XII as a promoter of axonal regeneration.

64 ho family small GTPase Rac1 and Rac1-induced axonal regeneration.

65 synaptic strength, activity, maturation, and axonal regeneration.

66 cruitment, a reduction in myelin removal and axonal regeneration.

67 they identify promising agents for promoting axonal regeneration.

68 ntire set of mammalian genes contributing to axonal regeneration.

69 of MT-I/II after optic nerve crush promotes axonal regeneration.

70 , is driven by kinesin-1 and is required for axonal regeneration.

71 n that uncovered novel molecules suppressing axonal regeneration.

72 he adult due to the very limited capacity of axonal regeneration.

73 end themselves to the analysis of successful axonal regeneration.

74 creates an environment that is permissive to axonal regeneration.

75 tein, as a key component of GDA(BMP)-induced axonal regeneration.

76 tes the gene expression necessary to enhance axonal regeneration.

77 plays an essential role in GDA(BMP)-mediated axonal regeneration.

78 n to affect signalling pathways that promote axonal regeneration(3).

79 ne expression signatures indicated attempted axonal regeneration, a metabolic switch to glycolysis, o

80 Despite the absence of axonal regeneration across the injury site, olfactory ce

81 ted that muscle CNTFRalpha contributes to MN axonal regeneration across the lesion site.

82 essentially involved in RGC degeneration or axonal regeneration after acute CNS injury.SIGNIFICANCE

83 Despite advances in promoting axonal regeneration after acute spinal cord injury (SCI)

84 To assess axonal regeneration after CBC lesions, we used biocytin

85 euronal Nogo-66 receptor (NgR/NgR1) to limit axonal regeneration after central nervous system injury.

86 Although axonal regeneration after CNS injury is limited, partial

87 go-66 and NgR have central roles in limiting axonal regeneration after CNS injury, and NEP1-40 provid

88 Nogo is a myelin-derived protein that limits axonal regeneration after CNS injury.

89 play a major role in preventing spontaneous axonal regeneration after CNS injury.

90 erve as redundant NgR ligands that may limit axonal regeneration after CNS injury.

91 g the role of GAGs in neural development and axonal regeneration after CNS injury.

92 age, thus becoming a significant obstacle to axonal regeneration after injury in maturity.

93 To achieve axonal regeneration after injury in the CNS, several for

94 in-derived proteins Nogo, MAG and OMgp limit axonal regeneration after injury of the spinal cord and

95 l synaptic morphology during development and axonal regeneration after injury.

96 kinase D and Akt1 are approaches to promote axonal regeneration after injury.

97 examine the role of CRE-binding proteins in axonal regeneration after injury.

98 Axonal regeneration after nerve cut has been demonstrate

99 sion of LOTUS enhances retinal ganglion cell axonal regeneration after optic nerve crush.

100 r after spinal cord injury (SCI), as well as axonal regeneration after optic nerve crush.

101 Schwann cells contribute to efficient axonal regeneration after peripheral nerve injury and, w

102 Ongoing efforts to promote axonal regeneration after SCI have involved multiple str

103 lts identify a therapeutic target to promote axonal regeneration after SCI.

104 optosis may be necessary in order to enhance axonal regeneration after SCI.

105 r BMP inhibition with Noggin, retarded early axonal regeneration after sciatic nerve crush injury.

106 istances and to bridge lesion sites, guiding axonal regeneration after spinal cord injury (SCI).

107 One strategy that has emerged for promoting axonal regeneration after spinal cord injury is the impl

108 actor signaling in adult neurons and promote axonal regeneration after spinal cord injury.

109 during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury.

110 guidance system may play a role in limiting axonal regeneration after spinal cord injury.

111 suppressing Nogo-A expression and enhancing axonal regeneration after TBI.

112 ich may partially contribute to the enhanced axonal regeneration after TBI.

113 Retinal ganglion cell (RGC) death and failed axonal regeneration after trauma or disease, including g

114 f an inhibitory fibrous scar, which prevents axonal regeneration after trauma.

115 PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regener

116 tion mutations in pathway components impairs axonal regeneration and degeneration after injury.

117 l nerve have been shown to modify peripheral axonal regeneration and functional outcome.

118 r provides a therapeutic basis for enhancing axonal regeneration and functional recovery after CNS in

119 Glial signals are known to inhibit axonal regeneration and functional recovery after mammal

120 ta confirm previous reports that ECs promote axonal regeneration and functional recovery after spinal

121 and NI250(Nogo), allows moderate degrees of axonal regeneration and functional recovery after spinal

122 entral nervous system (CNS) pose barriers to axonal regeneration and functional recovery following in

123 duced rapidly after injury and necessary for axonal regeneration and functional recovery.

124 onditioning lesions do significantly enhance axonal regeneration and indicate that axotomy rather tha

125 nctionally separated from the role of Wnd in axonal regeneration and injury signaling by the requirem

126 ation concerning the biological mechanism of axonal regeneration and its complexity has delayed the p

127 actors in the lesion site, thereby promoting axonal regeneration and locomotor function recovery.

128 port the hypothesis that GH-therapy enhances axonal regeneration and maintains chronically-denervated

129 egeneration as measured by both histological axonal regeneration and motor function.

130 ed on Schwann cells that modulate peripheral axonal regeneration and myelination are also recognized

131 hibitory molecule (growth-IM) which inhibits axonal regeneration and neurite regrowth after neural in

132 s, reveal that pericyte blockage facilitates axonal regeneration and neuronal integration into the lo

133 rug and therapeutic nucleic acids to promote axonal regeneration and plasticity after spinal cord inj

134 al anisotropy have been suggested to reflect axonal regeneration and plasticity, but the direct histo

135 DAC3 dephosphorylation discriminates between axonal regeneration and regenerative failure.

136 my of Drosophila neurons in culture triggers axonal regeneration and regrowth.

137 Return of potency is dependent on axonal regeneration and reinnervation of the penis.

138 onse in humans are able to induce elongative axonal regeneration and remyelination and restore impuls

139 these cells causes a catastrophic failure of axonal regeneration and remyelination in the PNS.

140 ccumulate in chronic CNS lesions and inhibit axonal regeneration and remyelination, making them signi

141 ne marrow resulted in significantly improved axonal regeneration and restoration of function.

142 of c-Jun specifically in SCs caused impaired axonal regeneration and severely increased neuronal cell

143 SA) and the cell adhesion molecule L1 during axonal regeneration and sprouting after injury to the ad

144 teraction in the eye and spinal cord promote axonal regeneration and sprouting of the optic nerve aft

145 e identify Pfn1 as an important regulator of axonal regeneration and suggest that AAV-mediated delive

146 nd and NgR receptor in situations of limited axonal regeneration and support the hypothesis that this

147 o peripheral nerve injury that both promotes axonal regeneration and suppresses cell identity.

148 t of functional recovery by restricting both axonal regeneration and synaptic plasticity.

149 olog (PTEN) has been shown to be involved in axonal regeneration and synaptic plasticity.

150 al cues for the survival of injured neurons, axonal regeneration and target reinnervation.

151 FGF2 priming facilitated the DPCs to promote axonal regeneration and to improve locomotor function in

152 nsheathing cells (OECs) are known to enhance axonal regeneration and to produce myelin after transpla

153 debris from degenerated fibers, accelerated axonal regeneration, and earlier reinnervation of neurom

154 eatments aimed at promoting neuroprotection, axonal regeneration, and neuroplasticity.

155 of tracers on nerve function and peripheral axonal regeneration, and therefore have implications in

156 s for neurorehabilitation and for the use of axonal regeneration as a therapeutic approach to disorde

157 tation in mediating descending propriospinal axonal regeneration as well as optimizing such regenerat

158 The arrest of dorsal root axonal regeneration at the transitional zone between the

159 Neuron survival and axonal regeneration become severely limited during early

160 Thus, clear axonal regeneration beyond spinal cord injury sites can

161 fter spinal cord injury promotes significant axonal regeneration beyond the distal end of a PN bridge

162 distal graft interface allows for functional axonal regeneration by chronically injured neurons.

163 ied a new way to alleviate the inhibition of axonal regeneration by CSPG GAGs.

164 g spinal cord transection in larval lamprey, axonal regeneration by descending brain neurons, rather

165 rategies, whereas immune neuroprotection and axonal regeneration can be achieved by transfer of activ

166 In the nematode Caenorhabditis elegans, axonal regeneration can proceed through axonal fusion, w

167 well known growth cone protein that promotes axonal regeneration, can be induced in rat brain astrocy

168 proposed mechanisms include abnormalities of axonal regeneration, collateral sprouting and synaptic p

169 toskeleton components, metabolic enzymes and axonal regeneration enhancers, was increased in the cent

170 oprotein (MAG), represent major obstacles to axonal regeneration following CNS injury.

171 en widely studied for its role in inhibiting axonal regeneration following injury to the central nerv

172 the injured neuron determines the extent of axonal regeneration following injury.

173 bitory factors (MAIFs) are inhibitors of CNS axonal regeneration following injury.

174 We investigated the role of MMPs in axonal regeneration following optic nerve crush (ONC) in

175 ly), but not single mutants, showed enhanced axonal regeneration following retro-orbital optic nerve

176 suggest a practical strategy for stimulating axonal regeneration following spinal cord injury.SIGNIFI

177 up) resulted in a significant enhancement of axonal regeneration for the total numbers of descending

178 rest for their potential capacity to support axonal regeneration, for example, after spinal cord inju

179 Axonal regeneration from the severed roots into the SC c

180 of the role of astrogliosis in inhibition of axonal regeneration has been challenged by recent findin

181 wn to mediate remyelination and to stimulate axonal regeneration in a number of in vivo rodent spinal

182 rapeutic for neurodegenerative disorders via axonal regeneration in Abeta25-35-treated cortical neuro

183 roduct, P0, has been implicated in promoting axonal regeneration in addition to its proposed structur

184 ere, we asked whether axonal degeneration or axonal regeneration in adult nerves might be affected by

185 noic acid receptor beta2 (RARbeta2) promoted axonal regeneration in adult sensory neurones located pe

186 ver, it is not known if RARbeta2 can promote axonal regeneration in cortical neurones of the CNS.

187 spinal lesion site is a major impediment to axonal regeneration in mammals.

188 Inhibitors of axonal regeneration in myelin are believed to be major c

189 he hypothesis that RAGE suppresses effective axonal regeneration in superimposed acute peripheral ner

190 Axonal regeneration in the adult central nervous system

191 s the contribution of Nogo to the failure of axonal regeneration in the adult CNS.

192 Axonal regeneration in the adult mammalian central nervo

193 Effective axonal regeneration in the adult mammalian nervous syste

194 nts and neurotrophins were used to influence axonal regeneration in the adult rat after complete spin

195 after injuries and form a strong barrier for axonal regeneration in the adult vertebrate CNS.

196 al nervous system (CNS) myelin that prevents axonal regeneration in the adult vertebrate CNS.

197 s, such as Nogo, may account for the lack of axonal regeneration in the central nervous system (CNS)

198 Failure of axonal regeneration in the central nervous system (CNS)

199 inhibit regeneration and toward encouraging axonal regeneration in the CNS after injury.

200 mising donors for transplantation to promote axonal regeneration in the CNS including the spinal cord

201 hypothesis that uPA binding to uPAR promotes axonal regeneration in the CNS.

202 The failure of axonal regeneration in the damaged CNS limits functional

203 The lack of axonal regeneration in the injured adult mammalian spina

204 Myelin-associated inhibitors limit axonal regeneration in the injured brain and spinal cord

205 ation and proliferation is a prerequisite to axonal regeneration in the injured peripheral nervous sy

206 ole of netrin and semaphorins in restricting axonal regeneration in the injured spinal cord.

207 secondary upregulation of NF message during axonal regeneration in the lamprey CNS may be part of an

208 In conclusion, axonal regeneration in the locust olfactory system appea

209 ssion may be an effective means of promoting axonal regeneration in the presence of diverse inhibitor

210 ibitory effects of myelin or promote central axonal regeneration in the spinal cord in vivo.

211 rom traumatic injury of the CNS, focusing on axonal regeneration in the spinal cord.

212 To induce axonal regeneration in the transected adult rat spinal c

213 transport and translation of mRNA cargos in axonal regeneration in vitro and in vivo.

214 o tested whether depleting fidgetin improves axonal regeneration in vivo after a dorsal root crush in

215 ) of zebrafish is a suitable system to study axonal regeneration in vivo because of both the superfic

216 Further, daidzein was effective in promoting axonal regeneration in vivo in an optic nerve crush mode

217 ach and found an enhancement or reduction of axonal regeneration in vivo, respectively.

218 ntification of a drug that is able to induce axonal regeneration in vivo.

219 and the actin-severing factor cofilin during axonal regeneration in vivo.

220 o test the importance of these molecules for axonal regeneration in vivo.

221 of treatments for ALS, approaches to improve axonal regeneration, including by inhibiting ROCK, shoul

222 Additionally, TANES may promote axonal regeneration, including those from supraspinal le

223 ured rat spinal cord resulted in compromised axonal regeneration, indicating that POSTN plays an esse

224 and as long as 15 months, after SCI promote axonal regeneration into and beyond a midcervical lesion

225 ether combinatorial treatments support motor axonal regeneration into and beyond the lesion.

226 Two weeks postrepair, axonal regeneration into BDNF(-/-) grafts was markedly l

227 2 or NGF, but not L1 or LacZ, induced robust axonal regeneration into normal as well as ectopic locat

228 Axonal regeneration into the grafts was assessed 4 and 8

229 both neuronal and neuronal-glial, results in axonal regeneration into the SC after dorsal root neurot

230 Aberrant axonal regeneration, irregularly sized myelinated fibers

231 Axonal regeneration is a major issue in the maintenance

232 Axonal regeneration is defective in both experimental an

233 Significantly increased axonal regeneration is detected in ephrinB3(-/-) mice.

234 After CNS injury, axonal regeneration is limited by myelin-associated inhi

235 Axonal regeneration is minimal after CNS injuries in adu

236 While axonal regeneration is more successful in peripheral ner

237 Axonal regeneration is normally limited within myelinate

238 ercoming these inhibitory cues and promoting axonal regeneration is one of the primary targets in dev

239 er axonal injury, their role specifically in axonal regeneration is unknown.

240 After a CNS injury in the adult mammals, axonal regeneration is very limited because of the reduc

241 rved some capability for remyelination while axonal regeneration is very limited.

242 have implicated c-Jun in neuronal death and axonal regeneration, it is unknown whether Jun function

243 Myelin inhibitors of axonal regeneration, like Nogo and MAG, block regrowth a

244 These actions, rather than axonal regeneration, may help ameliorate the effects of

245 are overexpressed sufficiently to accelerate axonal regeneration, myelination and function are restor

246 nstitutively active Pfn1 to rodents promoted axonal regeneration, neuromuscular junction maturation,

247 Little axonal regeneration occurs after spinal cord injury in a

248 g the 'nanoaxotomy' chip, we discovered that axonal regeneration occurs much faster than previously d

249 The molecular basis of axonal regeneration of central nervous system (CNS) neur

250 specific epigenetic mechanism that regulates axonal regeneration of CNS axons, suggesting novel targe

251 herefore, in spinal cord-transected lamprey, axonal regeneration of descending brain neurons probably

252 al cord at 20% BL to determine the extent of axonal regeneration of descending brain neurons.

253 CD8(+) T cells repressed the axonal regeneration of DRG neurons via caspase 3 activat

254 hile reduction in TDP-43 is shown to inhibit axonal regeneration of iPSC-derived motor neurons, rescu

255 6 domain on their surface potently inhibited axonal regeneration of mechanically injured cerebral cor

256 Our study provides proof of concept that axonal regeneration of motor neurons harboring SOD1(G93A

257 egenerated motor units with that expected if axonal regeneration of motor neurons were random.

258 This paper examines axonal regeneration of the primate median nerve lesioned

259 del studies: acute neuroprotection, enhanced axonal regeneration or plasticity, and treatment of demy

260 icative of a more inhibitory environment for axonal regeneration/plasticity, than MMP-9 null mice.

261 e examined whether their neuroprotective and axonal regeneration potentials can be identify in human

262 The three known inhibitors of axonal regeneration present in myelin--MAG, Nogo, and OM

263 Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf

264 a cell body responses and enhance subsequent axonal regeneration, probably by reducing the initial de

265 These findings show that RARbeta2 induces axonal regeneration programs within injured neurons and

266 njury, demonstrating its neuroprotection and axonal regeneration properties.

267 ount for this functional improvement include axonal regeneration, remyelination and neuroprotection.

268 after nerve injury is critical for favorable axonal regeneration, remyelination, and clinical improve

269 Progress in the field of axonal regeneration research has been like the process o

270 s suggest that the age-associated decline in axonal regeneration results from diminished Schwann cell

271 tomized adult rat sensory neurons to undergo axonal regeneration reveals new therapeutic targets to b

272 These results suggest that the axonal regeneration seen in in vivo studies using fibron

273 troxide-stained rat nerves including various axonal regeneration stages.

274 in Schwann cells during both development and axonal regeneration, suggesting that the developmental p

275 the mpz:egfp transgene was not dependent on axonal regeneration, suggesting that the primary signal

276 ar that changes in gene expression accompany axonal regeneration, the extent of this genomic response

277 he central nervous system as an inhibitor of axonal regeneration, the peripheral roles of Nogo isofor

278 ts into the mechanism by which Nogo inhibits axonal regeneration, this discovery may inspire new trea

279 pigenetic mechanisms that promote endogenous axonal regeneration, this provides possible avenues for

280 t dorsal root ganglion neurons for increased axonal regeneration through a neurotrophin-dependent mec

281 central nervous system (CNS) myelin prevents axonal regeneration through interaction with Nogo recept

282 evidence supports that Luman contributes to axonal regeneration through regulation of the unfolded p

283 pression of these molecules is necessary for axonal regeneration to occur.

284 ted axon growth to laminas I and II, shaping axonal regeneration toward the normal distribution patte

285 We examined blood vessel, Schwann cell and axonal regeneration using validated axotomy models to st

286 Axonal regeneration was analyzed by counting the number

287 Axonal regeneration was delayed in complement-depleted a

288 nse of DRG neurons, again, no evidence of DC axonal regeneration was detected.

289 for LRP-mediated chemoattraction to mediate axonal regeneration was examined in vivo in a model of c

290 In symptomatic SOD1(G93A) mice, axonal regeneration was markedly reduced compared to pre

291 To identify genes participating in axonal regeneration, we characterized mRNA expression pr

292 nerve injury in vivo and is associated with axonal regeneration, we have assayed axotomized adult ra

293 therapeutic potential of UPR manipulation to axonal regeneration, we locally delivered XBP1s or an sh

294 To test whether fidgetin knockdown assists axonal regeneration, we plated dissociated adult rat DRG

295 Changes in axonal localization of PKC and axonal regeneration were examined in cultured RGCs by im

296 any hits and some new mechanisms involved in axonal regeneration were identified.

297 into the area of the damaged nerve promoted axonal regeneration, which led to functional recovery as

298 These events parallel axonal regeneration with one critical difference: granul

299 fied in the peripheral nervous system during axonal regeneration, with overlap to axonal sprouting af

300 A direct histological assay of axonal regeneration would have many advantages over curr