ライフサイエンスコーパス: axon growth

1 (2+) (Cav) and K(+) (Kv) channels, modulates axon growth.

2 growth cones of embryonic neurons influences axon growth.

3 enes involved in cytoskeletal remodeling and axon growth.

4 ced by an optogenetic approach also inhibits axon growth.

5 ource of netrin1 promotes ventrally directed axon growth.

6 T2 triggers axonal degeneration or defective axon growth.

7 2 leads to an increase in BMP-Smad-dependent axon growth.

8 to determine its role in adolescent dopamine axon growth.

9 xonal mRNAs for local translation to support axon growth.

10 miR-155 KO neurons show enhanced spontaneous axon growth.

11 periments show that Magel2 directly promotes axon growth.

12 rate mechanisms exist for different modes of axon growth.

13 CD2AP; human CMS) as a positive regulator of axon growth.

14 dentify LZK as a novel positive regulator of axon growth.

15 stabilization reduces scarring and promotes axon growth.

16 , allows transport into axons, and increases axon growth.

17 hloride prevented mTORC1-induced accelerated axon growth.

18 hosphatase suppressors of injury-induced CNS axon growth.

19 associated inhibition and allow for improved axon growth.

20 es, and regulates both neuronal polarity and axon growth.

21 ehog (Shh) receptors in dendrites stimulates axon growth.

22 ell refinement and presynaptic photoreceptor axon growth.

23 mplicating a dual role of S6K1 in regulating axon growth.

24 dosome trafficking appears to be crucial for axon growth.

25 matodendritic early endosomes in L1-mediated axon growth.

26 CSPGs) act as barriers to cell migration and axon growth.

27 e a role controlling the rate of commissural axon growth.

28 ollows a distinct pattern from developmental axon growth.

29 n also inhibited local protein synthesis and axon growth.

30 suggests an essential role for NMNAT2 during axon growth.

31 fector by which BmprIb regulates commissural axon growth.

32 cord, which contains numerous impediments to axon growth.

33 tenuates the inhibitory activity of CSPGs on axon growth.

34 probable mechanism behind this regulation of axon growth.

35 triggering downstream pathways that inhibit axon growth.

36 uronal gene expression, differentiation, and axon growth.

37 d downstream functions of chodl during motor axon growth.

38 ndroitin sulfate-E (CS-E), potently inhibits axon growth.

39 ing pathways activated by many inhibitors of axon growth.

40 ne loop impaired early neurotrophin-promoted axon growth.

41 nown to be critical in neuronal survival and axon growth.

42 ding to promote axonal transport and restore axon growth.

43 and -9, and that knockdown of MTP18 promotes axon growth.

44 excessive scar formation, thereby protecting axon growth.

45 , accelerates the rate of spinal commissural axon growth.

46 in mAKAPalpha promotes neuronal survival and axon growth.

47 el mechanism underlying stimulation-mediated axon growth.

48 or lysosomes (LE/Lys) is crucial for proper axon growth.

49 ent decreases in mitochondrial transport and axon growth.

50 e signalling, had no effect on early sensory axon growth.

51 ulate actin interaction, polymerization, and axon growth.

52 ells, and callosal projection neurons during axon growth.

53 are likely to present physical obstacles to axon growth.

54 t that the complex is promoting longitudinal axon growth across the segment boundary.

55 ly undergo a developmental downregulation of axon growth activity as neurons mature.

56 omplex mediates myelin-induced inhibition of axon growth acutely in the CNS.

57 ss and elucidate a core mechanism underlying axon growth after CNS trauma.

58 en to identify endogenous suppressors of CNS axon growth after injury, and reveals Inpp5f (Sac2) as a

59 pment of a glial scar, while also increasing axon growth after spinal cord injury in vivo.

60 nules as well as increased phospho-G3BP1 and axon growth, although depletion of Csnk2a1 mRNA from PNS

61 Hsc70 was required for netrin-1-mediated axon growth and attraction in vitro, whereas Hsc70 activ

62 Thus, betaII-spectrin promotes both axon growth and axon stability through establishing the

63 monstrate an unexpected dissociation between axon growth and behavioral outcome, highlighting the nee

64 d that NGF-TrkA-PI3K signaling drives robust axon growth and branching in part by suppressing GSK3bet

65 erplay of the molecular programs that direct axon growth and cell specification, with activity-depend

66 plays an important role in the processes of axon growth and cellular motility.

67 After SCI, axon growth and circuit reorganization are determined by

68 In vitro DSCAM promotes RGC axon growth and fasciculation, and can act independently

69 d signaling strength, which in turn controls axon growth and growth cone sprouting.

70 ally, the extent to which Fz6 can rescue the axon growth and guidance defects in Fz3(-/-) mice.

71 e genes alter protein function and result in axon growth and guidance defects.

72 The fundamental problem in axon growth and guidance is to understand how cytoplasmi

73 The fundamental problem in axon growth and guidance is understanding how cytoplasmi

74 EphA/ephrin signaling regulates axon growth and guidance of neurons, but whether this pr

75 present data that extend the role for C1q in axon growth and guidance to include the sprouting patter

76 This enables them to control axon growth and guidance with remarkable specificity, bu

77 rcuits by assaying transcriptional identity, axon growth and guidance, and mRNA expression in Munc18-

78 Like axon growth and guidance, formation of collateral branch

79 cally diverse polarity processes - including axon growth and guidance, hair follicle orientation, and

80 through re-expression of genes necessary for axon growth and guidance, however, the gene regulatory m

81 tions of actin in the growth cone to produce axon growth and guidance.

82 etal transport, and microtubule dynamics for axon growth and guidance.

83 e essential for growth cone behaviors during axon growth and guidance.

84 development that might result from impaired axon growth and guidance.

85 fluctuations of growth cone actin to direct axon growth and guidance.

86 been characterized in the larger context of axon growth and guidance.

87 depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles,

88 for its function as an adhesion molecule in axon growth and in self-recognition between dendrites of

89 gram in basket cells that regulates targeted axon growth and inhibitory synapse formation.

90 mitochondrial fission reversibly suppressed axon growth and lamellar extension.

91 A requirement for NMNAT2 for both axon growth and maintenance suggests that reduced levels

92 Such stability is important for normal axon growth and maintenance, while hyperstability may co

93 been shown to function in such processes as axon growth and microtubule polymerization.

94 Importantly, labeled cells still exhibited axon growth and most cells retained markers of motor neu

95 after implantation, and was able to enhance axon growth and myelination.

96 tracellular matrix (ECM) play vital roles in axon growth and navigation, plasticity, and regeneration

97 cytoplasmic processes between NMJs to guide axon growth and NMJ reinnervation.

98 cular mechanisms of glial involvement in RGC axon growth and organization in the developing retinogen

99 ation, including motor neuron specification, axon growth and pathfinding, and mRNA expression, are un

100 tion works in the same way as IgCAM-mediated axon growth and pathfinding; it relies not only on extra

101 tin ligase, was discovered in the control of axon growth and patterning in the mammalian brain.

102 SMN effects, mediating part of the action on axon growth and random cell motility, as indicated by ch

103 iR-155 deletion would simultaneously improve axon growth and reduce neuroinflammation after SCI by ac

104 injury-specific kinesin that contributes to axon growth and regeneration by regulating and organizin

105 Thus, Set-beta differentially regulates axon growth and regeneration depending on subcellular lo

106 l ganglion cell (RGC) and hippocampal neuron axon growth and regeneration in a subcellular localizati

107 -gated calcium channels negatively regulates axon growth and regeneration of corticospinal neurons, t

108 es in neurons, as suggested by inhibition of axon growth and regeneration through the ARF activator E

109 syntaxin13 in cultured DRG neurons prevented axon growth and regeneration.

110 Integrins are involved in axon growth and regeneration.

111 adhesion molecule (NrCAM) is a regulator of axon growth and repellent guidance, and has been implica

112 NGF from TrkA-expressing neurons to modulate axon growth and survival.

113 y depleted neurons is compatible with normal axon growth and survival.

114 chanisms that regulate midbrain dopaminergic axon growth and target innervation are less clear.

115 ad signalling to limit midbrain dopaminergic axon growth and target innervation.

116 nfers cAMP regulation of neuroprotection and axon growth and that may be therapeutically targeted in

117 Chase significantly increased corticospinal axon growth and the number of synapses formed by cortico

118 lanar cell polarity (PCP) signaling in motor axon growth and they highlight the question of how PCP p

119 rgic neurons showed remarkable long-distance axon growth and topographical innervation of caudal SPNs

120 We identify a positive role for 14-3-3s in axon growth and uncover a developmental regulation of th

121 Endothelial Stat3 regulates angiogenesis, axon growth, and extracellular matrix remodeling and is

122 support intracellular transport, facilitate axon growth, and form a basis for neuronal morphology.

123 nectivity requires neuronal differentiation, axon growth, and precise target innervation.

124 uncover a retrograde extension mechanism for axon growth, and reveal the aetiology of axon-guidance d

125 ts show a specific role for Ret51 in pioneer axon growth, and suggest a critical role for long-range

126 ignaling pathway regulating RGC survival and axon growth, and suggest new neuroprotective or regenera

127 rowth in vivo, consistent with its effect on axon growth, and suggesting a role as a developmental ti

128 specification during neuronal polarization, axon growth, and terminal axon branching during synaptog

129 Sema3A and PNN GAGs is a potent inhibitor of axon growth, and this inhibition is reduced by the CS-E

130 Axon growth appeared normal in cultured knock-out neuron

131 actor ligand/receptor signaling that promote axon growth are incompletely understood.

132 Therapies that stimulate axon growth are needed to repair CNS damage.

133 d mRNAs - known as RNA regulons - that drive axon growth, axon guidance, injury responses, axon survi

134 cles (which carry many molecules involved in axon growth) became selectively targeted to the somatode

135 This relative suppression in axon growth behaviors is due to Coronin-1-dependent calc

136 developmental functions including control of axon growth, branching, neurite self-avoidance, and neur

137 e regeneration-associated elongating form of axon growth but had no impact on axon outgrowth in naive

138 h this, overexpression of neuritin increases axon growth but only when its mRNA localizes into the ax

139 thway but that Ttk69 likely also inhibits R7 axon growth by a TGF-beta/Activin-independent mechanism.

140 Neutralization of NG2's inhibitory effect on axon growth by anti-NG2 monoclonal antibodies (NG2-Ab) h

141 toxicity, and increases macrophage-elicited axon growth by approximately 40% relative to control con

142 of the transcription factor Sox11 increases axon growth by corticospinal tract (CST) neurons after s

143 Tp53inp2 is an atypical mRNA that regulates axon growth by enhancing NGF-TrkA signaling in a transla

144 dicate a critical role of force in promoting axon growth by facilitating microtubule (MT) polymerizat

145 PS1/gamma-secretase mediates axon growth by inhibiting RhoA signaling and cleaving Ep

146 Inhibition of axon growth by Nogo-A is mediated by the Nogo-66 recepto

147 Restriction of axon growth by patterned Nogo-A-Fc substrates suggests t

148 -secretase-dependent EphA3 cleavage mediates axon growth by regulating filament assembly through RhoA

149 ration is hindered by a decline of intrinsic axon growth capability in mature neurons.

150 r from such injuries due to a high intrinsic axon growth capacity and a less inhibitory environment.

151 he adult mammalian CNS decrease in intrinsic axon growth capacity during development in concert with

152 Promoting intrinsic axon growth capacity has been a major challenge in the f

153 injury and that this activity enhances their axon growth capacity.

154 ssessed how altering adolescent PFC dopamine axon growth changes the structural and functional develo

155 pinpoints ADF/cofilin as a key regulator of axon growth competence, irrespective of developmental st

156 Divergent regulation of CD2AP in different axon growth conditions suggests that separate mechanisms

157 he regulation of microtubule dynamics in the axon growth cone and enhances our understanding of this

158 development depends on the proper balance of axon growth cone attractive and repellent cues leading a

159 Netrin-1 induces axon growth cone collapse of mouse cerebellum external g

160 is required for dendrite elaboration but not axon growth cone collapse.

161 Ret, displayed defects in peripheral sensory axon growth cone morphology and dynamics.

162 ein (KBP) as critical for SCG10 transport to axon growth cones and complete axon extension.

163 As in other animals, axon growth cones in Caenorhabditis elegans integrate in

164 ear series of impenetrable barriers, forcing axon growth cones to traverse one half of each somite as

165 vel of endogenous phospho-JNK in commissural axon growth cones.

166 sentation of Frizzled3 in rodent commissural axon growth cones.

167 idence supports the idea that impairments in axon growth contribute to many clinical disorders, such

168 e of spinal neuron, we build models of their axon growth controlled by simple chemical gradients and

169 These deficits in axon growth could be rescued by transfecting with siRNA-

170 The SPG3A axon growth defects could be rescued with microtubule-bi

171 for the regulation of midbrain dopaminergic axon growth during central nervous system development.

172 adhesion and survival molecules involved in axon growth during CNS development, as well as axon rege

173 guidance mechanisms that control the rate of axon growth during development to accelerate the rate at

174 Different from physiological axon growth during development, a major limiting factor

175 trin is a key axon guidance cue that orients axon growth during neural circuit formation.

176 tiation between neighboring cells to guiding axon growth during neurogenesis.

177 another HDAC6 substrate contributes to this axon growth failure.

178 CD40L transiently enhanced axon growth from embryonic mouse DRG neurons cultured at

179 crovessels to induce and control directional axon growth from neural progenitor cells in vitro and ho

180 le enhancing integrin activation can promote axon growth from neurons cultured on inhibitory substrat

181 tion, miR-155 deletion increases spontaneous axon growth from neurons; adult miR-155 KO dorsal root g

182 n locally synthesize proteins, with roles in axon growth, guidance, and regeneration, but the mechani

183 Work on axon growth has classically focused on understanding how

184 Instead, the transcript supports axon growth in a coding-independent manner.

185 h receptors exhibits additive enhancement of axon growth in adult neuronal cultures in vitro.

186 oprotective effect in vitro, and it promotes axon growth in an animal model of optic nerve crush.

187 and promotes CST sprouting and regenerative axon growth in both acute and chronic injury paradigms.

188 are short and wavy, a defect reminiscent of axon growth in cells with depleted Atlastin-1.

189 KLFs regulate axon growth in CNS neurons including retinal ganglion ce

190 pendent) and promoting (receptor processing) axon growth in developing neurons.

191 by GSK-3 that is critical for SRF-dependent axon growth in mammalian central neurons.

192 tream effectors such as GSK3beta to abnormal axon growth in neurodevelopmental mTORopathies and open

193 ntly alter expression of genes that regulate axon growth in neurons.

194 previously studied the role of integrins in axon growth in PNS axons; in the present study, we inves

195 on integrin signaling and integrin-mediated axon growth in rat sensory neurons.

196 The prominent alterations in axon growth in SPG3A neurons may represent a particularl

197 gR1, a receptor previously shown to restrict axon growth in the adult, also functions in the dendrite

198 ivo promoted both sprouting and regenerative axon growth in the CST of adult mice.

199 ilin-1 (PS1)/gamma-secretase is required for axon growth in the developing mouse brain.

200 ploiting neurovascular interaction to direct axon growth in the injured spinal cord and the potential

201 for generating a supportive environment for axon growth in the injured spinal cord.

202 r (SRF), plays a critical role in regulating axon growth in the mammalian brain.

203 that mark (1) the beginning of regenerative axon growth in the optic nerve, and (2) the re-establish

204 Our results implicate impaired axon growth in the pathogenesis of AS and identify nonin

205 way promoting developmental and regenerative axon growth in the peripheral and central nervous system

206 3-3 protein-protein interactions, stimulates axon growth in vitro and regeneration in vivo.

207 tion dramatically decreased RGC survival and axon growth in vitro, and survival in vivo.

208 including PP2A, which we show also regulates axon growth in vitro.

209 tro, but the impact of hyperactive mTORC1 on axon growth in vivo and the mechanisms underlying those

210 Deletion of Tp53inp2 inhibits axon growth in vivo, and the defects are rescued by a no

211 sion in DRGs peaked in the period of maximum axon growth in vivo, consistent with its effect on axon

212 est the importance of mechanical signals for axon growth in vivo, we altered brain stiffness, blocked

213 irm crucial functions of this gene for motor axon growth in vivo.

214 athways (e.g., inflammation, cell death, and axon growth) in diverse cell types.

215 xplorative MTs: in growth cones they enhance axon growth, in axon shafts they cause excessive branchi

216 Whereas CD40L enhanced early axon growth independently of neurotrophins, disruption o

217 led to a shift toward an antiangiogenic and axon growth-inhibiting micromilieu after stroke, with an

218 al insights into the molecular mechanisms of axon growth inhibition and identify PARP1 as an effectiv

219 ing CRMP2, a cytosolic protein implicated in axon growth inhibition by Semaphorin/Plexin complexes.

220 teoglycans (CSPGs) are major contributors to axon growth inhibition following spinal cord injury and

221 dent deacetylation of Miro1 as a mediator of axon growth inhibition through decreased mitochondrial t

222 and polarity (Par) complex proteins mediate axon growth inhibition.

223 We found that the axon growth inhibitor chondroitin sulfate proteoglycan (

224 Following SCI, axon growth inhibitors and other inflammatory responses

225 local translation of RhoA contributes to the axon growth inhibitory effect of CSPGs.

226 Disheveled axon growth instead seems linked to Sfrp-mediated modula

227 Inhibition of either receptor increases axon growth into and beyond scar tissues after CNS injur

228 ith the idea that Sfrp1/2 normally constrain axon growth into the fiber layer and the optic disc.

229 s for axonal regrowth.SIGNIFICANCE STATEMENT Axon growth involves motion, and motion is driven by for

230 lonyl-CoA changes, and give insight into how axon growth is controlled by nutrients.

231 Overcoming these barriers to permit axon growth is critical for the development of any repai

232 e suggested that developmental regulation of axon growth is distinct in most regards from titration o

233 rticular organism, our approach to modelling axon growth is general and can be widely applied to stud

234 How cortical collapse factors influence axon growth is little understood.

235 n outgrowth in cultured sensory neurons, but axon growth is not affected when the overexpressed mRNA

236 neurospheres in vitro, we show that enteric axon growth is not inhibited by Shh.

237 The stimulus for axon growth is not postsynaptic cell inactivity because

238 Axon growth is primarily driven by microtubules.

239 Furthermore, TG axon growth is robustly inhibited by BMP4 and this inhib

240 late-onset Alzheimer's disease, its role in axon growth is unknown.

241 The role of Cav channels during axon growth is well understood, but it is unclear whethe

242 taII-spectrin-null neurons exhibited reduced axon growth, loss of actin-spectrin-based periodic membr

243 c growth programs that promote developmental axon growth may also facilitate axon regeneration in inj

244 capacity, which enhances neuron survival and axon growth of cocultured neurons.

245 dorsal root ganglion (DRG) neurons improves axon growth on an in vitro model of the inhibitory envir

246 not kindlin-2, in cultured neurons increased axon growth on an inhibitory aggrecan substrate.

247 ssion of constitutively active Rac1 inhibits axon growth on control surfaces.

248 e deacetylase 6 (HDAC6) was shown to support axon growth on the nonpermissive substrates myelin-assoc

249 s unknown whether complement proteins affect axon growth or regeneration.

250 and thereby contribute to the development of axon growth patterns.

251 that the ability of macrophages to create an axon growth-permissive microenvironment or cause neuroto

252 l dieback, and the molecular determinants of axon growth, plasticity, and regeneration in the context

253 e establish a correlation between diminished axon growth potential and histone 4 (H4) hypoacetylation

254 hibitory factors in the lesion scar and poor axon growth potential prevent axon regeneration.

255 ynthesis and induction of bdnf, ngf, and the axon growth promoter semaphorin 7a (sema7a), and as a co

256 tial for the previously described effects on axon growth promotion and angiogenesis.

257 tion by parthenolide or cnicin mimicked this axon growth promotion in wild-type animals, although it

258 sination by parthenolide fully mimicked this axon growth promotion in wild-type mice.

259 ral midbrain dopamine neurons enhanced their axon growth rate and induced axonal branching.

260 ar functions of cortical collapse factors to axon growth regulation and reveals new roles in axon bra

261 ecovery following CNS injury by manipulating axon growth regulators alone or in combination with acti

262 nt studies have found that integrin mediated axon growth relies on signalling via focal adhesion mole

263 rane excitability, but whether they regulate axon growth remains unclear.

264 olecular mechanisms underlying SRF-dependent axon growth remains unknown.

265 ort the survival of injured neurons, promote axon growth, remove myelin-associated growth inhibitors,

266 Axon growth requires long-range transport of organelles,

267 To examine axon growth responses to regulated NT-3 expression, adul

268 specifically, we found altered serotonergic axon growth resulting from increased 5-HT in the fetal f

269 2+)]i at an optimal concentration for normal axon growth.SIGNIFICANCE STATEMENT Accumulating evidence

270 d likely other factors) defines two distinct axon growth states, which are critical for proper circui

271 wn to influence both normal and regenerative axon growth, suggesting that understanding their mechani

272 ative differences in growth cone response or axon growth, suggesting that, despite their highly diver

273 rocyte cells in SCI lesions express multiple axon-growth-supporting molecules.

274 nt KLF9-JNK3 interaction that contributes to axon growth suppression in vitro and regenerative failur

275 N-terminal kinase 3) is critical for KLF9's axon-growth-suppressive activity.

276 Here, we found that knock-down of KLF9, an axon growth suppressor that is normally upregulated 250-

277 is a novel physiological regulator of early axon growth that acts by target-derived and autocrine me

278 We identified divergent modes of initial axon growth that prefigure disrupted differentiation of

279 erization into the axon tip, which propelled axon growth through an inhibitory environment.

280 we identified Olfm1 as a molecule promoting axon growth through interaction with the Nogo A receptor

281 Thus, CSPGs inhibit axon growth through multiple mechanisms, making them esp

282 nal gray matter with a focus on promotors of axon growth through the growth-inhibitory adult CNS, thi

283 early in development results in spontaneous axon growth through the injury, but this regenerative po

284 s of Nogo-A-Fc, KT5720 caused restriction of axon growth to areas devoid of Nogo-A-Fc.

285 olution imaging of growth cone dynamics from axon growth to synapse formation in cultured Drosophila

286 ugh blocking GSK3beta activity did not alter axon growth under physiological conditions in vivo, bloc

287 pression and the lack of additive effects on axon growth upon co-manipulation suggest complex functio

288 iquitination is not involved in the impaired axon growth upon deletion of Nedd4-1 and Nedd4-2.

289 inery to precisely and non-invasively direct axon growth using light.

290 by blood depressing substance II suppresses axon growth via an increase in the amplitude and frequen

291 Intrinsic axon growth was modulated by overexpressing Kruppel-like

292 E or a conditioning injury alone, propelling axon growth well beyond the spinal injury site.

293 Conversely, RGC survival and axon growth were unaltered in RGCs from AC1/AC8 double k

294 t midbrain during the period of dopaminergic axon growth, when BMP pathway components are upregulated

295 ex-2 of mTOR (mTORC2), and genes involved in axon growth, whereas genes related to neuropathic pain a

296 vators, significantly increased survival and axon growth, whereas pharmacologic or siRNA-mediated sAC

297 hese findings indicate that Shh can regulate axon growth, which may be critical for development of hi

298 e that Sfrps contribute to coordinate visual axon growth with a dual mechanism: by directly signaling

299 ould be an important endogenous mechanism of axon growth, with a potential for designing novel strate

300 that increasing mTORC1 activity accelerates axon growth without multiple axon formation.