ライフサイエンスコーパス: axon growth

1 hosphatase suppressors of injury-induced CNS axon growth.

2 associated inhibition and allow for improved axon growth.

3 ells, and callosal projection neurons during axon growth.

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

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

6 dosome trafficking appears to be crucial for axon growth.

7 matodendritic early endosomes in L1-mediated axon growth.

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

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

10 ollows a distinct pattern from developmental axon growth.

11 n also inhibited local protein synthesis and axon growth.

12 suggests an essential role for NMNAT2 during axon growth.

13 are likely to present physical obstacles to axon growth.

14 fector by which BmprIb regulates commissural axon growth.

15 cord, which contains numerous impediments to axon growth.

16 tenuates the inhibitory activity of CSPGs on axon growth.

17 probable mechanism behind this regulation of axon growth.

18 triggering downstream pathways that inhibit axon growth.

19 uronal gene expression, differentiation, and axon growth.

20 d downstream functions of chodl during motor axon growth.

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

22 ing pathways activated by many inhibitors of axon growth.

23 rons promoted dendrite growth but suppressed axon growth.

24 e axonal tip and inhibiting polarization and axon growth.

25 r transport of building materials to support axon growth.

26 (2+) (Cav) and K(+) (Kv) channels, modulates axon growth.

27 n impairs trigeminal and Rohon-Beard sensory axon growth.

28 important during ingrowth if GABA regulates axon growth.

29 growth cones of embryonic neurons influences axon growth.

30 enes involved in cytoskeletal remodeling and axon growth.

31 ced by an optogenetic approach also inhibits axon growth.

32 ource of netrin1 promotes ventrally directed axon growth.

33 T2 triggers axonal degeneration or defective axon growth.

34 2 leads to an increase in BMP-Smad-dependent axon growth.

35 to determine its role in adolescent dopamine axon growth.

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

37 periments show that Magel2 directly promotes axon growth.

38 rate mechanisms exist for different modes of axon growth.

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

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

41 stabilization reduces scarring and promotes axon growth.

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

43 hloride prevented mTORC1-induced accelerated axon growth.

44 Nogo-A allows corticospinal and raphespinal axon growth above and below the injury, as well as great

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

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

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

48 ltage-gated calcium channels--could suppress axon growth after injury.

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

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

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

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

53 , indicating that N-cadherin regulates motor axon growth and branching without severely affecting the

54 tent inflammatory stimulus known to increase axon growth and cause neurotoxicity.

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

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

57 phate levels in treated cultures, leading to axon growth and disinhibition by neurotrophin-induced re

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

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

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

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

62 hese signaling pathways function to regulate axon growth and guidance is fundamentally important to u

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

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

65 cellular signalling mechanisms that regulate axon growth and guidance, and also to test if its activa

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

67 a cascade of developmental events affecting axon growth and guidance, and suggest targeting the asso

68 As with axon growth and guidance, axon branching is tightly cont

69 Like axon growth and guidance, formation of collateral branch

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

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

72 n as a neuronal adaptor protein required for axon growth and guidance.

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

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

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

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

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

78 mitochondrial fission reversibly suppressed axon growth and lamellar extension.

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

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

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

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

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

84 from neuronal polarization and migration to axon growth and pathfinding to dendrite growth and branc

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

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

87 e data suggest that ACh negatively regulates axon growth and presynaptic specialization at the neurom

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

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

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

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

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

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

94 Integrins are involved in axon growth and regeneration.

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

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

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

98 Remarkably, TrkC-IgG reduced axon growth and synaptogenesis even in the presence of B

99 effects of transmitters such as dopamine on axon growth and synaptogenesis in developing neurons or

100 ng that endogenous NT-3 is necessary for SGN axon growth and synaptogenesis.

101 ther neurotrophin-3 (NT-3) or BDNF increases axon growth and synaptogenesis.

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

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

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

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

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

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

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

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

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

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

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

113 leptin include the following: neurogenesis, axon growth, and synaptogenesis.

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

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

116 Axon growth appeared normal in cultured knock-out neuron

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

118 of chodl induces arrest or stalling of motor axon growth at the horizontal myoseptum, an intermediate

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

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

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

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

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

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

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

126 omotes endocytosis of its TrkA receptors and axon growth by calcineurin-mediated dephosphorylation of

127 K3 activity levels to differentially control axon growth by coordinating the stability and configurat

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

129 In this study, we aim to promote axon growth by directly targeting the growth cone.

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

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

132 response mediator protein 2 (CRMP2), support axon growth by regulating the stability of axonal microt

133 and chicken commissural neurons, the rate of axon growth can either be stalled or accelerated.

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

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

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

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

138 he molecular mechanisms regulating intrinsic axon growth capacity in the adult CNS and discuss potent

139 ter injuries due to the diminished intrinsic axon growth capacity of mature neurons and the hostile e

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

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

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

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

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

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

146 as a negative regulator of neuronal cell and axon growth cone migrations.

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

148 as a prominently expressed E3 ligase in RGC axon growth cones and show that disrupting its function

149 orter segments by intermediate targets where axon growth cones are believed to coordinate guidance cu

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

151 that Stumpy is needed specifically for motor axon growth cones to proceed past intermediate targets.

152 In commissural axon growth cones, Vangl2 is predominantly localized on

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

154 sentation of Frizzled3 in rodent commissural axon growth cones.

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

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

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

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

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

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

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

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

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

164 yzed the role of N-cadherin in primary motor axons growth during development of the zebrafish (Danio

165 growth factor (NGF) is a potent survival and axon growth factor for neuronal populations in the perip

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

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

168 synapse formation is a crucial component of axon growth, GABA signalling may also shape the axon arb

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

170 Work on axon growth has classically focused on understanding how

171 that mechanical stimulation also can affect axon growth; however, whether mechanical force contribut

172 that specific lipids can powerfully inhibit axon growth, identify sulfatide as a novel myelin-associ

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

174 tent AMPK activators, inhibit axogenesis and axon growth in an AMPK-dependent manner.

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

176 that the two MT-binding activities regulate axon growth in an opposing manner: The lattice-binding a

177 lesion demonstrated a significant decline of axon growth in animals with transient NT-3 expression, o

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

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

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

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

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

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

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

185 A Cdh1, the 9D Cdh1 mutant failed to inhibit axon growth in primary cerebellar granule neurons.

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

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

188 ced by ZAMs enhanced cell death and impaired axon growth in surviving neurons.

189 d for NGF-dependent TrkA internalization and axon growth in sympathetic neurons.

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

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

192 Tnc inhibits olfactory sensory neuron (OSN) axon growth in the developing OB before glomerulogenesis

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

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

195 role, not mimicked by BDNF, in promoting SGN axon growth in the organ of Corti and synaptogenesis on

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

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

198 3-3 protein-protein interactions, stimulates axon growth in vitro and regeneration in vivo.

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

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

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

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

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

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

205 ons of SSDP in neural patterning and sensory axon growth, in part due to the stabilization of LIM-HD/

206 s able to partially rescue the inhibition of axon growth induced by a dominant-negative form of CLIM

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

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

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

210 anner: The lattice-binding activity mediates axon growth inhibition induced by suppression of GSK3 ac

211 ents, tackling a common target that mediates axon growth inhibition offers an alternative strategy to

212 ut the substrate(s) and mechanisms conveying axon growth inhibition remain elusive.

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

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

215 ntify sulfatide as a novel myelin-associated axon growth inhibitor, and provide evidence that sulfati

216 Following SCI, axon growth inhibitors and other inflammatory responses

217 After CNS injuries, axon growth inhibitors from the myelin and the scar tiss

218 known central nervous system scar associated axon growth inhibitors, semaphorin 3A has been shown to

219 regenerate is the presence of myelin-derived axon growth inhibitors, the role of which, however, rema

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

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

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

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

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

225 Axon growth is driven by the movement of a growth cone,

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

227 myelin or Semaphorin-mediated inhibition of axon growth is insufficient to promote 5-HT axon regener

228 derived neurotrophic cues, but whether local axon growth is mediated by endocytosis-dependent signali

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

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

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

232 Axon growth is primarily driven by microtubules.

233 Axon growth is regulated by many proteins, including adh

234 Inhibition of central nervous system axon growth is reportedly mediated in part by calcium-de

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

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

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

238 owever, how mitochondrial dynamics influence axon growth largely is unstudied.

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

240 We show that inhibition of axon growth mediated by AMPK overactivation requires TSC

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

242 cord transection injuries induce significant axon growth of descending serotonergic fibers in the vic

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

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

245 d macrophage response, but without enhancing axon growth or notable toxicity.

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

247 muscle myosin II (NMII) markedly accelerates axon growth over permissive and nonpermissive substrates

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

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

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

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

252 Axon growth potential is highest in young neurons but di

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

254 ontributes to the age-related decline of the axon growth potential.

255 " lesion) triggers a transcription-dependent axon growth program.

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

257 axon terminals in neurons, and activates the axon growth-promoting kinase JNK (c-Jun N-terminal prote

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

259 ns yields pleiotropic outcomes, causing both axon growth promotion and inhibition.

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

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

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

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

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

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

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

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

268 Axon growth requires long-range transport of organelles,

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

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

271 hic factor actions (i.e., ability to promote axon growth, selection of neurochemical phenotype and en

272 2+)]i at an optimal concentration for normal axon growth.SIGNIFICANCE STATEMENT Accumulating evidence

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

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

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

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

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

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

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

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

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

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

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

284 ed KLF family members suppressed or enhanced axon growth to differing extents, and several growth-sup

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 ing this approach, a significant increase in axon growth up to macrophage foci was evident.

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

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

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 mportantly, the ability of ZAMs to stimulate axon growth was transient; prolonged exposure to factors

293 Locomotion and raphespinal axon growth were assessed during 3 months of treatment b

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

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

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 of guidance factors required for directional axon growth, with a particular emphasis on the role of m

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