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1 ry creates physical and chemical barriers to axon regeneration.
2 ke Factor) family RBP UNC-75 is required for axon regeneration.
3 e inhibitory properties of the glial scar in axon regeneration.
4 ic kinases that regulated neuronal death and axon regeneration.
5 e activation of GSK3beta reduces AKT-induced axon regeneration.
6 es both GSK3beta and AKT-mediated effects on axon regeneration.
7 ich mTORC2 and pAKT-S473 negatively regulate axon regeneration.
8 ion of eIF2Bepsilon is sufficient to promote axon regeneration.
9 F and RhoGAP, respectively, as regulators of axon regeneration.
10 onal cues to create a supportive pathway for axon regeneration.
11 tive and negative cues to regulate adult CNS axon regeneration.
12 s) in post-transcriptional regulation during axon regeneration.
13  and that Celf2 mutant mice are defective in axon regeneration.
14 that chemical inhibition of PARPs can elicit axon regeneration.
15 o critical parallel pathways for AKT-induced axon regeneration.
16 DLK knockout, while simultaneously promoting axon regeneration.
17 ion of neuronal polarity is not required for axon regeneration.
18 erve injury, mitochondrial localization, and axon regeneration.
19  rather than prevents central nervous system axon regeneration.
20 r kinase 1 (DLK-1), a conserved regulator of axon regeneration.
21  and PARGs mediate DLK function in enhancing axon regeneration.
22 led their unexpected activity in suppressing axon regeneration.
23  indispensable role in mediating AKT-induced axon regeneration.
24 K3beta, as both GSK3(S/A) knock-ins improved axon regeneration.
25 ownstream effector of GSK3beta in regulating axon regeneration.
26 red C. elegans GABA motor neurons to enhance axon regeneration.
27 nthesis through the Kennedy pathway promoted axon regeneration.
28 cant spontaneous axonal sprouting instead of axon regeneration.
29 y and chemically inhibitory scar that limits axon regeneration.
30 ensive view of the complex biology governing axon regeneration.
31 nockdown of Lrig2 significantly improves CNS axon regeneration.
32 onditional knock out in vivo impairs sensory axon regeneration.
33  limits their utility for assessments of CST axon regeneration.
34 nd growth cone re-formation are required for axon regeneration.
35 njury, and is cell-autonomously required for axon regeneration.
36  scar and poor axon growth potential prevent axon regeneration.
37  of the intrinsic elongating form of sensory axon regeneration.
38 tify PARP1 as an effective target to promote axon regeneration.
39 injured neurons and contributes to stimulate axon regeneration.
40 adopted this mechanism for their spontaneous axon regeneration.
41 l deficits due to the absence of spontaneous axon regeneration.
42 keleton that are prerequisites for effective axon regeneration.
43 rminal phosphate cyclase) as an inhibitor of axon regeneration.
44  and suggests hypoxia as a tool to stimulate axon regeneration.
45  may have therapeutic potential in promoting axon regeneration.
46 promoting retinal ganglion cell survival and axon regeneration.
47  NG2+ cells is an additional obstacle to CNS axon regeneration.
48  damage, inflammatory spillover and hampered axon regeneration.
49 ulated by mTOR in injured neurons to promote axon regeneration.
50 t 4E-BP inhibition, is sufficient to promote axon regeneration.
51 y hostile environment and further inhibiting axon regeneration.
52 ivate intrinsic signaling pathways to enable axon regeneration.
53  4E-BP is required for PTEN deletion-induced axon regeneration.
54 al elongation and forming potent barriers to axon regeneration.
55 RSKS-1 as a new cell-autonomous inhibitor of axon regeneration.
56 athways, and the role of stress in promoting axon regeneration.
57  and leads to enhanced retinal ganglion cell axon regeneration.
58 owth-inert retraction bulbs and facilitating axon regeneration.
59  modulates growth cone actin dynamics during axon regeneration.
60 portant in sealing the lesion and inhibiting axon regeneration.
61  a potential therapeutic strategy to enhance axon regeneration.
62 y progressing growth cones is a major aim in axon regeneration.
63 linical investigations to promote functional axon regeneration.
64  these cell types might be key inhibitors of axon regeneration.
65 ased dendrite regeneration without affecting axon regeneration.
66 models of dorsal root ganglion neuron (DRGN) axon regeneration.
67 have been few direct analyses of age-related axon regeneration.
68 DAC5 as a transcriptional switch controlling axon regeneration.
69 nd that PI3K pathway is required for sensory axon regeneration.
70 ortant for providing a permissive bridge for axon regeneration.
71 ein futsch/MAP1B, which is also required for axon regeneration.
72 ical treatment with 7,8 DHF had no effect on axon regeneration.
73 ecline in anterior ventral microtubule (AVM) axon regeneration.
74 survival, migration, and polarity as well as axon regeneration.
75 s and that associate with their survival and axon regeneration.
76 ynthesis and toward PL synthesis may promote axon regeneration.
77 entify features critical for its function in axon regeneration.
78 hat its recruitment after injury facilitates axon regeneration.
79 ng neuronal survival, axon degeneration, and axon regeneration.
80 ress granule protein and phase separation in axon regeneration.
81           THBS1 knockdown in RGCs eliminated axon regeneration.
82  not form granules and are unable to inhibit axon regeneration.
83 otein functions cell autonomously to inhibit axon regeneration.
84 r mechanosensitive ion channels may regulate axon regeneration.
85 d upregulated in oligodendrocytes during RGC axon regeneration.
86  reconcile conflicting data on GSK3-mediated axon regeneration.
87 al activation, with very limited spontaneous axon regeneration.
88 d Sox11 as one that could induce substantial axon regeneration.
89 gnaling between SCs and axons for successful axon regeneration.
90 of fatty acid synthase (Fasn) in SGC impairs axon regeneration.
91 Cs) survive with relatively high spontaneous axon regeneration.
92 neurons, Caenorhabditis elegans neurons lose axon regeneration ability as they age, but it is not kno
93  a novel mechanism for controlling intrinsic axon regeneration ability.
94 ons for 12 weeks post-crush in vivo enhances axon regeneration across a chondroitinase-digested DREZ
95 thway, that poly-(ADP ribosylation) inhibits axon regeneration across species, and that chemical inhi
96            Available strategies of promoting axon regeneration act on only some of these types.
97 nt of the mTOR pathway facilitates human RGC axon regeneration after axotomy, providing evidence that
98 1) by initiating retinal ganglion cell (RGC) axon regeneration after axotomy.
99                                     Enabling axon regeneration after central nervous system (CNS) inj
100  as a novel therapeutic target for promoting axon regeneration after CNS injury.
101 le of mitochondrial transport for successful axon regeneration after injury and provide new insights
102 on growth during CNS development, as well as axon regeneration after injury in the peripheral nervous
103 lar membranes promoted adult rat optic nerve axon regeneration after injury in vivo.
104                                              Axon regeneration after injury requires the extensive re
105 lation patterns and transcriptomes, promotes axon regeneration after injury, and reverses vision loss
106 cx1 also promotes both neuronal survival and axon regeneration after injury, and these effects depend
107 one directive molecules known for inhibiting axon regeneration after injury.
108 we show that RtcB acts in neurons to inhibit axon regeneration after nerve injury.
109  its function promoted retinal ganglion cell axon regeneration after optic nerve crush in mice.
110 or 9 (KLF9) via shRNA promotes long-distance axon regeneration after optic nerve injury and uncover a
111 ay in retinal ganglion cells (RGCs) promotes axon regeneration after optic nerve injury.
112 r injury, promotes dramatic RGC survival and axon regeneration after optic nerve injury.
113 ugh the glycerol phosphate pathway, enhanced axon regeneration after optic nerve injury.
114  phenocopied enriched conditioning-dependent axon regeneration after SCI leading to improved function
115                                              Axon regeneration after spinal cord injury (SCI) fails d
116                                              Axon regeneration after spinal cord injury (SCI) fails d
117 )/cofilin controls actin turnover to sustain axon regeneration after spinal cord injury through its a
118 ults in functional improvements and promotes axon regeneration after spinal cord injury.
119 ortive environment for neuronal survival and axon regeneration after spinal cord injury.
120  while DCXs synergize with mTOR to stimulate axon regeneration, alone they can promote neuronal survi
121 ntrol of the neurite outgrowth length in our axon regeneration analysis.
122  involvement of mechanosensitive channels in axon regeneration and add a potential target for modulat
123  proper navigational abilities for effective axon regeneration and correct targeting of higher-order
124   Here we present a protocol for analyses of axon regeneration and density in unsectioned adult mouse
125 itical extrinsic and intrinsic regulators of axon regeneration and establishes shRNA as a viable mean
126 n, protect tissue around the lesion, support axon regeneration and form myelin.
127 th neural progenitor cells (NPCs) to support axon regeneration and form new 'neural relays' across si
128 iting may provide a new option for promoting axon regeneration and functional recovery after CNS trau
129 s their potential implications for promoting axon regeneration and functional recovery after nerve in
130 with parthenolidein vivomarkedly accelerated axon regeneration and functional recovery.
131 ctivate a pro-regenerative program to enable axon regeneration and functional recovery.
132 generative transcriptional program to enable axon regeneration and functional recovery.
133 Inpp5f (Sac2) leads to robust enhancement of axon regeneration and growth cone reformation.
134 ates had not previously been associated with axon regeneration and implicate new pathways of interest
135 a circuit-based mechanism that regulates CNS axon regeneration and implicate primary cilia as a regen
136 gether, these drug-elicited effects promoted axon regeneration and improved motor function after SCI.
137  either small-molecule trkB agonist enhanced axon regeneration and muscle reinnervation after periphe
138 ormation in the lesion site that facilitated axon regeneration and neuron preservation.
139 R tip concentration was observed only during axon regeneration and not during dendrite regeneration.
140  IL-10-null mice was accompanied by impaired axon regeneration and poor recovery of motor and sensory
141 Furthermore, lack of IL-10 leads to impaired axon regeneration and poor recovery of motor and sensory
142 ter peripheral nerve injury is essential for axon regeneration and recovery.
143 ing a nonpermissive environment that impairs axon regeneration and remyelination.
144 ation, downstream of Pten deletion, promotes axon regeneration and RGC survival.
145 roRNA-138 (miR-138) as a novel suppressor of axon regeneration and show that SIRT1, the NAD-dependent
146 esults also underline the key role of SCs in axon regeneration and successful target reinnervation.SI
147 cial effects of OSK-induced reprogramming in axon regeneration and vision require the DNA demethylase
148 athway regulates nervous system development, axon regeneration, and neuronal degeneration after acute
149 anism selectively contributing to myelinated axon regeneration, and point out the role of Cl(-) modul
150 TOR can serve as powerful tool for enhancing axon regeneration, and they highlight the remarkable cap
151 tes, however, are capable of spontaneous CNS axon regeneration, and we have shown that retinal gangli
152 ene expression, but their roles in mammalian axon regeneration are not well explored.
153            Implications of GSK3 activity for axon regeneration are often inconsistent, if not controv
154                    Stroked eyes showed minor axon regeneration around the optic nerve lesion site at
155                            Human SCs support axon regeneration as do rat SCs.
156 ce suggests that reduced levels could impair axon regeneration as well as axon survival in aging and
157         HDAC5 nuclear export is required for axon regeneration, as expression of a nuclear-trapped HD
158 lot assays, transmission EM of exosomes, and axon regeneration assays, we explored the secretion and
159   While traditionally viewed as a barrier to axon regeneration, beneficial functions of the glial sca
160 ased peripheral conditioning-lesion-enhanced axon regeneration beyond the epicenter.
161  (CSPGs) found within the glial scar inhibit axon regeneration but the intracellular signaling mechan
162 cell-intrinsic and extrinsic pathways govern axon regeneration, but only a limited number of factors
163 ns were described as regulatory proteins for axon regeneration, but they appear to function in many c
164 iated activation of 5-HT signalling promotes axon regeneration by activating both the RhoA and cAMP p
165                          SER-7 also promotes axon regeneration by activating the cyclic AMP (cAMP) si
166  factor, and that 5-HT subsequently promotes axon regeneration by autocrine signalling through the SE
167 he HSP proteins spastin and atlastin promote axon regeneration by coordinating concentration of the E
168 diated RNA repair/splicing pathway restricts axon regeneration by inhibiting the nonconventional spli
169                       Inhibition of cortical axon regeneration by Nogo-A depends on a NgR1/PlexinA2 g
170 ta are well positioned to regulate intrinsic axon regeneration capacity, which declines developmental
171 dults, dip-2 also inhibits initial stages of axon regeneration cell autonomously and acts in parallel
172 lion cells at specific time points along the axon regeneration continuum from early growth to target
173  phases of nerve repair, resulting in slowed axon regeneration, cutaneous reinnervation, and function
174 ation of STMN2 rescued neurite outgrowth and axon regeneration deficits induced by TDP-43 depletion.
175                                              Axon regeneration fails in the adult CNS, resulting in p
176                                              Axon regeneration failure causes neurological deficits a
177 nal program is a critical step in successful axon regeneration following injury.
178 r remyelination, macrophage recruitment, and axon regeneration following nerve injury.
179 f these genes improved neuronal survival and axon regeneration following ONC.
180 egies to enhance neuroplasticity and promote axon regeneration following spinal cord injury, and resu
181                           The probability of axon regeneration for individual identified neurons was
182 odels of SCI, we report robust corticospinal axon regeneration, functional synapse formation and impr
183                     The factors that control axon regeneration have been examined in many systems, bu
184                     While many regulators of axon regeneration have been identified, very little is k
185 tegrins can overcome inhibition and increase axon regeneration, however integrins are not transported
186 pulsive guidance responses and inhibition of axon regeneration; however, the cytoskeletal mechanisms
187 S6K1 decrease the effect of PTEN deletion on axon regeneration, implicating a dual role of S6K1 in re
188 t reduction of spastin leads to a deficit in axon regeneration in a Drosophila model.
189 on of multiple RAGs and promotion of sensory axon regeneration in a mouse model of spinal cord injury
190 stream of FASN in SGC contributes to promote axon regeneration in adult peripheral nerves and highlig
191  of alpha9 integrin and kindlin-1 on sensory axon regeneration in adult rat spinal cord after dorsal
192                            Here we show that axon regeneration in aging C. elegans motor neurons is i
193 oRaf or optoAKT activation not only enhanced axon regeneration in both regeneration-competent and -in
194                  To identify genes affecting axon regeneration in Caenorhabditis elegans, we performe
195  active non-coding RNA (ncRNA) essential for axon regeneration in Caenorhabditis elegans.
196 onverted GD1a ganglioside to GM1 and rescued axon regeneration in CNS axons and in PNS axons after Ne
197 r, others have demonstrated mTOR-independent axon regeneration in different cell types, raising the q
198 , and deficiency of Archease or Xbp1 impeded axon regeneration in Drosophila.
199 nel, functions as an intrinsic inhibitor for axon regeneration in Drosophila.
200 evelopmental axon growth may also facilitate axon regeneration in injured adult neurons.
201 nomous defects in macrophage recruitment and axon regeneration in injured nerves following loss of Gp
202  potential therapeutic approaches to promote axon regeneration in injury and other degenerative disea
203  mechanisms of neuronal injury responses and axon regeneration in mammals.
204 pha agonist fenofibrate rescues the impaired axon regeneration in mice lacking Fasn in SGC.
205 rently lack a therapy that potently enhances axon regeneration in patients with traumatic nerve injur
206  wild Antheraea pernyi silkworms can support axon regeneration in peripheral nerve injury.
207 s with age, yet the mechanisms that regulate axon regeneration in response to age are not known.
208 elongation in hippocampal neurons as well as axon regeneration in sensory neurons.
209 re neurons, growth factors minimally promote axon regeneration in the adult central nervous system (C
210 uggest new therapeutic strategies to promote axon regeneration in the adult CNS.SIGNIFICANCE STATEMEN
211 -eIF2Bepsilon signaling module in regulating axon regeneration in the adult mammalian CNS.
212 emoved by active DNA demethylation to permit axon regeneration in the adult mammalian nervous system.
213                                    Promoting axon regeneration in the central and peripheral nervous
214                                     The poor axon regeneration in the central nervous system (CNS) of
215 trolling myelination after injury and during axon regeneration in the central nervous system (CNS).
216                                              Axon regeneration in the CNS requires reactivating injur
217  might be a viable approach for facilitating axon regeneration in the diseased or injured human CNS,
218 ckdown undermines both neuronal survival and axon regeneration in the high regenerative capacity mode
219                                              Axon regeneration in the injured adult CNS is reportedly
220 tified gene expression patterns and promotes axon regeneration in the injured adult mouse CNS, demons
221 l ganglion cells from apoptosis and promotes axon regeneration in the injured optic nerve.
222 thesis might be involved in the mechanism of axon regeneration in the lamprey spinal cord.
223  the presence of Nogo-A does not inhibit RGC axon regeneration in the lizard visual pathway.
224                    Overcoming the failure of axon regeneration in the mammalian central nervous syste
225 protein Nogo-A contributes to the failure of axon regeneration in the mammalian central nervous syste
226 ng as a central module for promoting sensory axon regeneration in the mammalian nervous system.
227 h ability is the major reason for the failed axon regeneration in the mature mammalian CNS.
228                       The main limitation on axon regeneration in the peripheral nervous system (PNS)
229 hila CNS, whereas its overexpression reduced axon regeneration in the periphery.
230 lay a key role in spontaneous lizard retinal axon regeneration in the presence of Nogo-A.
231 ce demonstrated a 2-fold increase in sensory axon regeneration in the spinal cord in comparison to wi
232                                   Studies of axon regeneration in the spinal cord often assess regene
233 ture of the mechanisms behind successful CNS axon regeneration in this vertebrate model organism.
234 oth an RNAi-based screen for defective motor axon regeneration in unc-70/beta-spectrin mutants and a
235 duction of HIF-1alpha using hypoxia enhances axon regeneration in vitro and in vivo in sensory neuron
236 reas enhancing HDAC5 nuclear export promotes axon regeneration in vitro and in vivo.
237 h and branching defects in vivo and impaired axon regeneration in vitro.
238 n4b seems to represent no major obstacle for axon regeneration in vivo because it is less inhibitory
239 ite growth suppression in vitro and promoted axon regeneration in vivo These findings demonstrate a n
240 nd neuronal viability in vitro and restricts axon regeneration in vivo, and demonstrate a novel, non-
241 had neuroprotective properties and drove CNS axon regeneration in vivo, in part via secretion of a co
242 ce that miR-138 and SIRT1 regulate mammalian axon regeneration in vivo.
243 te depletion of Smad1 in adult mice prevents axon regeneration in vivo.
244 eletion or inactivation of GSK3beta promotes axon regeneration independently of the mTORC1 pathway, w
245  RGCs to block AIS reassembly did not affect axon regeneration, indicating that preservation of neuro
246                    DmPiezo activation during axon regeneration induces local Ca(2+) transients at the
247        Significance statement: The extent of axon regeneration is a critical determinant of neurologi
248                            After CNS injury, axon regeneration is blocked by an inhibitory environmen
249                                              Axon regeneration is essential to restore the nervous sy
250 dentified and it is not clear to what extent axon regeneration is evolutionarily conserved.
251  imaging, and whole-mount analysis show that axon regeneration is fueled by elevated actin turnover.
252                                              Axon regeneration is hindered by a decline of intrinsic
253 er, the neuronal cell biology that underlies axon regeneration is incompletely understood.
254                   Furthermore, inhibition of axon regeneration is independent of the RtcB cofactor ar
255      This reciprocal inhibition ensures that axon regeneration is inhibited only in older neurons.
256       Understanding the mechanism underlying axon regeneration is of great practical importance for d
257                       In the absence of TTL, axon regeneration is reduced severely.
258                             A determinant of axon regeneration is the intrinsic growth ability of inj
259 ment, a major limiting factor for successful axon regeneration is the poor intrinsic regenerative cap
260  trkB is knocked out selectively in neurons, axon regeneration is very weak, and topical treatment wi
261 rfering CASP2-mediated retinal ganglion cell axon regeneration, Muller cell activation and CNTF produ
262 ry strategy to promote functionally-relevant axon regeneration of adult neurons into the CNS after in
263         The deletion of KLF4 in vivo induces axon regeneration of adult retinal ganglion cells (RGCs)
264 ch add poly(ADP-ribose) to proteins, inhibit axon regeneration of both C. elegans GABA neurons and ma
265    Functionally, Tet3 is required for robust axon regeneration of DRG neurons and behavioral recovery
266           In addition, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adu
267                     Loss of DmPiezo enhances axon regeneration of sensory neurons in the peripheral a
268      Severe motoneuron death and inefficient axon regeneration often result in devastating motor dysf
269                     Ror was not required for axon regeneration or normal dendrite development, sugges
270 on associated with Wallerian degeneration or axon regeneration or the clearance of myelin debris by m
271 oves intrinsic growth potential to result in axon regeneration out of a growth-supportive peripheral
272 tudy demonstrates that long-distance sensory axon regeneration over a normal pathway and with sensory
273 r genetic loss of PARP1 markedly facilitates axon regeneration over nonpermissive substrates.
274 e, we identify novel intrinsic regulators of axon regeneration: poly(ADP-ribose) glycohodrolases (PAR
275                   We therefore conclude that axon regeneration promoted by suppression of CASP2 and C
276  by down-regulating LIN-41, an important AVM axon regeneration-promoting factor.
277 transmission that doubles as a suppressor of axon regeneration, providing a molecular clue for the sy
278  the growth potential and induce spontaneous axon regeneration remain poorly understood.
279 ury responses, such as neuronal survival and axon regeneration, remain largely unknown.
280 tory logic driving successful vertebrate CNS axon regeneration, revealing key gene regulatory candida
281 oform in CNS, AKT3, induces much more robust axon regeneration than AKT1 and that activation of mTORC
282 ection of the cross-regulating mechanisms in axon regeneration that involve the downstream effectors
283 LF4 and activated STAT3 in the regulation of axon regeneration that might have therapeutic implicatio
284  the negative regulator of PI3K, induces CNS axon regeneration through the activation of PI3K-mTOR si
285                         Our study thus links axon regeneration to cellular stress and RNA metabolism,
286 ole for active DNA demethylation in allowing axon regeneration to occur in the mature nervous system
287 nt state with little axonal growth to robust axon regeneration upon injury.
288                                              Axon regeneration was enhanced when the fibrin glue cont
289                                              Axon regeneration was similarly impaired in neurons when
290 rstand genetic determinants of mammalian CNS axon regeneration, we completed an unbiased RNAi gene-si
291    In an established mouse model with robust axon regeneration, we show that Armcx1, a mammalian-spec
292        Extending these findings to mammalian axon regeneration, we show that mouse Celf2 expression i
293 tinal ganglion cell (RGC) loss and extent of axon regeneration were determined at 8 and 14 days after
294 roglia depletion, spontaneous and LI-induced axon regeneration were unaffected by PLX5622 treatment o
295 urthermore, chemical PARP inhibitors improve axon regeneration when administered after injury.
296 ctive therapeutic strategy for promoting CNS axon regeneration when combined with neurotrophic factor
297 n of a nuclear-trapped HDAC5 mutant prevents axon regeneration, whereas enhancing HDAC5 nuclear expor
298 wing spinal cord injury is due to failure of axon regeneration, which has been ascribed to environmen
299 types, such as the maintenance of memory and axon regeneration with age, in both mammals and C. elega
300 fully enhance the repair capacity of SCs and axon regeneration, without substantial off-target damage
301 aling that drives both neurodegeneration and axon regeneration, yet little is known about the factors

 
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