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1 d upregulated in oligodendrocytes during RGC axon regeneration.
2 al activation, with very limited spontaneous axon regeneration.
3 K3beta, as both GSK3(S/A) knock-ins improved axon regeneration.
4 ownstream effector of GSK3beta in regulating axon regeneration.
5 red C. elegans GABA motor neurons to enhance axon regeneration.
6 cant spontaneous axonal sprouting instead of axon regeneration.
7 y and chemically inhibitory scar that limits axon regeneration.
8 ensive view of the complex biology governing axon regeneration.
9 nockdown of Lrig2 significantly improves CNS axon regeneration.
10 onditional knock out in vivo impairs sensory axon regeneration.
11 limits their utility for assessments of CST axon regeneration.
12 nd growth cone re-formation are required for axon regeneration.
13 scar and poor axon growth potential prevent axon regeneration.
14 of the intrinsic elongating form of sensory axon regeneration.
15 tify PARP1 as an effective target to promote axon regeneration.
16 injured neurons and contributes to stimulate axon regeneration.
17 l deficits due to the absence of spontaneous axon regeneration.
18 keleton that are prerequisites for effective axon regeneration.
19 rminal phosphate cyclase) as an inhibitor of axon regeneration.
20 and suggests hypoxia as a tool to stimulate axon regeneration.
21 may have therapeutic potential in promoting axon regeneration.
22 promoting retinal ganglion cell survival and axon regeneration.
23 NG2+ cells is an additional obstacle to CNS axon regeneration.
24 ulated by mTOR in injured neurons to promote axon regeneration.
25 t 4E-BP inhibition, is sufficient to promote axon regeneration.
26 y hostile environment and further inhibiting axon regeneration.
27 ivate intrinsic signaling pathways to enable axon regeneration.
28 4E-BP is required for PTEN deletion-induced axon regeneration.
29 al elongation and forming potent barriers to axon regeneration.
30 RSKS-1 as a new cell-autonomous inhibitor of axon regeneration.
31 athways, and the role of stress in promoting axon regeneration.
32 and leads to enhanced retinal ganglion cell axon regeneration.
33 owth-inert retraction bulbs and facilitating axon regeneration.
34 d Sox11 as one that could induce substantial axon regeneration.
35 modulates growth cone actin dynamics during axon regeneration.
36 portant in sealing the lesion and inhibiting axon regeneration.
37 a potential therapeutic strategy to enhance axon regeneration.
38 y progressing growth cones is a major aim in axon regeneration.
39 linical investigations to promote functional axon regeneration.
40 these cell types might be key inhibitors of axon regeneration.
41 models of dorsal root ganglion neuron (DRGN) axon regeneration.
42 have been few direct analyses of age-related axon regeneration.
43 DAC5 as a transcriptional switch controlling axon regeneration.
44 nd that PI3K pathway is required for sensory axon regeneration.
45 ortant for providing a permissive bridge for axon regeneration.
46 ical treatment with 7,8 DHF had no effect on axon regeneration.
47 gnaling between SCs and axons for successful axon regeneration.
48 ecline in anterior ventral microtubule (AVM) axon regeneration.
49 survival, migration, and polarity as well as axon regeneration.
50 PTEN-Akt pathway that is also important for axon regeneration.
51 ) are regulators of synaptic development and axon regeneration.
52 hnRNP K that is essential for successful CNS axon regeneration.
53 elicits profound cellular changes, including axon regeneration.
54 se that results in a dense scar that impedes axon regeneration.
55 Cs) survive with relatively high spontaneous axon regeneration.
56 f tubulin modifications that is required for axon regeneration.
57 tegy for identifying conserved mechanisms of axon regeneration.
58 n essential role in growth cone dynamics and axon regeneration.
59 ormation of this "glial bridge" and prevents axon regeneration.
60 -induced retrograde axonal degeneration, and axon regeneration.
61 ors is insufficient to trigger long-distance axon regeneration.
62 l nervous system is incapable of restorative axon regeneration.
63 omponents as effective targets for promoting axon regeneration.
64 dulation of BMP signaling influences sensory axon regeneration.
65 h a possible role of NFs in the mechanism of axon regeneration.
66 ys must be coordinately activated to promote axon regeneration.
67 r the role of c-Jun in regulation of in vivo axon regeneration.
68 that act synergistically to promote enhanced axon regeneration.
69 ecular mechanisms within neurons that govern axon regeneration.
70 ry creates physical and chemical barriers to axon regeneration.
71 ke Factor) family RBP UNC-75 is required for axon regeneration.
72 e inhibitory properties of the glial scar in axon regeneration.
73 e activation of GSK3beta reduces AKT-induced axon regeneration.
74 es both GSK3beta and AKT-mediated effects on axon regeneration.
75 ich mTORC2 and pAKT-S473 negatively regulate axon regeneration.
76 ion of eIF2Bepsilon is sufficient to promote axon regeneration.
77 F and RhoGAP, respectively, as regulators of axon regeneration.
78 onal cues to create a supportive pathway for axon regeneration.
79 tive and negative cues to regulate adult CNS axon regeneration.
80 s) in post-transcriptional regulation during axon regeneration.
81 and that Celf2 mutant mice are defective in axon regeneration.
82 reconcile conflicting data on GSK3-mediated axon regeneration.
83 that chemical inhibition of PARPs can elicit axon regeneration.
84 o critical parallel pathways for AKT-induced axon regeneration.
85 ion of neuronal polarity is not required for axon regeneration.
86 erve injury, mitochondrial localization, and axon regeneration.
87 rather than prevents central nervous system axon regeneration.
88 r kinase 1 (DLK-1), a conserved regulator of axon regeneration.
89 and PARGs mediate DLK function in enhancing axon regeneration.
90 indispensable role in mediating AKT-induced axon regeneration.
91 neurons, Caenorhabditis elegans neurons lose axon regeneration ability as they age, but it is not kno
93 heathing glia (OEG) transplantation promotes axon regeneration across a complete spinal cord transect
94 thway, that poly-(ADP ribosylation) inhibits axon regeneration across species, and that chemical inhi
95 nglion neurons to express kindlin-1 promoted axon regeneration across the dorsal root entry zone and
100 le of mitochondrial transport for successful axon regeneration after injury and provide new insights
101 on growth during CNS development, as well as axon regeneration after injury in the peripheral nervous
104 cx1 also promotes both neuronal survival and axon regeneration after injury, and these effects depend
110 or 9 (KLF9) via shRNA promotes long-distance axon regeneration after optic nerve injury and uncover a
114 ganglioside Ab with GD1a reactivity inhibits axon regeneration after PNS injury in an animal model.
119 while DCXs synergize with mTOR to stimulate axon regeneration, alone they can promote neuronal survi
122 itical extrinsic and intrinsic regulators of axon regeneration and establishes shRNA as a viable mean
125 s their potential implications for promoting axon regeneration and functional recovery after nerve in
130 ates had not previously been associated with axon regeneration and implicate new pathways of interest
131 gether, these drug-elicited effects promoted axon regeneration and improved motor function after SCI.
132 that anti-GD1a Abs can mediate inhibition of axon regeneration and limit recovery in some patients wi
133 either small-molecule trkB agonist enhanced axon regeneration and muscle reinnervation after periphe
136 R tip concentration was observed only during axon regeneration and not during dendrite regeneration.
137 iscusses possible strategies for stimulating axon regeneration and perhaps functional recovery after
138 IL-10-null mice was accompanied by impaired axon regeneration and poor recovery of motor and sensory
139 Furthermore, lack of IL-10 leads to impaired axon regeneration and poor recovery of motor and sensory
143 roRNA-138 (miR-138) as a novel suppressor of axon regeneration and show that SIRT1, the NAD-dependent
144 esults also underline the key role of SCs in axon regeneration and successful target reinnervation.SI
145 ulation of integrins is a route to promoting axon regeneration and understanding regeneration failure
146 athway regulates nervous system development, axon regeneration, and neuronal degeneration after acute
147 anism selectively contributing to myelinated axon regeneration, and point out the role of Cl(-) modul
148 TOR can serve as powerful tool for enhancing axon regeneration, and they highlight the remarkable cap
149 tes, however, are capable of spontaneous CNS axon regeneration, and we have shown that retinal gangli
150 death, scarring, and a failure of tissue and axon regeneration are not ameliorated by current treatme
155 ce suggests that reduced levels could impair axon regeneration as well as axon survival in aging and
157 While traditionally viewed as a barrier to axon regeneration, beneficial functions of the glial sca
158 Combinatorial treatment generated motor axon regeneration beyond both C5 hemisection and T3 comp
161 (CSPGs) found within the glial scar inhibit axon regeneration but the intracellular signaling mechan
163 cell-intrinsic and extrinsic pathways govern axon regeneration, but only a limited number of factors
164 iated activation of 5-HT signalling promotes axon regeneration by activating both the RhoA and cAMP p
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 ta are well positioned to regulate intrinsic axon regeneration capacity, which declines developmental
169 phases of nerve repair, resulting in slowed axon regeneration, cutaneous reinnervation, and function
176 odels of SCI, we report robust corticospinal axon regeneration, functional synapse formation and impr
178 ress made in understanding the mechanisms of axon regeneration, how a neuron responds to an injury an
179 tegrins can overcome inhibition and increase axon regeneration, however integrins are not transported
180 pulsive guidance responses and inhibition of axon regeneration; however, the cytoskeletal mechanisms
181 S6K1 decrease the effect of PTEN deletion on axon regeneration, implicating a dual role of S6K1 in re
183 on of multiple RAGs and promotion of sensory axon regeneration in a mouse model of spinal cord injury
184 vely in adult DRG neurons results in sensory axon regeneration in a mouse model of spinal cord injury
185 pathways as key for sustaining long-distance axon regeneration in adult CNS, a crucial step towards f
186 of alpha9 integrin and kindlin-1 on sensory axon regeneration in adult rat spinal cord after dorsal
190 onverted GD1a ganglioside to GM1 and rescued axon regeneration in CNS axons and in PNS axons after Ne
192 r, others have demonstrated mTOR-independent axon regeneration in different cell types, raising the q
195 nomous defects in macrophage recruitment and axon regeneration in injured nerves following loss of Gp
196 potential therapeutic approaches to promote axon regeneration in injury and other degenerative disea
198 rently lack a therapy that potently enhances axon regeneration in patients with traumatic nerve injur
200 s with age, yet the mechanisms that regulate axon regeneration in response to age are not known.
202 uggest new therapeutic strategies to promote axon regeneration in the adult CNS.SIGNIFICANCE STATEMEN
204 emoved by active DNA demethylation to permit axon regeneration in the adult mammalian nervous system.
208 ckdown undermines both neuronal survival and axon regeneration in the high regenerative capacity mode
210 tified gene expression patterns and promotes axon regeneration in the injured adult mouse CNS, demons
214 protein Nogo-A contributes to the failure of axon regeneration in the mammalian central nervous syste
216 protein Nogo-A contributes to the failure of axon regeneration in the mammalian central nervous syste
219 describes current progress in understanding axon regeneration in the model organism Caenorhabditis e
220 one machinery as a novel strategy to promote axon regeneration in the nervous system after injury.
223 ce demonstrated a 2-fold increase in sensory axon regeneration in the spinal cord in comparison to wi
225 ture of the mechanisms behind successful CNS axon regeneration in this vertebrate model organism.
226 oth an RNAi-based screen for defective motor axon regeneration in unc-70/beta-spectrin mutants and a
227 duction of HIF-1alpha using hypoxia enhances axon regeneration in vitro and in vivo in sensory neuron
229 n4b seems to represent no major obstacle for axon regeneration in vivo because it is less inhibitory
230 ngs identify a unique means of promoting CST axon regeneration in vivo by reengineering a development
231 ite growth suppression in vitro and promoted axon regeneration in vivo These findings demonstrate a n
232 nd neuronal viability in vitro and restricts axon regeneration in vivo, and demonstrate a novel, non-
238 review focuses on recent advances in sensory axon regeneration, including studies assessing the abili
239 eletion or inactivation of GSK3beta promotes axon regeneration independently of the mTORC1 pathway, w
240 RGCs to block AIS reassembly did not affect axon regeneration, indicating that preservation of neuro
243 ture cortical neurons, Nogo-22 inhibition of axon regeneration is abolished by genetic deletion of Ng
258 ment, a major limiting factor for successful axon regeneration is the poor intrinsic regenerative cap
259 trkB is knocked out selectively in neurons, axon regeneration is very weak, and topical treatment wi
260 rfering CASP2-mediated retinal ganglion cell axon regeneration, Muller cell activation and CNTF produ
262 ch add poly(ADP-ribose) to proteins, inhibit axon regeneration of both C. elegans GABA neurons and ma
263 Functionally, Tet3 is required for robust axon regeneration of DRG neurons and behavioral recovery
266 Severe motoneuron death and inefficient axon regeneration often result in devastating motor dysf
267 on associated with Wallerian degeneration or axon regeneration or the clearance of myelin debris by m
268 oves intrinsic growth potential to result in axon regeneration out of a growth-supportive peripheral
269 tudy demonstrates that long-distance sensory axon regeneration over a normal pathway and with sensory
271 e, we identify novel intrinsic regulators of axon regeneration: poly(ADP-ribose) glycohodrolases (PAR
274 transmission that doubles as a suppressor of axon regeneration, providing a molecular clue for the sy
277 le ZMB provides a novel context for studying axon regeneration, Schwann cell migration, and remyelina
279 8 months after injury demonstrated that this axon regeneration suppressed locomotor performance and d
280 oform in CNS, AKT3, induces much more robust axon regeneration than AKT1 and that activation of mTORC
281 ection of the cross-regulating mechanisms in axon regeneration that involve the downstream effectors
282 LF4 and activated STAT3 in the regulation of axon regeneration that might have therapeutic implicatio
283 the negative regulator of PI3K, induces CNS axon regeneration through the activation of PI3K-mTOR si
285 ole for active DNA demethylation in allowing axon regeneration to occur in the mature nervous system
289 rstand genetic determinants of mammalian CNS axon regeneration, we completed an unbiased RNAi gene-si
290 In an established mouse model with robust axon regeneration, we show that Armcx1, a mammalian-spec
292 tinal ganglion cell (RGC) loss and extent of axon regeneration were determined at 8 and 14 days after
293 roglia depletion, spontaneous and LI-induced axon regeneration were unaffected by PLX5622 treatment o
295 ctive therapeutic strategy for promoting CNS axon regeneration when combined with neurotrophic factor
296 n of a nuclear-trapped HDAC5 mutant prevents axon regeneration, whereas enhancing HDAC5 nuclear expor
297 wing spinal cord injury is due to failure of axon regeneration, which has been ascribed to environmen
298 types, such as the maintenance of memory and axon regeneration with age, in both mammals and C. elega
299 fully enhance the repair capacity of SCs and axon regeneration, without substantial off-target damage
300 aling that drives both neurodegeneration and axon regeneration, yet little is known about the factors
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