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1 rks and cell types pertinent for fetal neuro-gliogenesis.
2 fects in neurogenesis, but severe defects in gliogenesis.
3  quiescent progenitor cells in posttraumatic gliogenesis.
4 h the induction of GLAST, an early marker of gliogenesis.
5 tate gyrus neurogenesis as well as forebrain gliogenesis.
6 nto post-mitotic neurons before the onset of gliogenesis.
7 nstructive role for Notch-Delta signaling in gliogenesis.
8 ating, undergoing neurogenesis or undergoing gliogenesis.
9 g1 regulates the switch from neurogenesis to gliogenesis.
10 cells remained high through the beginning of gliogenesis.
11 dition to its established role in peripheral gliogenesis.
12 hout SVZ formation and the postnatal peak of gliogenesis.
13 transcription factors that are necessary for gliogenesis.
14  during CNS development, particularly during gliogenesis.
15 d in vivo to prevent premature and excessive gliogenesis.
16 f neuronal migration, neurite outgrowth, and gliogenesis.
17 al zones of p27Kip1(-/-) mice at the peak of gliogenesis.
18 differentiated OLs during postnatal cortical gliogenesis.
19  reaches maximal levels during the period of gliogenesis.
20 ages of neurogenesis and the early stages of gliogenesis.
21  models due to the delayed onset of cortical gliogenesis.
22 rol the temporal switch from neurogenesis to gliogenesis.
23 r Casz1 to promote the rod fate and suppress gliogenesis.
24 cal areas during peak neurogenesis and early gliogenesis.
25 ion, disrupts both cortical neurogenesis and gliogenesis.
26 vous system, neurogenesis generally precedes gliogenesis.
27 genesis, while the host embryo advanced into gliogenesis.
28 iption factors that coordinate initiation of gliogenesis.
29 genesis, neuronal migration, myelination and gliogenesis.
30 , its degradation at the SVZ correlates with gliogenesis.
31 in the molecular control of neurogenesis and gliogenesis.
32  of neural fate to cortical neurogenesis and gliogenesis.
33 trol the transition between neurogenesis and gliogenesis.
34 s and reduces neurogenesis at the expense of gliogenesis.
35 es Olig2 expression, indicative of premature gliogenesis.
36 mounts of neurogenesis coexist with waves of gliogenesis.
37  target of mTORC1 and has been implicated in gliogenesis.
38  the neural tube during neurogenesis but not gliogenesis.
39 rallel study of the ongoing neurogenesis and gliogenesis.
40 this relationship mediates the initiation of gliogenesis.
41 pression coordinates neurogenesis and cortex gliogenesis.
42 providing a powerful model for understanding gliogenesis.
43 -X3 and STAT3, which are known regulators of gliogenesis.
44 riod of neurogenesis followed by a period of gliogenesis.
45 on time plan of newborn neurons, and ongoing gliogenesis.
46 umulation was still able to completely block gliogenesis.
47 g that yet-unidentified factors regulate gut gliogenesis.
48 ense of proliferation, function similarly in gliogenesis.
49 r the induction of neurogenesis, but not for gliogenesis.
50  therefore may play a role in injury-induced gliogenesis.
51 pment as a regulatory target for REPO during gliogenesis.
52                                Later, during gliogenesis, activated Notch1 triggers a rapid cellular
53 underlie axonal sprouting, neurogenesis, and gliogenesis after stroke have recently been identified.
54  the greatest potential for neurogenesis and gliogenesis among all taxa, partly due to their indeterm
55 ypotheses that BMPs are required for enteric gliogenesis and act by promoting responsiveness of ENCDC
56  LIN28 expression caused a complete block of gliogenesis and an increase in neurogenesis.
57 n neocortex encompasses a critical period of gliogenesis and cortical expansion.
58 ation, with upregulation of gene modules for gliogenesis and decreases in neurogenesis.
59    However, the molecular cues that instruct gliogenesis and determine glial cell type are poorly und
60 itor character, and in some contexts promote gliogenesis and drive binary fate choices.
61  The trajectory map shows that neurogenesis, gliogenesis and early postmitotic maturation in the embr
62 scade that operates during the initiation of gliogenesis and identifies a unique set of genes that re
63  uncover new physiological roles for GDE3 in gliogenesis and identify GDE3 as a key regulator of CNTF
64 he entire midbrain ventricular zone, reduced gliogenesis and increased generation of neurons, includi
65          Noggin, by suppressing subependymal gliogenesis and increasing progenitor availability, pote
66 d from discrete precursor populations during gliogenesis and migrate extensively from their origins,
67             Eroded genes are associated with gliogenesis and myelination, suggesting a previously und
68 te throughout the RMS and contribute to both gliogenesis and neurogenesis in the postnatal OB.
69 fic (anti-Hu) antigens, indicating that both gliogenesis and neurogenesis occurred after spinal cord
70 or the transcription factor Ascl1 in enteric gliogenesis and neurogenesis.
71 h the switch from excitatory neurogenesis to gliogenesis and OB interneuron neurogenesis in the corte
72 by the upregulation of genes associated with gliogenesis and phagocytosis, with the depletion of brai
73                              GGF2 stimulated gliogenesis and proliferation and inhibited glial cell d
74 ; overexpression of either factor suppresses gliogenesis and promotes neurogenesis; each can substitu
75                   However, the activation of gliogenesis and the role of newly formed astrocytes in t
76 vival, neurite outgrowth, synapse formation, gliogenesis) and neurodegeneration (neuronal death, peri
77 t affecting proliferation in early phases of gliogenesis, and a p27Kip1-independent event leading to
78 f prenatal nicotine on neurogenesis, but not gliogenesis, and also on the number of newly generated n
79 ic Lhx2 overexpression and suppress baseline gliogenesis, and also to compensate for loss of Lhx2 and
80 scribed is implicated in adult neurogenesis, gliogenesis, and angiogenesis.
81 ion as a key driver of NSC proliferation and gliogenesis, and identify a unique mechanism for conferr
82 terations linked to changes in cytoskeleton, gliogenesis, and impaired synaptogenesis.
83 and inflammation on reduced neurogenesis and gliogenesis, and increased apoptosis and depressive-like
84 base of neuronal columns at the beginning of gliogenesis, and later within the cortical layers, sugge
85                                Neurogenesis, gliogenesis, and neural migration were altered during di
86 nical molecular pathways of neurogenesis and gliogenesis, and predict two distinct trajectories for c
87 pression is both robust and sustained during gliogenesis, and the cis-regulatory region of the dvdup1
88 f these mice, whereas their distribution and gliogenesis appeared normal.
89                          The role of Cdk5 in gliogenesis appeared specific to the early postnatal per
90 hat regulate peripheral nervous system (PNS) gliogenesis are incompletely understood.
91   Dendritic arborization, axonal growth, and gliogenesis are observed along with a strong maturation
92 tain neurogenic potential into the period of gliogenesis argues that they do not self-renew.
93 xiety, point to hippocampal neurogenesis and gliogenesis as key in this modulation, and underscore FG
94  identify a new mechanism regulating enteric gliogenesis as well as novel functions for Lgi4 regulati
95 d NFIA are key transcriptional regulators of gliogenesis associated with OL and AS.
96 nate ability of progenitors to switch toward gliogenesis at later passages.
97 amplifying progenitors, leading to increased gliogenesis at the expense of neurogenesis in neonatal a
98        The enriched pathways in the dHC were gliogenesis, axon development, and lipid modification, w
99         The RAS/RAF/MEK/ERK pathway promotes gliogenesis but the kinetic role of RAF1, a key RAF kina
100 ral crest, neuregulin instructively promotes gliogenesis, but how alternative fates are determined is
101  we demonstrate that oli is not required for gliogenesis, but plays pivotal roles in regulating larva
102  activation of the Notch pathway can promote gliogenesis by peripheral (PNS) and central (CNS) nervou
103                             Neurogenesis and gliogenesis continue in discrete regions of the adult ma
104  required to maintain Sox9 expression during gliogenesis, demonstrating that Notch signaling promotes
105 sly been shown to be important for promoting gliogenesis during development, this is the first demons
106 olfactory bulb neurogenesis, or neurogenesis/gliogenesis during development.
107 ration of enteric neurons and for regulating gliogenesis during postnatal development.
108 2 mRNAs were found during the peak period of gliogenesis (E15-E19) in the telencephalic and mesenceph
109 monstrating extensive cell proliferation and gliogenesis following central nervous system (CNS) traum
110 larly distinct APC subgroups at the start of gliogenesis from both dorsal and ventral forebrains.
111 pression enhances it, without any effects on gliogenesis from NPCs in vitro.
112             In examining the early stages of gliogenesis from progenitors in the SVZ, we noted that i
113 diate progenitor cells that express critical gliogenesis genes Ascl1, Egfr, and Olig2.
114 role in brain homeostasis, the importance of gliogenesis has been overlooked, both in healthy and dis
115 urce of Shh throughout both neurogenesis and gliogenesis, has not been clearly defined.
116              However, bHLH factors linked to gliogenesis have not been described.
117 with the ability of BMP signaling to promote gliogenesis, Hipk2(-/-) mutants show a significant incre
118 S development, neurogenesis largely precedes gliogenesis: how is this timing achieved?
119 entral nervous system, neurogenesis precedes gliogenesis; however, when and how progenitors are speci
120 enesis is delayed and reduced, and posterior gliogenesis impaired.
121  progenitors transition from neurogenesis to gliogenesis in a stereotyped sequence that is in part in
122 ury at the beginning (E11) and peak (E15) of gliogenesis in an avian tectal model of penetrating embr
123 his review examines the role of Notch during gliogenesis in both fruit flies and vertebrates, as well
124  have defined functions of MEK in regulating gliogenesis in developing cerebral cortex using loss- an
125 pmental window encompassing neurogenesis and gliogenesis in human primary tissue.
126 ively to instruct a cell-heritable switch to gliogenesis in neighboring stem cells.
127 ndergo primarily neurogenesis in the gut but gliogenesis in nerves.
128          Thus, the primary event controlling gliogenesis in neural progenitors is the transcription o
129                  We show that Lhx2 regulates gliogenesis in part by regulating directly the expressio
130 tal alcohol exposure triggers an increase in gliogenesis in the adult motor cortex.
131 oss leads to increased NSC proliferation and gliogenesis in the brainstem, but not in the cortex.
132 o smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats.
133 ors and that levels of MEK activity regulate gliogenesis in the developing cortex.
134 priate amount and timing of neurogenesis and gliogenesis in the developing hippocampus.
135 a inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous
136 ecific temporal sequence of neurogenesis and gliogenesis in the developing spinal cord.
137 n controlling the timing of neurogenesis and gliogenesis in the developing ventral spinal cord.
138 and suppress the resulting enhanced level of gliogenesis in the hippocampus.
139 onmental factors can affect neurogenesis and gliogenesis in the hippocampus.
140 nt with decreased neurogenesis and increased gliogenesis in the mature hippocampus.
141 ion factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-aut
142  pathways that control perineural and cortex gliogenesis in the post-embryonic brain and have shown t
143 ostmitotic neurons non-autonomously enhances gliogenesis in the progenitors via FGF signalling.
144 try, a reduction in striatal neuroglia, with gliogenesis in the subventricular zone and the somatosen
145 trolling the transition from neurogenesis to gliogenesis in the vertebrate CNS are incompletely under
146 hysiological Notch signaling is required for gliogenesis in vivo, independent of the role of Notch in
147 ther physiological Notch signaling regulates gliogenesis in vivo.
148 s hastened cell cycle withdrawal and blocked gliogenesis in vivo.
149               Plagl1 and Sox9 did not induce gliogenesis in wildtype animals, but nonetheless activat
150  induced by N1ICD electroporation, inhibited gliogenesis in wildtype animals, but rescued MG developm
151 the adult V-SVZ contains spatial domains for gliogenesis, in addition to those for neurogenesis.
152 tion of neurogenesis to a generic program of gliogenesis, in both astrocyte and oligodendrocyte VZ pr
153           We further demonstrate that Muller gliogenesis induced by misexpression of the potently gli
154 the mechanism by which Lgi4 promotes enteric gliogenesis involves binding the ADAM22 receptor.
155  The mechanism underlying the later onset of gliogenesis is poorly understood, although the cytokine-
156 rentiation by G34R/V mutations and malignant gliogenesis is promoted by co-option of a potentially ta
157           Our findings demonstrate that mPFC gliogenesis is vulnerable to psychostimulant abuse and p
158 or proliferation rate, along with a delay in gliogenesis, is also observed in Gdf11(-/-) spinal cord
159 hat the impairment of postnatal hypothalamic gliogenesis markedly alters sexual maturation by prevent
160 rmalization of drug-impaired neurogenesis or gliogenesis may help reverse neuroplasticity during abst
161  the molecular regulation of early postnatal gliogenesis may provide clues to normal and pathological
162 at long-term alterations in neurogenesis and gliogenesis might contribute to the observed hippocampal
163 atrix predominantly impacted in males, while gliogenesis, myelination and synaptic plasticity were pr
164 y CNS; (2) during most of the year, baseline gliogenesis occurs mainly in the ependyma with substanti
165 he balance between stem-cell maintenance and gliogenesis of hypothalamic ventricular zone radial glia
166  dependency of Mek-Erk/MAPK signaling during gliogenesis of one of the two developmentally transient
167 ressed at early developmental stages, before gliogenesis or angiogenesis take place in the neural ret
168 ated by Lhx2: loss of either factor promotes gliogenesis; overexpression of either factor suppresses
169  during the wave of cortical and hippocampal gliogenesis (P2-P4), significantly fewer YFP+ cells were
170 ed by activation of a micro-(mi)RNA-mediated gliogenesis pathway.
171 ne and oSVZ is phased out and transitions to gliogenesis prior to gyral development.
172                  Our data indicate that oSVZ gliogenesis, rather than neurogenesis, correlates with r
173 he impact of Abeta pathology on neurogenesis/gliogenesis remains unclear.
174                                              Gliogenesis requires the careful orchestration of migrat
175 y migratory and metabolic roles during astro-gliogenesis, respectively.
176 n-specific increase in NSC proliferation and gliogenesis results from selective Akt hyperactivation.
177 electrophysiological changes observed during gliogenesis, suggesting that astrocytes undergoing secon
178 ations in regulating mammalian neurogenesis, gliogenesis, synaptic formation, and brain function.
179 receptors can regulate both neurogenesis and gliogenesis that may be developmentally dependent.
180 tenuates self-renewal and induces precocious gliogenesis through modulation of the responsiveness to
181 ggest that Xenopus prune may regulate Muller gliogenesis through phosphodiesterase-mediated regulatio
182 born neurons (neurogenesis) and glial cells (gliogenesis) throughout life, is highly impaired in seve
183                   The susceptibility of mPFC gliogenesis to even modest doses of methamphetamine coul
184  will peer through the lens of developmental gliogenesis to gain a clearer understanding of the proce
185 epithelium differentiation, neurogenesis and gliogenesis, to neural circuit formation.
186 ogenitor subtypes during the neurogenesis-to-gliogenesis transition.
187 nvolved in cell adhesion, axon guidance, and gliogenesis upon silencing of FoxO6 We then show that Fo
188 etric division via Prospero, and a switch to gliogenesis via Glial Cell Missing (Gcm); however, these
189                      This effect on cortical gliogenesis was accompanied by a decrease in YFP+ prolif
190                                      Enteric gliogenesis was analyzed in mice that overexpress the BM
191 m of LRRK2 in the control of neurogenesis or gliogenesis was investigated.
192                             In contrast, ENS gliogenesis was readily observed under steady-state cond
193                        Neurogenesis, but not gliogenesis, was affected in HAP1-null neurospheres and
194 RA and it is a known moderator of neuro- and gliogenesis, we were interested in testing whether these
195 or that plays a crucial role in the onset of gliogenesis; we found that its induction is regulated by
196 ression promotes neurogenesis and suppresses gliogenesis, whereas loss of Lhx2 has the opposite effec
197 l densities peak during the latter stages of gliogenesis, which occurs in the SVZ of the lateral vent
198                     The mechanistic basis of gliogenesis, which occurs late in human development, is
199 A (NFIA) as a key regulator of developmental gliogenesis, while miR-223 has been shown to repress NFI
200 d voluntary exercise had profound effects on gliogenesis with differential regulation of oligodendroc
201               This dataset captures prenatal gliogenesis with high temporal resolution and is provide

 
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