ライフサイエンスコーパス: SVZ

1 SVZ and RMS microglia thus appear to comprise a function

2 SVZ cells also gave rise to proliferative subventricular

3 removal of Gli2 or Gli3 does not alter adult SVZ neurogenesis.

4 delivery of Fezf2 in the neonatal and adult SVZ niche, we showed that ectopic Fezf2 expression is su

5 results demonstrate that neonatal and adult SVZ stem cells retain neuronal fate plasticity.

6 The plastic capacity of neonatal and adult SVZ stem/progenitor cells is still largely unknown.

7 ectable in multiple cell types in both adult SVZ and corpus callosum.

8 ated GLI3(R) is a primary inhibitor of adult SVZ NSC function.

9 hic effects of recombinant PEDF on the adult SVZ and corpus callosum, demonstrate induction of endoge

10 identify molecular cues present in the adult SVZ niche during injury, and analyzed their role on NPCs

11 that Notch1 is a key component of the adult SVZ niche, promoting maintenance of aNSCs, and that this

12 ntial factor in the maintenance of the adult SVZ, and demonstrate that NSCs within the SVZ maintain t

13 n in nestin-expressing NSCs within the adult SVZ.

14 and Sox10 double-positive cells in the adult SVZ.

15 tion arrest and differentiation in the adult SVZ.

16 ses Reln in neural stem cells from the adult SVZ.

17 on associated with a decline of the affected SVZ-stem cell niche in aged mice.

18 and in vitro suggest the potential that aged SVZ manipulation is associated with DAergic functional r

19 r, the overall neurogenic output of the aged SVZ is reduced.

20 eural stem or progenitor cells in the DG and SVZ after injury.

21 unctional difference between the SC-NPCs and SVZ-NPCs during homeostatic conditions.

22 vast majority of CUX2(+) cells in the VZ and SVZ are migrating interneurons derived from the subcorti

23 o the rostral migratory stream, the anterior SVZ, and the dorsal part of the medial and posterior SVZ

24 regulatory role of H3K4me3 within the baboon SVZ, we developed a technique to purify undifferentiated

25 ifferentiated progenitor cells of the baboon SVZ.

26 In the human brain, SVZ cells including local astroglia also express EZH2, c

27 urce of CNTF in adult healthy brains changes SVZ-derived neural progenitors' migratory behavior that

28 ated levels of H3K4me3 in the MRI-classified SVZ-associated Glioblastoma Multiforme (GBM), which has

29 results reveal an unknown gateway connecting SVZ neurogenesis to neuronal activity-dependent control

30 oarchitecture and neurogenic potential of cV-SVZ.

31 ibe the cytoarchitecture of canine V-SVZ (cV-SVZ), to assess its neurogenic potential, and to compare

32 ltrastructural studies indicated that the cV-SVZ is organized in layers as in humans, but including m

33 ction of Cre recombinase into Pbx2-deficient SVZ stem and progenitor cells carrying floxed alleles of

34 ion, as Ink4a/Arf-deficiency in Ezh2-deleted SVZ NSCs rescues cell proliferation, but neurogenesis re

35 (SVZ), the function of ECM in the developing SVZ remains unknown.

36 and biochemical experiments revealed direct SVZ NSC responses to local acetylcholine release, synerg

37 used to test for the presence of a distinct SVZ and to define the boundaries of the SVZ in developin

38 Tbr2(+) cells are organized into a distinct SVZ in the dorsal ventricular ridge (DVR) of turtle fore

39 Tbr2(+) cells into an anatomically distinct SVZ, both developmentally and evolutionarily, may be sha

40 tomical integration of nonimmortalized donor SVZ-derived murine aNPCs in the dysmyelinated brain at k

41 , most stem cells in the ganglionic eminence SVZ did not maintain radial fibers or orientation.

42 an enormous contribution from non-epithelial SVZ stem cells.

43 Cells expressing SVZ markers infiltrated surrounding brain regions.

44 al hyperproliferation of oncogene expressing SVZ cells by facilitating an antiproliferative expressio

45 insult, provides a favorable environment for SVZ-derived oligodendrocyte progenitor generation.

46 roducing cells expressing Dcx migrating from SVZ to the injury sites.

47 ed whether the fate of postnatally generated SVZ neurons can be altered.

48 However, SVZ NSCs can also differentiate into astrocytes.

49 i and reduced OB-size without alterations in SVZ neurogenesis.

50 s that underlie aging-associated declines in SVZ neurogenesis for the early detection of differences

51 rease in cell death-levels and a decrease in SVZ-derived neuroblasts in the distal RMS, as compared t

52 Adult-onset receptor disruption in SVZ NSP cells with a recombinant adeno-associated virus

53 hat Lnk expression after stroke increased in SVZ through the transcription factors STAT1/3.

54 expression in NSP cells, led to increases in SVZ-associated neuroblasts and new olfactory bulb neuron

55 rived IGF2 contributes to NSC maintenance in SVZ but not in the SGZ, and that this is regulated by th

56 enuates prolactin-stimulated neurogenesis in SVZ-derived adult neural stem/progenitor cells (aNPCs).

57 at revealed a higher neurogenic potential in SVZ-NPCs compared with SC-NPCs.

58 loss of NSCs and a progressive reduction in SVZ proliferation, without an increase in glial cell pro

59 for neurogenesis independent of its role in SVZ NSC proliferation, as Ink4a/Arf-deficiency in Ezh2-d

60 s inactivation caused rostrocaudal shifts in SVZ and CP gene expression, with loss of corticospinal a

61 l growth factor receptor (EGFR) signaling in SVZ NPCs stimulates the interaction between N-cadherin a

62 uption of in vivo CNTF receptor signaling in SVZ NSP cells, with a "floxed" CNTF receptor alpha (CNTF

63 ing mechanisms contributing to aging-induced SVZ stem/neuroprogenitor cell (NPC) inhibition in aging

64 ed severe defects in cortical-injury-induced SVZ astrogenesis, instead producing cells expressing Dcx

65 imary neurospheres produced from the injured SVZ increased approximately twofold versus controls, and

66 -mutant cells from the neonatal and juvenile SVZ generate brain lesions and structural abnormalities,

67 s of the transcriptome of dorsal and lateral SVZ in early postnatal mice, including neural stem cells

68 all molecules that can be used to manipulate SVZ microdomain-specific lineages.

69 I, the number of Ki67(+) cells in the medial SVZ of the injured hemisphere increased.

70 neural stem cells (NSCs) of the adult mouse SVZ, but its role there has not been elucidated.

71 rotein fascin is highly upregulated in mouse SVZ-derived migratory neuroblasts.

72 Mutant SVZ cells overexpressed Wnt, cell-cycle and stem cell ge

73 iate activation of genes associated with non-SVZ neuronal subtypes.

74 mical, proteomic, and functional analyses of SVZ NPC-secreted factors revealed the neurite outgrowth-

75 Proteomic analysis of SVZ tissue from mice with experimental demyelination ide

76 is ratio with KLK3 and RUNX3; association of SVZ involvement with Ras oncogene family members, such a

77 maging, we examined the dynamic behaviors of SVZ progenitors in the ferret, a gyrencephalic carnivore

78 pict microglia as a conspicuous component of SVZ and its anterior extension, the rostral migratory st

79 Our results show an initial decrease of SVZ proliferation at 24 h, followed by a recovery leadin

80 generated neurons modulate cell division of SVZ stem cells.

81 ession is sufficient to redirect the fate of SVZ stem cells.

82 , were causally related to the impairment of SVZ-NPCs.

83 sult in ventriculomegaly with an increase of SVZ neuroblast in rostral migratory stream, whereas VEGF

84 nstrated that proliferation and migration of SVZ neuroprogenitor cells were enhanced by 9cRA.

85 that CNTF controls the directed migration of SVZ-derived progenitors and oligodendrocyte precursors.

86 We investigated the evolutionary origin of SVZ neural precursor cells in the prenatal cerebral cort

87 s are expressed during the normal program of SVZ neurogenesis, suggesting that PBX1 might act as a pr

88 s a marked reduction in the proliferation of SVZ cells in the mutant.

89 that N-cadherin enhances the recruitment of SVZ NPCs into demyelinated lesions.

90 now show that Pbx1 is an early regulator of SVZ neurogenesis.

91 ur study is the first to demonstrate ongoing SVZ astrogliogenesis in the normal adult mammalian foreb

92 Significantly, analysis of the neonatal (P5) SVZ reveals that although progenitors remain sensitive t

93 the dorsal part of the medial and posterior SVZ.

94 the ventral part of the medial and posterior SVZ.

95 restructuring of ECM in the early postnatal SVZ.

96 itical role for Nf1 in maintaining postnatal SVZ-derived neurogenesis and identifies a potential ther

97 hether Tsc-mutant neurons from the postnatal SVZ contribute to brain lesions and abnormal circuit rem

98 (hi) astrocyte production from the postnatal SVZ niche.

99 sociated with an exacerbated proinflammatory SVZ microenvironment converging to dysregulate the Wingl

100 Elevated levels of SOX5/6/21 promoted SVZ cells to exit the cell cycle, whereas genetic ablati

101 d radial unit production together with rapid SVZ growth and heightened localized neurogenesis can cau

102 genesis and the limited ability of recruited SVZ neuroblasts to survive long-term and differentiate i

103 from discrete circuits can directly regulate SVZ neurogenesis.

104 ctivity apply to SHH signaling in regulating SVZ-derived olfactory bulb interneurons and maintaining

105 ust post-injury astrogenic response required SVZ Notch activation modulated by Thbs4 via direct Notch

106 lasts and disorganized astrocytes in the RMS/SVZ, linking EphA4 forward signaling to SVZ and RMS spat

107 ase (ChAT)(+) neurons residing in the rodent SVZ neurogenic niche.

108 Tsc1(null) newborn neurons although sparing SVZ stem cells.

109 quirement for GLI(A) function in stimulating SVZ neurogenesis.

110 Here we show in mice that SVZ-generated astrocytes express high levels of thrombos

111 However, recent studies have shown that SVZ size and the abundance of resident progenitors do no

112 howed a progressive loss of NSCs both at the SVZ and the DG of the hippocampus.

113 oduction of neuroblasts is controlled by the SVZ microenvironmental niche.

114 ns this propensity of glioma to colonize the SVZ through secretion of chemoattractant signals toward

115 stained AZ and PSD markers; in contrast, the SVZ-AZ spatial coupling is decreased.

116 NPCs were isolated and propagated from the SVZ and cervical, thoracic, and caudal regions of the SC

117 pact (CCI) injury, and isolated RNA from the SVZ and DG at different post-injury time points.

118 ped astrocytes also flow anteriorly from the SVZ in association with the rostral migratory stream, bu

119 The entry of new astrocytes from the SVZ into the corpus callosum appears to be balanced by a

120 ural stem cells (NSCs) were derived from the SVZ on postnatal 7 d, 1 m, and 12 m-old mice.

121 lasts that appeared to be recruited from the SVZ to the striatum.

122 of the neuroblast ectopic migration from the SVZ toward the lesion showed an increase in this process

123 A migratory stream was indicated from the SVZ up to the MOB, consisting of neuroblasts that formed

124 versity of neural cells originating from the SVZ.

125 We found that microglia residing in the SVZ and adjacent rostral migratory stream (RMS) comprise

126 romodeoxyuridine-immunoreactive cells in the SVZ and dentate gyrus following focal ischemia.

127 , BMP, and activin signaling pathways in the SVZ and DG after injury, suggesting that these pathways

128 transgenic mice inhibits neurogenesis in the SVZ and OB following prolactin infusion or mating/pregna

129 neural precursor cell (NPC) turnover in the SVZ but it was not addressed if a reduced demand specifi

130 role of APP in regulating NSC number in the SVZ clearly demonstrate that endothelial deletion of App

131 at the number of new neurons produced in the SVZ declines through aging; however, age-related changes

132 Expression of the PBC protein PBX1 in the SVZ has been reported, but its functional role(s) has no

133 The "intermediate map" in the SVZ is modulated by Eomes (also known as Tbr2), a T-box

134 IP1 and found that expression of DKK3 in the SVZ is restricted to NPCs.

135 favour astrogenesis over neurogenesis in the SVZ niche, and whether astrocytes produced there have di

136 to other unique populations residing in the SVZ niche, microglia display distinct morphofunctional p

137 matory genes, such as Heme oxygenase1 in the SVZ niche, starting by middle age, amplified upon neurot

138 br2-expressing neural precursor cells in the SVZ produce excitatory neurons for each cortical layer i

139 ediate progenitor cells, which divide in the SVZ to produce cortical neurons.

140 decreased proliferation and pool size in the SVZ zone, and were associated with elevated inflammatory

141 e cells (resembling neural stem cells in the SVZ), (2) neuronal cells, and (3) a cell type with an in

142 ophin expression is strongly enriched in the SVZ, and pleiotrophin knock down starkly reduced glioma

143 In the SVZ, paracrine IGF2 is a cerebrospinal fluid and endothe

144 e number of BrdU label-retaining NSCs in the SVZ, whereas NSC/astrocyte deletion of App has no detect

145 molecules to direct germinal activity in the SVZ, which has therapeutic potential in neurodegenerativ

146 ectively, miR17-92 cluster expression in the SVZ.

147 ntermediate progenitors, which divide in the SVZ.

148 NSC growth to control the NSC number in the SVZ.

149 d migration of the multipolar neurons in the SVZ/IZ.

150 cs of alternatively activated microglia, the SVZ/RMS microglia were clearly distinguished by their lo

151 e in one of the adult neurogenic niches, the SVZ.

152 rogenitors of the MGE in the VZ, but not the SVZ, for proper cortical interneuron migration.

153 within the dense astroglial meshwork of the SVZ and rostral migratory stream (RMS), yet are permissi

154 t neonatal H-I alters the composition of the SVZ and that LIF is a key regulator for a subset of inte

155 inct SVZ and to define the boundaries of the SVZ in developing cortices.

156 down starkly reduced glioma invasion of the SVZ in the murine brain.

157 on, leading to enhanced migration out of the SVZ into demyelinated lesions of the SCWM.

158 rating both the assembly and function of the SVZ neural stem cell niche.

159 ed by ADAM10 cleavage is the response of the SVZ niche to promote repair of the injured brain.

160 nance of adult NSCs and stabilization of the SVZ vascular niche using conditional, tamoxifen-inducibl

161 as preceded by significant regression of the SVZ vasculature at 14 d, and concomitant decrease of VEG

162 lps NSCs maintain their stemness outside the SVZ in Nes-CreER(T2); Qk(L/L); Pten(L/L); Trp53(L/L) mic

163 as are GFAP(+) astrocytes found outside the SVZ.

164 s but fails to maintain stemness outside the SVZ.

165 re-GEPCOT cells survived and repopulated the SVZ.

166 In rodents, the SVZ is a lifelong source of new neurons fated to migrate

167 rigin of the dopaminergic innervation to the SVZ and SGZ in rodents.

168 ted changes attributable specifically to the SVZ neural stem cell (NSC) population have not been full

169 prominent in rostral regions adjacent to the SVZ where NPC-derived oligodendrocytes significantly out

170 as been found to innervate proximally to the SVZ, causes motor and cognitive impairments.

171 midbrain dopaminergic projections toward the SVZ.

172 a significant loss of YFP(+) NSCs within the SVZ by 45 d post recombination, which was preceded by si

173 Deletion of either gene within the SVZ does not cause any obvious defects in cortical inter

174 lt SVZ, and demonstrate that NSCs within the SVZ maintain the integrity of their vascular niche throu

175 undifferentiated progenitor cells within the SVZ of adult baboon brain.

176 thin the RMS and progenitor cells within the SVZ.

177 ons of neuroblasts and astrocytes within the SVZ/RMS/OB system resulting in a cell-specific mosaic, s

178 ineage tracing demonstrated that it is these SVZ-generated Thbs4(hi) astrocytes, and not Dcx(+) neuro

179 e found preferentially in close proximity to SVZ neural stem cells (NSCs) that produce interleukin-15

180 RMS/SVZ, linking EphA4 forward signaling to SVZ and RMS spatial organization, orientation, and regul

181 nd ROCK inhibition decreased invasion toward SVZ NPC-secreted factors.

182 loped a technique to purify undifferentiated SVZ cells while preserving the endogenous nature without

183 ration of purified quiescent and activated V-SVZ stem cells and transit-amplifying cells.

184 to describe the cytoarchitecture of canine V-SVZ (cV-SVZ), to assess its neurogenic potential, and to

185 onist or antagonist increased or decreased V-SVZ proliferation, respectively.

186 ulting in loss of adult NSCs and defective V-SVZ regeneration.

187 Understanding how V-SVZ NSCs establish and maintain lifelong neurogenesis co

188 However, V-SVZ NSCs are heterogeneous: they have different embryoni

189 great similarity between canine and human V-SVZ indicating that the dog may be better representative

190 dulating the activity of this hypothalamic-V-SVZ connection.

191 purified vascular cells from a neurogenic (V-SVZ) and non-neurogenic brain region (cortex) on the V-S

192 cal signals had the most potent effects on V-SVZ proliferation and neurogenesis, highlighting the int

193 ic Hh-regulated subregion of the postnatal V-SVZ.

194 endothelial-derived mitogen that promotes V-SVZ cell proliferation.

195 -3 acts as a mediator of quiescence in the V-SVZ adult neural stem cell niche.

196 cond-most common dividing cell type in the V-SVZ and had a T(C) of 18 h and T(S) of 9 h.

197 adult progenitor cell proliferation in the V-SVZ and how large numbers of new neurons continue to be

198 C cells), and neuroblasts (A cells) in the V-SVZ and the number of times these cells divide remain un

199 osis, suggesting a supportive role for the V-SVZ environment in tumor initiation or progression.

200 vides long-range regionalized input to the V-SVZ niche and can regulate specific NSC subpopulations.

201 s regarding the unique organization of the V-SVZ NSC niche, the multiple regulatory controls of neuro

202 on-neurogenic brain region (cortex) on the V-SVZ stem cell lineage in vitro.

203 A largely ignored component of the V-SVZ stem cell niche is the lateral ventricle choroid ple

204 view, we describe unique components of the V-SVZ that may permit or promote tumor growth within the r

205 l circuitry, via mosaic innervation of the V-SVZ, can recruit distinct NSC pools, allowing on-demand

206 presented perivascular niches outside the V-SVZ.

207 selectively innervate the anterior ventral V-SVZ and promote the proliferation of Nkx2.1(+) NSCs and

208 MC) neurons innervate the anterior ventral V-SVZ and regulate deep granule interneuron production dep

209 progenitor domains in the anterior ventral V-SVZ of both the neonatal and adult mouse brain.

210 decreased neurogenesis only in the ventral V-SVZ.

211 rain, the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ), with signaling path

212 ls in the ventricular-subventricular zone (V-SVZ) contact the cerebrospinal fluid (CSF), which flows

213 ult mouse ventricular-subventricular zone (V-SVZ) exhibit a regional identity and, depending on their

214 The ventricular-subventricular zone (V-SVZ) is an extensive germinal niche containing neural st

215 st in the ventricular-subventricular zone (V-SVZ) of the adult mammalian brain.

216 ns of the ventricular-subventricular zone (V-SVZ) of the adult rodent brain generate several subtypes

217 mammalian ventricular-subventricular zone (V-SVZ) presents the highest neurogenic potential in the br

218 s) in the ventricular-subventricular zone (V-SVZ) produce diverse olfactory bulb (OB) neurons.

219 is in the ventricular-subventricular zone (V-SVZ) shortly after birth was also largely unaffected, ex

220 he of the ventricular-subventricular zone (V-SVZ), beyond serving as a potential site of origin, affe

221 the adult ventricular-subventricular zone (V-SVZ), NSCs are a specialized form of astrocyte that gene

222 In the ventricular-subventricular zone (V-SVZ), quiescent neural stem cells (qNSCs) become activat

223 rain, the ventricular-subventricular zone (V-SVZ), replenish olfactory neurons throughout life.

224 ulate the ventricular-subventricular zone (V-SVZ).

225 tomes of fetal human and embryonic mouse VZ, SVZ, and cortical plate.

226 ergo increased apoptosis, indicating that VZ/SVZ-derived and rhombic lip-derived progenitor cells sho

227 of EphB2 disrupted the separation of the VZ/SVZ and IZ migratory routes.

228 promoting tangential migration along the VZ/SVZ but not IZ.

229 In contrast, neural progenitors of the VZ/SVZ did not undergo increased apoptosis, indicating that

230 the ventricular zone/subventricular zone (VZ/SVZ) and intermediate zone (IZ) of the dorsal telencepha

231 ld greater in R6/2 vs. wild type mice, while SVZ cell proliferation was not affected.

232 ed in NPCs of the mouse subventricular zone (SVZ) and aged animals with genetically enhanced WIP1 exp

233 ed cells in the rostral subventricular zone (SVZ) and hippocampus of DCX-TK transgenic mice, but not

234 ult neurogenesis in the subventricular zone (SVZ) and in the subgranular zone (SGZ) of the hippocampu

235 ridine (+) cells in the subventricular zone (SVZ) and lesioned cortex in the stroke brain.

236 protein changes in the subventricular zone (SVZ) and neurodegenerative diseases with age.

237 ult neurogenesis in the subventricular zone (SVZ) and olfactory bulb (OB) mediates several reproducti

238 of the brain, e.g., the subventricular zone (SVZ) and substantia nigra (SN), have promising potential

239 the elaboration of the subventricular zone (SVZ) and the associated increase in neural progenitors.

240 enesis in the forebrain subventricular zone (SVZ) and the hippocampal dentate gyrus (DG).

241 ammals occurring in the subventricular zone (SVZ) and the subgranular zone (SGZ), is subject to compl

242 tem cells (NSCs) in the subventricular zone (SVZ) and to astrocytes in the adult mouse forebrain.

243 s (NPCs) from the adult subventricular zone (SVZ) can also generate new oligodendrocytes after demyel

244 We challenged subventricular zone (SVZ) cells in vivo with low concentrations of CNTF to an

245 ostnatal forebrain, the subventricular zone (SVZ) contains a pool of undifferentiated cells, which pr

246 The subventricular zone (SVZ) continuously supplies new interneurons that incorpo

247 e retained in the brain subventricular zone (SVZ) during the chronic phase of multiple sclerosis in h

248 nces and found that the subventricular zone (SVZ) expanded massively during the early second trimeste

249 last chain formation in subventricular zone (SVZ) explants are compromised when clusterin, which is p

250 SCs) in the adult mouse subventricular zone (SVZ) express the histone methyltransferase EZH2.

251 irth, stem cells in the subventricular zone (SVZ) generate neuroblasts that migrate along the rostral

252 l niche in the affected subventricular zone (SVZ) in aging mice.

253 neurogenesis within the subventricular zone (SVZ) in the rodent model.

254 within the adult neural subventricular zone (SVZ) in vivo, we show distinct responses to ionising rad

255 ality, mass effect, and subventricular zone (SVZ) involvement-were independently evaluated and correl

256 The lateral ventricle subventricular zone (SVZ) is a frequent and consequential site of pediatric a

257 The subventricular zone (SVZ) is greatly expanded in primates with gyrencephalic

258 The subventricular zone (SVZ) is one of the two major neurogenic regions in the a

259 The subventricular zone (SVZ) is the largest germinal zone of the forebrain and i

260 enerated from nestin(+) subventricular zone (SVZ) neural progenitor cells (NPCs) in normal adult mice

261 neurogenesis from adult subventricular zone (SVZ) neural stem cells (NSCs) in culture.

262 newly generated rodent subventricular zone (SVZ) neuroblasts as they transit along the lateral ventr

263 Subventricular zone (SVZ) neurogenesis continuously provides new GABA- and do

264 in the control of adult subventricular zone (SVZ) neurogenesis in rodents.

265 Postnatal and adult subventricular zone (SVZ) neurogenesis is believed to be primarily controlled

266 e dentate gyrus and the subventricular zone (SVZ) next to the lateral ventricles, continuously self-r

267 lls (NPCs) of the adult subventricular zone (SVZ) niche are fairly well understood, the pathways acti

268 of these cells in their subventricular zone (SVZ) niches but fails to maintain stemness outside the S

269 mouse lateral ventricle subventricular zone (SVZ) NICs as Glast(mid)EGFR(high)PlexinB2(high)CD24(-/lo

270 genitor cells or in the subventricular zone (SVZ) of ischemic animals significantly increased cell pr

271 ation in the neurogenic subventricular zone (SVZ) of neonatal mice, we deleted Tsc1 and generated olf

272 esis is impaired in the subventricular zone (SVZ) of postmortem human PD brains, in primate nonhuman

273 ssed Idh1(R132H) in the subventricular zone (SVZ) of the adult mouse brain.

274 ent from the neurogenic subventricular zone (SVZ) of the adult mouse striatum.

275 he cortex, striatum and subventricular zone (SVZ) of the ischemic rat brain, while simultaneously enh

276 lar niche signal in the subventricular zone (SVZ) of the lateral ventricle of the adult mouse brain.

277 esis takes place is the subventricular zone (SVZ) of the lateral ventricles.

278 The subventricular zone (SVZ) provides a constant supply of new neurons to the ol

279 ural progenitors in the subventricular zone (SVZ) region of mouse brain.

280 se in stem cells of the subventricular zone (SVZ) upon oncogenic stress, whereas their expression in

281 re we show that the VZ, subventricular zone (SVZ), and CP contain distinct molecular maps of regional

282 In the adult mammalian subventricular zone (SVZ), GFAP-positive neural stem cells (NSCs) generate ne

283 Aging and PD impair the subventricular zone (SVZ), one of the most important brain regions for adult

284 lactosidase outside the subventricular zone (SVZ), subarachnoid hemorrhage, and ventriculomegaly.

285 quiescence in the adult subventricular zone (SVZ), the function of ECM in the developing SVZ remains

286 oglial functions in the subventricular zone (SVZ), the major postnatal neurogenic niche.

287 d RhoA and Cdc42 in the subventricular zone (SVZ), where more fate-restricted progenitors are located

288 Subventricular zone (SVZ)-derived adult neural precursor cells (aNPCs) were i

289 ntrols the migration of subventricular zone (SVZ)-derived neural progenitors toward the demyelinated

290 ursors (NPs) within the subventricular zone (SVZ).

291 regions, including the subventricular zone (SVZ).

292 ced neurogenesis in the subventricular zone (SVZ).

293 s of FGF2 on the VZ and subventricular zone (SVZ).

294 n was injected into the subventricular zone (SVZ).

295 enitor cells within the subventricular zone (SVZ).

296 NPCs derived from the subventricular zone (SVZ-NPCs) were also included in the study as a reference

297 NSCs) within the rodent subventricular zone (SVZ; also called subependymal zone) generate doublecorti

298 lls located within the Sub-Ventricular Zone (SVZ).

299 t zones, including presynaptic vesicle zone (SVZ), active zone (AZ) and postsynaptic density (PSD).

300 c ventricular (VZ) and subventricular zones (SVZ), which give rise to excitatory neurons, are divided