ライフサイエンスコーパス: NSC

1 NSC-311068 and especially NSC-370284 significantly repre

2 NSC-370284 and UC-514321 both directly target STAT3/5, t

3 NSCs are 'hard-to-transfect' but amenable to 'magnetofec

4 NSCs are clonally expandable, genetically stable, and ea

5 NSCs in the adult mouse ventricular-subventricular zone

6 Z and promote the proliferation of Nkx2.1(+) NSCs and the generation of deep granule neurons.

7 aling enables direct communication between a NSC and its descendants, so that progeny can send feedba

8 e necessary and sufficient to maintain adult NSC quiescence and ablating them leads to NSC activation

9 llular transport functions in cultured adult NSCs.

10 ion culture conditions, Kdm5b-depleted adult NSCs migrated from neurospheres with increased velocity.

11 n migratory velocity of Kdm5b-depleted adult NSCs.

12 ith Kdm5b depletion in differentiating adult NSCs.

13 f postnatal NSCs, resulting in loss of adult NSCs and defective V-SVZ regeneration.

14 re observed along the SGZ, composed of adult NSCs and early IPCs, and oxidative byproducts were prese

15 to sustain the neurogenic potential of adult NSCs and identify alpha-SYN and DA as potential targets

16 on to efficient lineage progression of adult NSCs and identify mitochondrial function as a potential

17 rnessed for preferential modulation of adult NSCs in the hippocampus.

18 also show that premature senescence of adult NSCs into non-neurogenic astrocytes in mice lacking alph

19 nonical Wnt signaling in proliferating adult NSCs and non-canonical Wnt signaling in differentiating

20 ed depletion of Kdm5b in proliferating adult NSCs decreased proliferation rates and reduced neurosphe

21 iding RGCs gives rise to the quiescent adult NSCs that populate the ventricular-subventricular zone (

22 protein previously found in quiescent adult NSCs, is expressed by a subpopulation of embryonic RGCs,

23 ostasis and how its dysregulation may affect NSC metabolism/development and contribute to disease.

24 maging were performed daily up to 48 h after NSC injection.

25 With age, NSCs exhibited increased SA-beta-gal activity and decrea

26 Furthermore, an NSC-like cell-of-origin enhanced tumor incidence, malign

27 entified two compounds (i.e., NSC-311068 and NSC-370284) that selectively suppress TET1 transcription

28 and reset neuronal competition dynamics and NSC activation, leaving the DG modified by a functionall

29 starch-at-maturity, sucrose-at-maturity and NSC-at-heading.

30 oblasts harboring a TDP-43M337V mutation and NSC-34 motor neuronal cell line expressing TDP-43Q331K m

31 Multiscale invariance of LMA, leaf water and NSC mark these traits as candidates for tracking forest

32 rient-dependent way in niche glial cells and NSCs.

33 ked whether cross-talk between pericytes and NSCs was induced by CORM-3, thereby promoting neurogenes

34 ly active topoisomerase I inhibitors such as NSC 314622, LMP-400, LMP-776.

35 at reducing miR-210 significantly attenuated NSC proliferation upon induction of differentiation.

36 Because NSCs seemed to be in close proximity to pericytes, we as

37 e cascade of reciprocal interactions between NSCs and ECs in this process was determined by quantifyi

38 light on the reciprocal interactions between NSCs and ECs, which are pivotal for our mechanistic unde

39 reveal that reciprocal interactions between NSCs and NK cells regulate neurorepair.

40 ne-pyrrole 2,3-dioxygenase (IDO), but not by NSC-398, a specific inhibitor of COX-2, suggesting IDO a

41 HA is synthesized by NSCs and increases in the SGZ with aging.

42 za sativa) stem nonstructural carbohydrates (NSC) at two critical developmental time-points using a s

43 a (LMA), water, nonstructural carbohydrates (NSCs) and polyphenols with increasing elevation.

44 the content of nonstructural carbohydrates (NSCs) of distal branches in woody plants with contrastin

45 substantial amounts of nonstructural carbon (NSC) for later use, storage regulation and mobilization

46 (TBI) promotes neural stem/progenitor cell (NSC) proliferation in an attempt to initiate innate repa

47 , few lncRNAs that control neural stem cell (NSC) behavior are known.

48 nery, regulates Drosophila neural stem cell (NSC) development through Ca(2)(+) mito homeostasis contr

49 d gel was found to promote neural stem cell (NSC) differentiation into neurons and neurite extension.

50 age-related reductions in neural stem cell (NSC) expansion and differentiation in the hippocampus.

51 Mammalian neural stem cell (NSC) lines provide a tractable model for discovery acros

52 lar niche signals regulate neural stem cell (NSC) quiescence and growth.

53 erated exhaustion of the neuronal stem cell (NSC) reserve, thereby allowing neurogenesis to proceed a

54 is crucial for maintaining neural stem cell (NSC) self-renewal and heterogeneity; however, the underl

55 MFN1/2 deletion, impaired neural stem cell (NSC) self-renewal, with consequent age-dependent depleti

56 Genetically engineered neural stem cell (NSC) transplant populations offer key benefits in regene

57 otrophin-based therapy and neural stem cell (NSC)-based strategies have progressed to clinical trials

58 for engrafted neural stem/progenitor cells (NSC/NPCs).

59 Transplanted neural stem cells (NSC) interact with the host brain microenvironment.

60 of origin reminiscent of neural stem cells (NSC) or oligodendrocyte precursor cells (OPC).

61 ation of new neurons from neural stem cells (NSC), in offspring.

62 n by human neural stem and progenitor cells (NSCs) in vitro via a PAR1-PAR3-sphingosine-1-phosphate-r

63 lls, including neural stem/progenitor cells (NSCs).

64 selectively expressed in neural stem cells (NSCs) and astrocytes.

65 uronal differentiation of neural stem cells (NSCs) and dendritic branching of differentiated neurons.

66 trols the self-renewal of neural stem cells (NSCs) and has been implied as an oncogene which initiate

67 role in normal mammalian neural stem cells (NSCs) and in SCZ pathogenesis remains unknown.

68 the number of hippocampal neural stem cells (NSCs) and investigated the expression of several miRNAs

69 erentiation are silent in neural stem cells (NSCs) and occupy black chromatin and a TrxG-repressive s

70 postnatal mice, including neural stem cells (NSCs) and their immediate progenies, which generate dist

71 Neural stem cells (NSCs) are a heterogeneous population of cells that gener

72 Neural stem cells (NSCs) are defined by their ability to self-renew and to

73 Adult neural stem cells (NSCs) are defined by their inherent capacity to self-ren

74 Drosophila neural stem cells (NSCs) are quiescent at early larval stages, when they ar

75 linical interest in using neural stem cells (NSCs) as carriers for targeted delivery of therapeutics

76 Neural stem cells (NSCs) differentiate into both neurons and glia, and stra

77 g Drosophila development, neural stem cells (NSCs) divide asymmetrically and generate intermediate pr

78 central question: How do neural stem cells (NSCs) divide in different ways to produce heterogeneous

79 ity of individual pallial neural stem cells (NSCs) from embryo to adult.

80 acturing patient specific neural stem cells (NSCs) from iPSCs.

81 subventricular zone (SVZ) neural stem cells (NSCs) in culture.

82 on and differentiation of neural stem cells (NSCs) in development has not been studied.

83 Neural stem cells (NSCs) in specialized niches in the adult mammalian brain

84 ycling and maintenance of neural stem cells (NSCs) in the brain subependymal zone of adult male and f

85 ely reduced the number of neural stem cells (NSCs) in the postnatal dentate gyrus (DG), drastically i

86 Adult neural stem cells (NSCs) in the ventricular-subventricular zone (V-SVZ) pro

87 Hippocampal neural stem cells (NSCs) integrate inputs from multiple sources to balance

88 differentiation of murine neural stem cells (NSCs) into neurons and astroglial-like cells.

89 on of neurons and glia by neural stem cells (NSCs) is essential for neural circuit assembly.

90 The quiescence of adult neural stem cells (NSCs) is regulated by local parvalbumin (PV) interneuron

91 f Pten and Trp53 in mouse neural stem cells (NSCs) leads to the expansion of these cells in their sub

92 Neural stem cells (NSCs) play an essential role in shaping the developing b

93 Neural stem cells (NSCs) reside in a unique microenvironment within the cen

94 in close proximity to SVZ neural stem cells (NSCs) that produce interleukin-15 and sustain functional

95 During development, neural stem cells (NSCs) undergo transitions from neuroepithelial cells to

96 In the present study, neural stem cells (NSCs) were derived from the SVZ on postnatal 7 d, 1 m, a

97 Neural stem cells (NSCs) within the hippocampal niche integrate local cues,

98 al neurons from quiescent neural stem cells (NSCs).

99 ir capacity of endogenous neural stem cells (NSCs).

100 liferation of hippocampal neural stem cells (NSCs).

101 ric oxide synthase within neural stem cells (NSCs).

102 apoptosis in hippocampal neural stem cells (NSCs).

103 etween neonatal and adult neural stem cells (NSCs).

104 oliferation of endogenous neural stem cells (NSCs); however, the survival of young neurons is sharply

105 is compared with nearest shrunken centroids (NSCs) and sparse discriminant analysis (SDA) with k-near

106 ivity to the neurogenic niche in controlling NSC quiescence and hippocampal neurogenesis.

107 Non-syndromic craniosynostosis (NSC) is a frequent congenital malformation in which one

108 Expression of SMAD1 in YAP-deficient NSCs partially rescued the astrocytic differentiation de

109 It also inhibited hippocampal derived NSC proliferation and differentiation, as evident by the

110 odevelopment and in SCZ patient iPSC-derived NSCs.

111 e c oxidase and aconitase in differentiating NSC cultures exposed to inflammatory mediators.

112 nervation of the V-SVZ, can recruit distinct NSC pools, allowing on-demand neurogenesis in response t

113 val type II neuroblasts (NBs, the Drosophila NSCs) and transforms type II NBs into type I NBs.

114 creening, we identified two compounds (i.e., NSC-311068 and NSC-370284) that selectively suppress TET

115 od vessel function is required for efficient NSC differentiation in the developing cerebral cortex by

116 gest that although stimulation of endogenous NSCs following TBI might offer new avenues for cell-base

117 magnetofection technology to safely engineer NSCs to overexpress BDNF.

118 All daughter cell types of engineered NSCs (neurons, astrocytes and oligodendrocytes) were tra

119 g both approaches by genetically-engineering NSCs to express BDNF is an attractive approach to achiev

120 al, maturation, and integration of engrafted NSC/NPCs as a restorative treatment for PD.

121 entiated neuronal recruitment from engrafted NSCs might offer a new approach to the treatment of stro

122 ng manifested in transition of the enigmatic NSC terminal arbor onto long cytoplasmic processes engag

123 NSC-311068 and especially NSC-370284 significantly repressed TET1-high AML progres

124 CD44-expressing NSCs isolated from the mouse SGZ are self-renewing and c

125 Remarkably, VEGF caused extensive NSC remodelling manifested in transition of the enigmati

126 porous silica nanoparticle (MSN)-facilitated NSC tracking in the brain via SPECT.

127 Four familial NSC kindreds had mutations in genes previously implicate

128 In vitro, endogenous Lmnb1 depletion favors NSC differentiation into glial fibrillar acidic protein

129 ted for two conditionally immortalized fetal NSC lines derived from the cortical anlage (CTXOE03) and

130 , the mutant DG neurospheres generated fewer NSCs with defects in proliferation, survival, and differ

131 demonstrate feasibility of this platform for NSC imaging.

132 ly tuned levels of Lamin B1 are required for NSC differentiation into neurons, proper expression of t

133 Yorkie is necessary and sufficient for NSC reactivation, growth and proliferation.

134 ng rosettes, which are abundant with founder NSCs and correspond to the early proliferative developin

135 he generation of specific cell lineages from NSCs in vivo, during postnatal life and adulthood, as we

136 potential to produce all three lineages from NSCs in vivo.

137 we report a histological analysis of the FT NSC niche in postnatal rats and humans.

138 signals from distal brain regions to govern NSC quiescence and activation.

139 gnaling appears to be a key factor governing NSC quiescence, division, and fate.

140 at deletion of Drosha in adult dentate gyrus NSCs activates oligodendrogenesis and reduces neurogenes

141 This work assessed human H9 NSCs that were implanted into sites of SCI in immunodefi

142 on a Pten(-/-); Trp53(-/-) background helps NSCs maintain their stemness outside the SVZ in Nes-CreE

143 hibition of neurogenesis in both hippocampal NSC cultures and the hippocampus, suggesting the specifi

144 ur findings establish that adult hippocampal NSCs inherently possess multilineage potential but that

145 down of NFIB in Drosha-deficient hippocampal NSCs restores neurogenesis, suggesting that the Drosha/N

146 In vivo, however, hippocampal NSCs do not generate oligodendrocytes for reasons that h

147 ound one of those previously described hits, NSC 60339 (1).

148 However, NSC in older aboveground and belowground tissues was enr

149 s via gene targeting in both mouse and human NSC lines, including: (1) efficient targeted transgene i

150 idate the signaling mechanisms between human NSCs and endothelial cells (ECs), these were cocultured

151 ver, the time period of maturation for human NSCs in adult injured CNS is not well defined, posing fu

152 -seq-based transcriptomic profiling in human NSCs treated with 1 muM Pb.

153 Thus, human NSCs retain an intrinsic human rate of maturation, despi

154 es neuronal production by transplanted human NSCs, promotes circuit restoration and improves function

155 neurons and glia, and strategies using human NSCs have the potential to restore function following sp

156 liferation; however, proliferation of type I NSCs was unchanged in response to fluoxetine.

157 ver, within the ventral hippocampus, type II NSC and neuroblast populations specifically responded to

158 ct of fluoxetine on proliferation of type II NSCs and neuroblast populations in the ventral hippocamp

159 Both conditions impaired NSC lineage progression.

160 tem cells, has not been exploited to date in NSC lines.

161 These findings implicate new genes in NSC and demonstrate related pathophysiology of common no

162 ase-retinoblastoma signaling is important in NSC proliferation and the reduction of this activation o

163 Mice lacking CD44 demonstrate increases in NSC proliferation in the SGZ.

164 Depletion of MYO9A in NSC-34 cells revealed a direct effect of MYO9A on neuron

165 tricted development of neuronal processes in NSC-34 cells and primary cortical neurons.

166 dentify Pb-induced transcriptomic changes in NSCs and to link these changes to neurodevelopmental out

167 Notch receptor, is selectively expressed in NSCs.

168 -219 and downregulation of TLX expression in NSCs derived from SCZ patient iPSCs and DISC1-mutant iso

169 n of an essential autophagy gene, FIP200, in NSCs increased expression of Ccl5 and Cxcl10 in a p53-in

170 Further, Lfng in NSCs and Notch ligands Delta1 and Jagged1, expressed by

171 in mitochondrial function and morphology in NSCs, these data link mitochondrial complex function to

172 increased proliferation is also observed in NSCs grown in vitro, suggesting that CD44 functions to r

173 temporal transcription factor progression in NSCs silences the module, thereby limiting mitotic poten

174 nd initiation of growth and proliferation in NSCs.

175 We further demonstrated that, in NSCs, MBD1 binds and represses directly specific genes a

176 YAP in NSCs was required for neocortical astrocytic differentia

177 integration of adult-born DGCs and increased NSC activation.

178 prevented the relief from hypoxia, increased NSC expansion at the expense of differentiation.

179 NSC cultures or in the SGZ induces increased NSC proliferation, and CD44-null as well as HA-disrupted

180 pressed by their progeny, together influence NSC recruitment, cell cycle duration, and terminal fate.

181 domain-containing Tyr phosphatase inhibitor (NSC 87877), or the MEK inhibitor PD98059 blocked FSH-dep

182 ese results suggest that carbofuran inhibits NSC proliferation and neuronal differentiation by alteri

183 type but not CD44-null NSCs with HA inhibits NSC proliferation.

184 Interestingly, NSC loss in alpha-SYN-deficient mice can be prevented by

185 ng iPSC expansion, iPSC differentiation into NSCs, the subsequent depletion of undifferentiated iPSCs

186 An alternative is to isolate NSCs from a donor, and expand them in vitro as transplan

187 on reminiscent of early postnatal "juvenile" NSCs.

188 In neurons, almost all key NSC genes are switched off via HP1-mediated repression.

189 canonical Hippo signalling pathway maintains NSC quiescence.

190 ile and scalable genome editing in mammalian NSCs, providing significant new opportunities for functi

191 g of 291 parent-offspring trios with midline NSC revealed 15 probands with heterozygous damaging de n

192 In vivo, SPECT visualizes actively migrating NSCs toward glioma xenografts in real time after both in

193 anisms by which this key regulator modulates NSC function, indicating that this engineered AAV varian

194 miR-219 suppresses mouse NSC proliferation downstream of TLX.

195 Primary mouse NSCs overexpressing BDNF generated increased daughter ne

196 it amplifying cells and neuroblasts) but not NSCs (quiescent and activated) undergo apoptosis after 2

197 Treating wild type but not CD44-null NSCs with HA inhibits NSC proliferation.

198 the deficient differentiation of FIP200-null NSCs from FIP200;p53hGFAP 2cKO mice.

199 ncreased chemokine expression in FIP200-null NSCs was induced by abnormal p62 aggregate formation and

200 al to inhibit differentiation of FIP200-null NSCs.

201 More than 95% of NSC is sporadic, suggesting a role for de novo mutations

202 UC-514321, a structural analog of NSC-370284, exhibited a more potent therapeutic effect a

203 slocation, leading to decreased apoptosis of NSC.

204 ed GC from these tumors showed that cells of NSC-like origin were more tumorigenic, had a higher rate

205 monstrate that the spatiotemporal control of NSC activity is an important driver of the macroarchitec

206 d to explain the role of NR2E1 in control of NSC self-renewal and cancer.

207 mechanistic understanding of the efficacy of NSC transplantation.

208 In contrast, the genetics of NSC is largely unexplored.

209 Multimodal dynamic in vivo imaging of NSC behaviors in the brain is necessary for developing s

210 tions about the design and implementation of NSC-based therapies.

211 4) C in stemwood NSC showed strong mixing of NSC across the youngest growth rings, with limited 'mixi

212 lear receptor TLX, an essential regulator of NSC proliferation and self-renewal, inhibits miR-219 pro

213 discovered that Qki is a major regulator of NSC stemness.

214 (HIF)-1alpha levels controlled the switch of NSC expansion to differentiation.

215 de evidence that high glycolytic activity of NSCs is required to prevent their precocious differentia

216 mplementing the cell replacement benefits of NSCs.

217 NK cells limited the reparative capacity of NSCs following brain inflammation.

218 ssues with an optimized seeding condition of NSCs, BMECs and MSCs.

219 The conversion of NSCs is strongly associated with PLC variations during d

220 ent enhanced the in vitro differentiation of NSCs into mature neurons.

221 accounted for the differential efficiency of NSCs to induce endothelial morphogenesis.

222 f the hippocampus while the mitotic index of NSCs in the dorsal portion of the hippocampus remained u

223 s important for maintaining the integrity of NSCs, which is critical for their neurogenic potency.

224 kinesis events that follow apical mitoses of NSCs; coordinating abscission with delamination from the

225 gest that MBD1 maintains the multipotency of NSCs by restraining the onset of differentiation genes a

226 An increased number of NSCs and new neurons in NDAN individuals is associated w

227 tine specifically increased proliferation of NSCs located in the ventral region of the hippocampus wh

228 ant and oncogene-induced malignant states of NSCs.

229 or maintaining the integrity and stemness of NSCs, which is critical for their ability to generate ne

230 ic neurons control activation of a subset of NSCs in response to feeding, providing insights into how

231 Loading efficiency and viability of NSCs with (111)In-MSN complex were optimized.

232 estingly, BPA-mediated inhibitory effects on NSC proliferation and neuronal differentiations were als

233 e (an extracellular superoxide scavenger) or NSC 23766 (a Rac GTPase inhibitor) completely inhibited

234 ure of this tissue and its relation to other NSC niches in the CNS has not yet been established.

235 n, yet little is known about how Pb perturbs NSC functions and whether such perturbation contributes

236 ling RGP-mediated glia genesis and postnatal NSC behavior.

237 es neurogenesis from embryonic and postnatal NSC populations.

238 stricting local immune response in postnatal NSCs through non-cell autonomous mechanisms.

239 diminished the embryonic origin of postnatal NSCs, resulting in loss of adult NSCs and defective V-SV

240 Recently, another potential NSC niche has been identified in the filum terminale (FT

241 bit strong fluorescent profiles in preloaded NSCs, allowing for ex vivo validation of the in vivo dat

242 vels (up to 54%) reported so far for primary NSCs.

243 concentrating and transporting the purified NSCs to the surgery room, could be integrated and comple

244 utated (ATM)-dependent and promote quiescent NSC (qNSC) activation, which does not occur in the subdo

245 y discriminates quiescent from non-quiescent NSCs in the Drosophila nervous system.

246 Radiolabeled NSCs were administered to glioma-bearing mice via either

247 n the niche only is sufficient to reactivate NSCs.

248 xpression) in the hippocampus, which reduced NSC proliferation because of increased p21 levels and re

249 , suggesting that CD44 functions to regulate NSC proliferation in a cell-autonomous manner.

250 A therefore signals through CD44 to regulate NSC quiescence and differentiation, and HA accumulation

251 suggesting that niche blood vessels regulate NSC differentiation at least in part by providing oxygen

252 s known about whether autophagy can regulate NSCs through cell-extrinsic mechanisms.

253 nicate with distal brain regions to regulate NSCs and hippocampal neurogenesis.

254 ile PI3K/AKT governs neurofibromin-regulated NSC proliferation, multilineage differentiation is MEK-d

255 cular niche signal that negatively regulates NSC growth to control the NSC number in the SVZ.

256 ivo studies on the role of APP in regulating NSC number in the SVZ clearly demonstrate that endotheli

257 by providing oxygen and possibly regulating NSC metabolism.

258 in part, attributed to rescue of age-related NSC quiescence.

259 exposure to increased oxygen levels rescued NSC differentiation in Gpr124 null embryos and increased

260 crease in the number of BrdU label-retaining NSCs in the SVZ, whereas NSC/astrocyte deletion of App h

261 SCZ NSCs exhibit reduced cell proliferation.

262 tion rescues the proliferative defect in SCZ NSCs.

263 wn PBD dimer, SJG-136 (also known as SG2000, NSC 694501 or BN2629), was synthesized in the 1990s and

264 rmediate progenitors; and capacity of single NSCs to generate the correct number and laminar fate of

265 The number of SOX2(+) NSCs in the DG was significantly increased in NDAN indiv

266 Further, the prevalence of SOX2(+) NSCs was found to correlate with cognitive capacity.

267 to the V-SVZ niche and can regulate specific NSC subpopulations.

268 alidate candidate genes underlying rice stem NSC and informs future comparative studies in other agro

269 C) as the mobilized component of stored stem NSC during early springtime.

270 Radial patterns of (14) C in stemwood NSC showed strong mixing of NSC across the youngest grow

271 Our findings suggest that ETH stimulates NSC proliferation and differentiation in vitro and adult

272 torage regulation and mobilization of stored NSC in long-lived organisms like trees are still not wel

273 sAPP suppresses NSC growth in culture.

274 However, V-SVZ NSCs are heterogeneous: they have different embryonic or

275 These results suggest that NSC-mediated neuron and glia production is tightly regul

276 hile previous studies have demonstrated that NSCs can be isolated from the FT, the in vivo architectu

277 VCAM1 affects the NSC fate by signaling through its intracellular domain t

278 the central nervous system (CNS) called the NSC niche.

279 gatively regulates NSC growth to control the NSC number in the SVZ.

280 C activation and subsequent depletion of the NSC pool.

281 etion of App has no detectable effect on the NSC number.

282 depletion of undifferentiated iPSCs from the NSCs, and concentrating and transporting the purified NS

283 endent upon the type and the position of the NSCs along the DV axis of the hippocampus.

284 ltimodal noninvasive tracking of therapeutic NSCs toward various brain malignancies.

285 that endothelial-derived IGF2 contributes to NSC maintenance in SVZ but not in the SGZ, and that this

286 lt NSC quiescence and ablating them leads to NSC activation and subsequent depletion of the NSC pool.

287 alpha-SYN regulates dopamine availability to NSCs.

288 ly employ viral vectors for gene delivery to NSCs though safety and scalability pose major concerns f

289 11)In-MSN complexes show minimal toxicity to NSCs and robust in vitro and in vivo stability.

290 HA digestion in wild type NSC cultures or in the SGZ induces increased NSC prolife

291 CD44-null as well as HA-disrupted wild type NSCs demonstrate delayed neuronal differentiation.

292 eads to the accumulation of undifferentiated NSCs and impaired transition into the neuronal lineage.

293 pitation followed by mass spectrometry using NSC-34 cells expressing human wild-type or mutant Matrin

294 rdU label-retaining NSCs in the SVZ, whereas NSC/astrocyte deletion of App has no detectable effect o

295 The molecular mechanism by which NSC number is controlled in the neurogenic regions of th

296 ere cocultured in an in vitro model in which NSC-induced endothelial morphogenesis produced a neurova

297 ood vessels temporo-spatially coincided with NSC differentiation.

298 omedical data, the results are compared with NSC and SDA models with four different types of imputati

299 ing pericyte death, rescuing cross-talk with NSCs and promoting neurogenesis.

300 h rings, with limited 'mixing in' of younger NSC to older rings.