ライフサイエンスコーパス: neurosphere

1 opulation or reduced cell density within the neurosphere.

2 tiation into differentiated embryoid body or neurospheres.

3 lizes flow and microstructures to dissociate neurospheres.

4 ne, Gpr17, resulted in a decreased number of neurospheres.

5 the male-specific Sry gene, and cultured as neurospheres.

6 ts of forced differentiation in glioblastoma neurospheres.

7 to form pluripotent, long-term self-renewing neurospheres.

8 ox2 in glioma cell lines and patient-derived neurospheres.

9 id not induce neuronal differentiation in WT neurospheres.

10 ly higher in Cx43-null than in WT littermate neurospheres.

11 ion of GABAergic cells derived from passaged neurospheres.

12 mouse models of GBM and in primary human GBM neurospheres.

13 ll lines and increased in stem cell enriched neurospheres.

14 inhibited IGF2-induced growth of GBM-derived neurospheres.

15 for EGF to support the growth of GBM-derived neurospheres.

16 maintained as free-floating undifferentiated neurospheres.

17 isogenic cultures of hiPSC-derived forebrain neurospheres.

18 ssed by neural progenitors grown as cultured neurospheres.

19 nb2 (-/-) neurons as they migrated away from neurospheres.

20 elomerase activity in cultured eNOS(-/-) SVZ neurospheres.

21 ease in differentiation in etoposide-treated neurospheres.

22 itions for inducing differentiation in human neurospheres.

23 Inhibition of OPN blocked the formation of neurospheres, affected the proliferative capacity of tra

24 Average diameters of individual cells and neurospheres after 1 week in culture were similar in mic

25 Incubation of neurospheres alone with rhEPO failed to increase progeni

26 However, in adult normal neurospheres, alpha(1)-adrenergic receptor stimulation i

27 grafts derived from EphB2-overexpressing GBM neurospheres also showed decreased cellular proliferatio

28 In vitro neurosphere and differentiation assays indicate that Bot

29 Using subventricular neurosphere and matrigel cultures, we demonstrated that

30 potential; and as few as six cells will form neurospheres and 20-30 cells will grow tumor in mice.

31 oplastic stem cell phenotype in glioblastoma neurospheres and clinical glioblastoma specimens.

32 Moreover, a fraction of GFP+ cells formed neurospheres and differentiated into neurons, astrocytes

33 ng cells accounted for the cells that formed neurospheres and differentiated to hair cells.

34 ay analysis on control and shMCT4-expressing neurospheres and found a dramatic reduction in the expre

35 3 negative cells, hypoxia was able to induce neurospheres and hESC markers.

36 hermore, GD3 synthase (GD3S) is increased in neurospheres and human GBM tissues, but not in normal br

37 inished the proliferation of patient-derived neurospheres and increased survival in mouse models of e

38 t not gliogenesis, was affected in HAP1-null neurospheres and mouse brain.

39 n of Musashi-Notch signaling by TRIM3 in GBM neurospheres and neural stem cells that may better expla

40 These cells were differentiated into neurospheres and neuronal precursors in vitro, providing

41 cture with combined features of hypothalamic neurospheres and pancreatic islets.

42 B proliferation in vitro compared to control neurospheres and substantially inhibited G3 MB prolifera

43 ZIKV infection of human organoids and mouse neurospheres and TLR3 inhibition reduced the phenotypic

44 nglioside D3 (GD3) is overexpressed on eight neurospheres and tumor cells; in combination with CD133,

45 in gene expression of patient-derived glioma neurospheres and uncover subpopulations similar to those

46 tion of embryonic and adult NPCs cultured as neurospheres and, in vivo, in the subventricular zone of

47 ir morphology, self-renewal, ability to form neurospheres, and gene expression profiles.

48 5p enhanced the self-renewal capacity of GBM neurospheres, and inhibition of endogenous miR-486-5p ac

49 aged IDH wild-type glioblastomas, derivative neurospheres, and single-cell gene expression profiles t

50 an exogenous signal but then regroup into a neurosphere as the signal is removed.

51 eration and differentiation both in cultured neurospheres as well as in vivo mouse and fly models of

52 Hh-pathway in TMZ-response on additional GBM neurospheres as well as on GBM patients, by extracting R

53 strating the applicability of this device to neurosphere assay applications.

54 greater differentiation of hair cells in the neurosphere assay showed that Lgr5-positive cells had th

55 istochemistry (IHC), electron microscopy and neurosphere assay the morphology, cytoarchitecture and n

56 ewal, and multipotentiality as assessed by a neurosphere assay.

57 ne (SVZ) are isolated and expanded using the neurosphere assay.

58 f neural progenitor cells measured by single neurosphere assay.

59 nd on forebrain signals not available in the neurosphere assay.

60 Neural precursor responses were evaluated by neurosphere assays as well as by stereological analyses.

61 In vitro NPC-derived neurosphere assays showed that Tat-containing conditione

62 ar movement in cortical slice assays, and in neurosphere assays, the percentage of migrating neurons

63 Our findings suggested that implementing a neurosphere-based culture enabled directing neural proge

64 layer-based culture for neural induction and neurosphere-based culture for neural proliferation and e

65 his study explores the use of a simple human neurosphere-based in vitro model to characterise the pha

66 ma cells and glioma-initiating cell-enriched neurospheres both in vitro and in vivo, and we show that

67 Pre-GEPCOT cells could not form neurospheres but expressed the stem cell markers Slc1a3-

68 ells had the ability to proliferate and form neurospheres but had an impaired response to mitogen sti

69 adiosensitizes GBM cells and patient-derived neurospheres by impairing DNA repair.

70 plantation of a clonally derived spinal cord neurosphere can result in reconstitution of all examined

71 Adult neurospheres can be collected in 1 week as a source of n

72 from the murine spinal cord and organized as neurospheres, can be triggered to migrate out in respons

73 EphB2 expression stimulated GBM neurosphere cell migration and invasion, and inhibited n

74 e cell migration and invasion, and inhibited neurosphere cell proliferation in vitro.

75 characteristics of neurosphere formation and neurosphere cell self-renewal.

76 ion with this, we confirmed that both normal neurosphere cells and ENU-im-mortalized subventricular z

77 rtib exerted similar effects on glioblastoma neurosphere cells in vivo and resulted in markedly reduc

78 Moreover, alisertib caused glioblastoma neurosphere cells to partially differentiate and enter s

79 Many glioblastoma neurosphere cells treated with alisertib for short perio

80 se in PrP(Sc) levels with time in the Tg4053 neurosphere cells, whereas the level of PrP(Sc) decayed

81 e and cell migration in EphB2-expressing GBM neurosphere cells.

82 -deficient embryos formed greater numbers of neurospheres compared with neurospheres from wild-type e

83 ote that an intact tumor microenvironment or neurosphere conditions in vitro are required for Gli act

84 The percent neurospheres containing differentiated neurons and the n

85 Neurospheres continued to generate differentiated progen

86 radial glial morphology) expressed YFP; YFP+ neurospheres could be generated in vitro after recombina

87 nol in a fetal mouse cerebral cortex-derived neurosphere culture model.

88 nsequences for DIPG self-renewal capacity in neurosphere culture.

89 eshly isolated human glioblastoma multiforme neurosphere cultures (containing "stem cell-like cells")

90 When GBM-derived neurosphere cultures are grown in 1% oxygen, hypoxia-ind

91 micked those seen in mice, validating use of neurosphere cultures as models for studying tau phosphor

92 binant murine TIMP-1 (rmTIMP-1) to TIMP-1 KO neurosphere cultures evoked a dose-dependent increase in

93 ry and qRT-PCR to screen fetal mouse-derived neurosphere cultures for ethanol-sensitive neural stem c

94 e central nervous system (CNS) SC-containing neurosphere cultures for studying heritable neurodegener

95 We produced neurosphere cultures from FVB/NCr (FVB) mice, from trans

96 table neurodegenerative disease, we compared neurosphere cultures from transgenic mice that express h

97 iments on bulk GBM cell line cultures and on neurosphere cultures of a human-origin GBM xenograft tum

98 In neurosphere cultures prepared from the SVZ of adult mice

99 Studies of neurosphere cultures prepared from the telencephalon at

100 ansient exposure of embryonic day 14.5 mouse neurosphere cultures to dexamethasone (DEX) limits proli

101 The susceptibility of neurosphere cultures to prions mirrored that of the mice

102 Neurosphere cultures treated with gamma-secretase inhibi

103 GL261 neurosphere cultures were used to evaluate GIC.

104 on is markedly reduced in human GBM samples, neurosphere cultures, and cell lines and its reconstitut

105 netically engineered mice and derivative NSC neurosphere cultures, we show that this brain region-spe

106 By using a conditional deletion system and neurosphere cultures, we showed that FoxM1 is important

107 nditioned media obtained from primary glioma neurosphere cultures.

108 th factor (EGF)-induced proliferation within neurosphere cultures.

109 ce impairs neuronal cell proliferation using neurosphere cultures.

110 contrast, ZSCAN21 silencing reduced SNCA in neurosphere cultures.

111 of differentiation in CNS progenitor cells (neurosphere) cultures from TIMP-1 KO mice revealed a spe

112 sion levels in undifferentiated, SVZ-derived neurospheres decline markedly with differentiation.

113 ties (80-85%) and the ability to regrow into neurospheres, demonstrating the applicability of this de

114 Moreover, neurospheres derived from animals with Copb2 variants gr

115 These changes can be preserved in vitro, as neurospheres derived from Gdf11(-/-) and wild-type litte

116 Neurospheres derived from raptor-deficient brains are sm

117 logy, the degree of neuronal maturation from neurospheres derived from wild-type (WT) and Cx43-null m

118 this, LY364947 treatment in irradiated GL261 neurosphere-derived cells decreased DNA damage responses

119 Olfactory neurosphere-derived cells from nine male schizophrenia p

120 investigate cell cycle dynamics in olfactory neurosphere-derived cells from nine male schizophrenia p

121 s study was to investigate whether olfactory neurosphere-derived cells from schizophrenia patients ha

122 The neurosphere-derived cells migrated, proliferated, and ge

123 In this study, we used neurosphere-derived cells to show that immature doubleco

124 ition, neural stem/progenitor cell cultures (neurosphere-derived cells) from nasal biopsies from indi

125 Neural stem/progenitor cell cultures (neurosphere-derived cells) from olfactory mucosa of schi

126 eptides in the background of human olfactory neurosphere-derived stem (ONS) cell matrix.

127 antagomirs to preestablished orthotopic GBM neurosphere-derived xenografts using advanced nanopartic

128 The neurosphere diameter also increased at day 10 post PPA t

129 e of the B2BkR antagonist HOE-140 during rat neurosphere differentiation, neuron-specific beta3-tubul

130 In cell culture, stem cells in hippocampal neurospheres display alterations in proliferation for wh

131 The Met(high) subpopulation within Met-pos neurospheres displayed clonogenic potential and long-ter

132 Met-positive and Met-negative neurospheres displayed distinct growth factor requiremen

133 ment of variant allele frequencies (VAFs) in neurospheres displaying contrasting phenotypes of sustai

134 tool for a wide range of applications where neurosphere dissociation is needed.

135 We show that this microfluidic-chip-based neurosphere-dissociation method can generate high yields

136 enitor cells in vivo, yet in vitro generated neurospheres, divided in response to bFGF (basic fibrobl

137 tivated and functional in glioblastoma (GBM) neurospheres enriched for glioblastoma tumor-initiating

138 CD133+ve cells form neurospheres, exhibit self-renewal and differentiation,

139 esting a loss of neurogenic potential in rat neurospheres expanded in vitro.

140 h beta-HB, SCFA receptor inhibitor, hindered neurosphere expansion (p < 0.001).

141 Here we report that cultured neurospheres expressing cellular prion protein (PrP(C))

142 sion of the MET oncogene was associated with neurospheres expressing the gene signature of mesenchyma

143 Met expression was almost absent from neurospheres expressing the signature of the classical s

144 evidence that TRBP is required for efficient neurosphere formation and for the expression of neural s

145 38 significantly reduced the cell viability, neurosphere formation and induced apoptosis of GSCs with

146 We show that TMZ + GSI treatment decreased neurosphere formation and inhibited neurosphere recovery

147 t to induce the stem cell characteristics of neurosphere formation and neurosphere cell self-renewal.

148 qualities of primary GBM cultures, including neurosphere formation and the expression of stem cell ma

149 Neurosphere formation assays showed that adult auditory

150 IR decreased primary neurosphere formation by 28%, but did not reduce seconda

151 y neurosphere formation by 75% and secondary neurosphere formation by 68%.

152 364947 treatment before IR decreased primary neurosphere formation by 75% and secondary neurosphere f

153 ut not control IgG, dramatically reduced the neurosphere formation frequency in mice that had exercis

154 Cs decreased proliferation rates and reduced neurosphere formation in culture.

155 activity and blocked cell proliferation and neurosphere formation in cultures of glioma stem cells,

156 layed an enhanced capacity for self-renewing neurosphere formation in response to Wnt and were conver

157 h reduced growth factor dependency, enhanced neurosphere formation in vitro, and increased sensitivit

158 duced proliferating (BrdU-labeled) cells and neurosphere formation in wild type but not TLR3(-/-)-der

159 Neurosphere formation is commonly used as a surrogate fo

160 equence of vascular regression, since YFP(+) neurosphere formation over serial passage was unaffected

161 k attenuated stem cell marker expression and neurosphere formation while having minimal effects on tu

162 expression of embryonic SCs and NC markers, neurosphere formation, and differentiation into neurons,

163 t by analyzing cell viability via MTT assay, neurosphere formation, and endoplasmic reticulum stress/

164 on of miR-124 and knockdown of SNAI2 reduced neurosphere formation, CD133(+) cell subpopulation, and

165 in CD133(+) glioma cells potently disrupted neurosphere formation, induced apoptosis, and inhibited

166 ved from eNOS-/- mice restored the decreased neurosphere formation, proliferation, neurite outgrowth,

167 increasing cell proliferation and stem cell neurosphere formation, with its ectopic overexpression s

168 nd that these cells have high propensity for neurosphere formation.

169 rmation by 28%, but did not reduce secondary neurosphere formation.

170 ndently increased the number and size of new neurosphere formation.

171 glioblastoma cells and GSCs and promoted GSC neurosphere formation.

172 tures, TMZ treatment significantly decreases neurosphere formation; however, a small percentage of ce

173 e retinal integration and differentiation of neurospheres formed by stem cells and mouse neural proge

174 development were also supported by a higher neurosphere forming ability at E11 than at E15.

175 Neurosphere forming cells (NSFCs) have been established

176 markers, inhibit the tumor-initiating cell's neurosphere-forming capacity, and migration.

177 RA treatment dramatically decreased neurosphere-forming capacity, inhibited the ability of n

178 47 had no effect on the primary or secondary neurosphere-forming capacity.

179 or, on a panel of unselected patient-derived neurosphere-forming cells and found that GBM cells can b

180 at allows the purification to homogeneity of neurosphere-forming neural precursors from the adult mou

181 uorescence-activated cell sorting to isolate neurosphere-forming neural stem cells (NSCs) from embryo

182 Importantly, these cells constitute the neurosphere-forming population among SVZ astrocytes.

183 population, which comprises the majority of neurosphere-forming precursors, there are two distinct s

184 Production of neurospheres from auditory nerve cells was stimulated by

185 Using cultured neurospheres from PPT1-KO and wild-type mouse fetuses, w

186 compared FTD-hallmark tau phosphorylation in neurospheres from rTg(tau(P301L))4510 mice and from rTg(

187 pon differentiation, more than twice as many neurospheres from the damaged brain were tripotential, s

188 h the Notch intracellular domain rescued GBM neurospheres from the RA-induced differentiation and ste

189 reater numbers of neurospheres compared with neurospheres from wild-type embryos.

190 ntiated cells (GBMDC) grown in serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro.

191 Consistently, the mutant DG neurospheres generated fewer NSCs with defects in prolif

192 We transplanted neurospheres generated from fetal and postnatal intestin

193 cells represent <2% of the cells present in neurospheres generated from postnatal rat brain but >95%

194 Re-engraftment of these primary tumor neurospheres generates secondary tumors with features ch

195 l interfering RNA increased the number of WT neurospheres generating differentiated neurons.

196 Alpelisib inhibited GSC neurosphere growth and these effects were more pronounce

197 phenotype defined by glioblastoma invasion, neurosphere growth, and endothelial tube formation was m

198 In vitro IL-6 enhanced neurosphere growth, self-renewal, and tripotentiality an

199 ted TMZ-sensitization of a TMZ non-responder neurosphere in vitro by treating them with the FDA-appro

200 strocytes and oligodendrocytes, and can form neurospheres in culture.

201 GBM-SCs were grown as non-adherent neurospheres in growth factor supplemented serum-free me

202 k genes important in hypoxia, we treated GBM neurospheres in hypoxia and identified monocarboxylate t

203 They grew as neurospheres in serum-free medium with epidermal growth

204 adherent in serum-containing media and forms neurospheres in supplemented serum-free media was develo

205 oliferation of NPCs was further found in SVZ neurospheres in tissue culture.

206 but not proliferation or differentiation, in neurospheres in vitro and in newly born SGZ cells in viv

207 ne in three EGFR(+) astrocytes gives rise to neurospheres in vitro, a 20-fold enrichment over unsorte

208 Using enteric neurons differentiated from neurospheres in vitro, we show that enteric axon growth

209 age of CD44+ cells in glioblastoma multiform neurospheres in vitro.

210 serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro.

211 apitulated all of these findings in cultured neurospheres, in which overexpression and depletion of B

212 each gene in LGE or MGE cells propagated as neurospheres, indicating that these newly identified mol

213 Neurospheres infected with lentiviral vectors expressing

214 (NSC) function but the relationship between neurosphere-initiating cells (NICs) and NSCs remains unc

215 The effect of sera on differentiation of NPC neurospheres into neuronal colonies was tested in 72-h-l

216 Obtaining single dissociated cells from neurospheres is difficult using nonenzymatic methods.

217 neurons in 1 d differentiated FMRP-deficient neurospheres is normalized.

218 ation were altered during differentiation of neurospheres isolated from B2BkR knock-out mice.

219 h factor receptor was reduced in hippocampal neurospheres isolated from db/db mice.

220 Neonatal neurospheres isolated from normal mice expressed a mixtu

221 Under these conditions neurosphere-like bodies (NLB) developed.

222 tative PCR analysis showed that treatment of neurosphere-like ReN cell aggregate cultures with gamma-

223 ensitive in vitro bioassay for mouse prions; neurosphere lines from other Tg mice overexpressing PrP

224 Neurosphere lines from Tg4053 mice provide a sensitive i

225 lf-renewal potential of several glioblastoma neurosphere lines in vitro, and this activity was furthe

226 Neurosphere lines isolated from the brains of mice at em

227 osphorylation patterns, the observation that neurosphere lines maintained their cell line-specific-di

228 anti-proliferative actions in GBM stem-like neurospheres mediated, in part, by interactions between

229 n: more than 80% of the NSCs obtained by the neurosphere method express GD3.

230 r 7 days following a single application with neurosphere method.

231 enotype-specific phosphorylation patterns in neurospheres mimicked those seen in mice, validating use

232 This neurosphere model might provide the basis of a human-bas

233 Using patient-derived mutant IDH1 neurosphere models, we showed that PDH activity was esse

234 Neural progenitor cell viability and neurosphere morphology (neurosphere number, size and cha

235 onditioning also modulated alteration in the neurosphere morphology in response to oxidative stress.

236 logical disorders, on the cell viability and neurosphere morphology of NPCs derived from the perivent

237 cells isolated from Sox1 null embryos formed neurospheres normally, but were specifically deficient i

238 ristics of groups of progenitor cells called neurosphere (NS) cells, including individual cell diamet

239 1 of age, hypothalamic NPCs were cultured as neurospheres (NS) and treated with leptin/insulin.

240 for the detection of spikes recorded from 3D neurospheres (NS) with a very low signal-to-noise ratio.

241 r cell viability and neurosphere morphology (neurosphere number, size and chain migration) were asses

242 that neither mirror nor AgNPs affect on the neurosphere number.

243 ration and neurosphere size while decreasing neurosphere numbers, specially in the cultures that were

244 me, on development of neuronal colonies from neurospheres of HNPCs in the presence of Abeta1-40.

245 high yields of single cells from dissociated neurospheres of mouse KT98 and DC115 cell models (passag

246 Growth as neurospheres or in co-culture with younger cells did not

247 Neurospheres, or neural progenitor and stem cells (NPSCs

248 PCs, namely the chain migration of NPCs from neurospheres, perhaps as a result of its effect on cell

249 latent neural precursor cells when added to neurosphere preparations from sedentary mice.

250 In neurospheres prepared from progenitor cells obtained fro

251 Notably, GL261 neurospheres produced 3.7-fold more TGF-beta per cell co

252 Similarly, the number and size of primary neurospheres produced from the injured SVZ increased app

253 millions of cortical, hippocampal neurons or neurosphere progenitors from each brain.

254 fferences between neuron differentiation and neurosphere proliferation: adhesion dependence and the d

255 elial cells (hBMEC) or NOTCH ligand with GBM neurospheres promoted GBM cell growth and increased CSLC

256 Using a neurosphere recovery assay and xenograft experiments, we

257 ecreased neurosphere formation and inhibited neurosphere recovery.

258 In 3-dimensional co-culture with neurospheres, red fluorescent human LNCaP cells formed a

259 CD24(depleted) cells retained neurosphere regeneration capacity, but following ethanol

260 ation of gliomas from Sulf2(-/-) tumorigenic neurospheres resulted in decreased growth in vivo in mic

261 idative stress increased chain migration and neurosphere size while decreasing neurosphere numbers, s

262 Using both SVZ neurosphere stem cell and parasagittal brain slice cultu

263 embryonic stem cells, neural stem cells and neurosphere stem/progenitor cells.

264 sistant cancer cells as well as glioblastoma neurosphere stemlike cell cultures derived from patients

265 ts, and leads biologically to maintenance of neurosphere stemness in conjunction with FOXM1 and EZH2.

266 human LNCaP cells formed agglomerates on the neurosphere surface.

267 with a lower frequency and produced smaller neurospheres than control cells in vitro, indicating red

268 ltured in serum-free medium form 3-fold more neurospheres than do CD133- cells.

269 cohort yielded significantly lower number of neurospheres than the WKY cohort (by 69+/-7%; p<0.05).

270 cytes, some of which, when cultured, produce neurospheres that differentiate into neurons and glia.

271 We utilized GBM neurospheres that display GSC characteristics and found

272 Neprilysin increased the number of neurospheres that formed colonies of neuron-like cells.

273 ferate late into embryogenesis, can generate neurospheres that passage extensively, and differentiate

274 hat these iMuSCs have the capability to form neurospheres that represent multiple neural phenotypes.

275 lastoma cell lines and patient-derived tumor neurospheres, the E3 ligase is confined to the nucleus a

276 Pten (p53(-/-) Pten(-/-)) as well as tumour neurospheres (TNSs) derived from this model.

277 e-forming capacity, inhibited the ability of neurospheres to form colonies in soft agar and inhibited

278 n in vitro model of neural cell development (neurospheres) to evaluate, through immunocytochemistry,

279 rom postnatal rat brain but >95% of cells in neurospheres treated with the anti-mitotic agent Ara C.

280 xhibits potent efficacy against glioblastoma neurosphere tumor stem-like cells in vitro and in vivo.

281 mice bearing intracranial human glioblastoma neurosphere tumor xenografts.

282 he reduced Notch1 and Hes1 expression in LBW neurosphere, under both basal and stimulated conditions,

283 antation of spinal cord tissue and nonclonal neurospheres, we show that the central spinal cord repre

284 After seven days, the primary neurospheres were counted and their mean number was obta

285 Differentiation capacity of the resulting neurospheres were evaluated in vitro by immunocytochemis

286 Neurospheres were generated from mouse ES cells (ES-NS)

287 th following early CVB3 infection, surviving neurospheres were readily observed and continued to expr

288 Mouse G3 MBs neurospheres were screened against a library of approxim

289 -positive and NG2(+) progenitor cells within neurospheres were shown to preferentially express high l

290 In all, 1.5% of attached cells form neurospheres when transferred to serum-free medium.

291 roliferation of patient-derived glioblastoma neurospheres, whereas a STAT3 inhibitor reversed this ef

292 Here, we demonstrate that cultured murine neurospheres, which comprise neural stem cells and their

293 f function in glioblastoma-derived stem-like neurospheres, whose in vivo growth pattern closely repli

294 Cultures of the SVZ contained 1) neurospheres with a core of Musashi-1-, nestin-, and nuc

295 nsduced neural progenitor cells gave rise to neurospheres with a lower frequency and produced smaller

296 Treatment of cultured embryonic cortical neurospheres with a TLR3 ligand (polyIC) significantly r

297 Transfection of Cx43-null neurospheres with Cx43 mutants revealed that Cx43 carbox

298 cells and glioblastoma stem cell-containing neurospheres with EGFRvIIIAb-IONPs.

299 ons, Kdm5b-depleted adult NSCs migrated from neurospheres with increased velocity.

300 requirement for MCT4 in vitro, we transduced neurospheres with lentiviruses encoding short-hairpin RN

301 n central nervous system stem cells grown as neurospheres with magnetic nanoparticles does not advers