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1 opulation or reduced cell density within the neurosphere.
2 itions for inducing differentiation in human neurospheres.
3 ne, Gpr17, resulted in a decreased number of neurospheres.
4  the male-specific Sry gene, and cultured as neurospheres.
5 ts of forced differentiation in glioblastoma neurospheres.
6 to form pluripotent, long-term self-renewing neurospheres.
7 id not induce neuronal differentiation in WT neurospheres.
8 ly higher in Cx43-null than in WT littermate neurospheres.
9 ease in differentiation in etoposide-treated neurospheres.
10 ion of GABAergic cells derived from passaged neurospheres.
11 mouse models of GBM and in primary human GBM neurospheres.
12 inhibited IGF2-induced growth of GBM-derived neurospheres.
13 for EGF to support the growth of GBM-derived neurospheres.
14 maintained as free-floating undifferentiated neurospheres.
15 ssed by neural progenitors grown as cultured neurospheres.
16 elomerase activity in cultured eNOS(-/-) SVZ neurospheres.
17 cell sorting and can generate multipotential neurospheres.
18 tiation into differentiated embryoid body or neurospheres.
19 lizes flow and microstructures to dissociate neurospheres.
20   Inhibition of OPN blocked the formation of neurospheres, affected the proliferative capacity of tra
21    Average diameters of individual cells and neurospheres after 1 week in culture were similar in mic
22                                        Using neurospheres - aggregate cultures, derived from single s
23                                Incubation of neurospheres alone with rhEPO failed to increase progeni
24                     However, in adult normal neurospheres, alpha(1)-adrenergic receptor stimulation i
25 grafts derived from EphB2-overexpressing GBM neurospheres also showed decreased cellular proliferatio
26 y properties of RA activation in the SVZ; in neurospheres, altered retinoid signaling elicits neither
27                                     In vitro neurosphere and differentiation assays indicate that Bot
28                         Using subventricular neurosphere and matrigel cultures, we demonstrated that
29 potential; and as few as six cells will form neurospheres and 20-30 cells will grow tumor in mice.
30 fied prominin+ lin- cells form self-renewing neurospheres and can differentiate into astrocytes, olig
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 B proliferation in vitro compared to control neurospheres and substantially inhibited G3 MB prolifera
42  ZIKV infection of human organoids and mouse neurospheres and TLR3 inhibition reduced the phenotypic
43 nglioside D3 (GD3) is overexpressed on eight neurospheres and tumor cells; in combination with CD133,
44 in gene expression of patient-derived glioma neurospheres and uncover subpopulations similar to those
45 tion of embryonic and adult NPCs cultured as neurospheres and, in vivo, in the subventricular zone of
46 ir morphology, self-renewal, ability to form neurospheres, and gene expression profiles.
47 aged IDH wild-type glioblastomas, derivative neurospheres, and single-cell gene expression profiles t
48  an exogenous signal but then regroup into a neurosphere as the signal is removed.
49 eration and differentiation both in cultured neurospheres as well as in vivo mouse and fly models of
50 Hh-pathway in TMZ-response on additional GBM neurospheres as well as on GBM patients, by extracting R
51 strating the applicability of this device to neurosphere assay applications.
52 greater differentiation of hair cells in the neurosphere assay showed that Lgr5-positive cells had th
53 istochemistry (IHC), electron microscopy and neurosphere assay the morphology, cytoarchitecture and n
54 f neural progenitor cells measured by single neurosphere assay.
55 nd on forebrain signals not available in the neurosphere assay.
56 ewal, and multipotentiality as assessed by a neurosphere assay.
57 Neural precursor responses were evaluated by neurosphere assays as well as by stereological analyses.
58                         In vitro NPC-derived neurosphere assays showed that Tat-containing conditione
59 ar movement in cortical slice assays, and in neurosphere assays, the percentage of migrating neurons
60 his study explores the use of a simple human neurosphere-based in vitro model to characterise the pha
61 ma cells and glioma-initiating cell-enriched neurospheres both in vitro and in vivo, and we show that
62              Pre-GEPCOT cells could not form neurospheres but expressed the stem cell markers Slc1a3-
63 ells had the ability to proliferate and form neurospheres but had an impaired response to mitogen sti
64 plantation of a clonally derived spinal cord neurosphere can result in reconstitution of all examined
65                                        Adult neurospheres can be collected in 1 week as a source of n
66 from the murine spinal cord and organized as neurospheres, can be triggered to migrate out in respons
67              EphB2 expression stimulated GBM neurosphere cell migration and invasion, and inhibited n
68 e cell migration and invasion, and inhibited neurosphere cell proliferation in vitro.
69 characteristics of neurosphere formation and neurosphere cell self-renewal.
70 ion with this, we confirmed that both normal neurosphere cells and ENU-im-mortalized subventricular z
71 rtib exerted similar effects on glioblastoma neurosphere cells in vivo and resulted in markedly reduc
72      Moreover, alisertib caused glioblastoma neurosphere cells to partially differentiate and enter s
73                            Many glioblastoma neurosphere cells treated with alisertib for short perio
74 se in PrP(Sc) levels with time in the Tg4053 neurosphere cells, whereas the level of PrP(Sc) decayed
75 e and cell migration in EphB2-expressing GBM neurosphere cells.
76 neurons through the formation of multipotent neurosphere clones.
77 -deficient embryos formed greater numbers of neurospheres compared with neurospheres from wild-type e
78 ote that an intact tumor microenvironment or neurosphere conditions in vitro are required for Gli act
79                                  The percent neurospheres containing differentiated neurons and the n
80                                              Neurospheres continued to generate differentiated progen
81 radial glial morphology) expressed YFP; YFP+ neurospheres could be generated in vitro after recombina
82 nol in a fetal mouse cerebral cortex-derived neurosphere culture model.
83 nsequences for DIPG self-renewal capacity in neurosphere culture.
84 eshly isolated human glioblastoma multiforme neurosphere cultures (containing "stem cell-like cells")
85                             When GBM-derived neurosphere cultures are grown in 1% oxygen, hypoxia-ind
86 micked those seen in mice, validating use of neurosphere cultures as models for studying tau phosphor
87 binant murine TIMP-1 (rmTIMP-1) to TIMP-1 KO neurosphere cultures evoked a dose-dependent increase in
88 ry and qRT-PCR to screen fetal mouse-derived neurosphere cultures for ethanol-sensitive neural stem c
89 e central nervous system (CNS) SC-containing neurosphere cultures for studying heritable neurodegener
90                                  We produced neurosphere cultures from FVB/NCr (FVB) mice, from trans
91 table neurodegenerative disease, we compared neurosphere cultures from transgenic mice that express h
92 iments on bulk GBM cell line cultures and on neurosphere cultures of a human-origin GBM xenograft tum
93                                           In neurosphere cultures prepared from the SVZ of adult mice
94                                   Studies of neurosphere cultures prepared from the telencephalon at
95                         In vitro analysis of neurosphere cultures revealed that proliferation of Id4-
96 ansient exposure of embryonic day 14.5 mouse neurosphere cultures to dexamethasone (DEX) limits proli
97                        The susceptibility of neurosphere cultures to prions mirrored that of the mice
98                                              Neurosphere cultures treated with gamma-secretase inhibi
99                                        GL261 neurosphere cultures were used to evaluate GIC.
100 sic fibroblast growth factor (bFGF)-expanded neurosphere cultures with the EGF-like domain of neuregu
101 on is markedly reduced in human GBM samples, neurosphere cultures, and cell lines and its reconstitut
102 netically engineered mice and derivative NSC neurosphere cultures, we show that this brain region-spe
103   By using a conditional deletion system and neurosphere cultures, we showed that FoxM1 is important
104 th factor (EGF)-induced proliferation within neurosphere cultures.
105 ce impairs neuronal cell proliferation using neurosphere cultures.
106  contrast, ZSCAN21 silencing reduced SNCA in neurosphere cultures.
107 nditioned media obtained from primary glioma neurosphere cultures.
108  of differentiation in CNS progenitor cells (neurosphere) cultures from TIMP-1 KO mice revealed a spe
109 sion levels in undifferentiated, SVZ-derived neurospheres decline markedly with differentiation.
110 ties (80-85%) and the ability to regrow into neurospheres, demonstrating the applicability of this de
111 A activation in similar cells in SVZ-derived neurospheres depends on retinoid synthesis from the prem
112                                    Moreover, neurospheres derived from animals with Copb2 variants gr
113  These changes can be preserved in vitro, as neurospheres derived from Gdf11(-/-) and wild-type litte
114 hat relatively mature neurons generated from neurospheres derived from postnatal subependymal zone or
115                                              Neurospheres derived from raptor-deficient brains are sm
116 logy, the degree of neuronal maturation from neurospheres derived from wild-type (WT) and Cx43-null m
117 this, LY364947 treatment in irradiated GL261 neurosphere-derived cells decreased DNA damage responses
118      However, when ectopically transplanted, neurosphere-derived cells from either region are largely
119 investigate cell cycle dynamics in olfactory neurosphere-derived cells from nine male schizophrenia p
120                                    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 e of the B2BkR antagonist HOE-140 during rat neurosphere differentiation, neuron-specific beta3-tubul
127   The Met(high) subpopulation within Met-pos neurospheres displayed clonogenic potential and long-ter
128                Met-positive and Met-negative neurospheres displayed distinct growth factor requiremen
129 ment of variant allele frequencies (VAFs) in neurospheres displaying contrasting phenotypes of sustai
130  tool for a wide range of applications where neurosphere dissociation is needed.
131    We show that this microfluidic-chip-based neurosphere-dissociation method can generate high yields
132 enitor cells in vivo, yet in vitro generated neurospheres, divided in response to bFGF (basic fibrobl
133 tivated and functional in glioblastoma (GBM) neurospheres enriched for glioblastoma tumor-initiating
134                          CD133+ve cells form neurospheres, exhibit self-renewal and differentiation,
135 esting a loss of neurogenic potential in rat neurospheres expanded in vitro.
136                 Here we report that cultured neurospheres expressing cellular prion protein (PrP(C))
137 sion of the MET oncogene was associated with neurospheres expressing the gene signature of mesenchyma
138        Met expression was almost absent from neurospheres expressing the signature of the classical s
139 evidence that TRBP is required for efficient neurosphere formation and for the expression of neural s
140 38 significantly reduced the cell viability, neurosphere formation and induced apoptosis of GSCs with
141   We show that TMZ + GSI treatment decreased neurosphere formation and inhibited neurosphere recovery
142 t to induce the stem cell characteristics of neurosphere formation and neurosphere cell self-renewal.
143 qualities of primary GBM cultures, including neurosphere formation and the expression of stem cell ma
144                                              Neurosphere formation assays showed that adult auditory
145                         IR decreased primary neurosphere formation by 28%, but did not reduce seconda
146 y neurosphere formation by 75% and secondary neurosphere formation by 68%.
147 364947 treatment before IR decreased primary neurosphere formation by 75% and secondary neurosphere f
148 ut not control IgG, dramatically reduced the neurosphere formation frequency in mice that had exercis
149 Cs decreased proliferation rates and reduced neurosphere formation in culture.
150  activity and blocked cell proliferation and neurosphere formation in cultures of glioma stem cells,
151 layed an enhanced capacity for self-renewing neurosphere formation in response to Wnt and were conver
152 duced proliferating (BrdU-labeled) cells and neurosphere formation in wild type but not TLR3(-/-)-der
153                                              Neurosphere formation is commonly used as a surrogate fo
154 equence of vascular regression, since YFP(+) neurosphere formation over serial passage was unaffected
155 k attenuated stem cell marker expression and neurosphere formation while having minimal effects on tu
156 t by analyzing cell viability via MTT assay, neurosphere formation, and endoplasmic reticulum stress/
157 on of miR-124 and knockdown of SNAI2 reduced neurosphere formation, CD133(+) cell subpopulation, and
158  in CD133(+) glioma cells potently disrupted neurosphere formation, induced apoptosis, and inhibited
159 ved from eNOS-/- mice restored the decreased neurosphere formation, proliferation, neurite outgrowth,
160                    In addition, cultured SVZ neurosphere formation, proliferation, telomerase activit
161  increasing cell proliferation and stem cell neurosphere formation, with its ectopic overexpression s
162 rmation by 28%, but did not reduce secondary neurosphere formation.
163 ndently increased the number and size of new neurosphere formation.
164 glioblastoma cells and GSCs and promoted GSC neurosphere formation.
165 nd that these cells have high propensity for neurosphere formation.
166 tures, TMZ treatment significantly decreases neurosphere formation; however, a small percentage of ce
167 e retinal integration and differentiation of neurospheres formed by stem cells and mouse neural proge
168  development were also supported by a higher neurosphere forming ability at E11 than at E15.
169                                              Neurosphere forming cells (NSFCs) have been established
170          RA treatment dramatically decreased neurosphere-forming capacity, inhibited the ability of n
171 47 had no effect on the primary or secondary neurosphere-forming capacity.
172 at allows the purification to homogeneity of neurosphere-forming neural precursors from the adult mou
173 uorescence-activated cell sorting to isolate neurosphere-forming neural stem cells (NSCs) from embryo
174      Importantly, these cells constitute the neurosphere-forming population among SVZ astrocytes.
175  population, which comprises the majority of neurosphere-forming precursors, there are two distinct s
176  show that Shh regulates the self-renewal of neurosphere-forming stem cells and that it modulates pro
177 l glia in the GEs where ActN1 increases FGF2 neurosphere frequency, but not in the septum where it do
178                                Production of neurospheres from auditory nerve cells was stimulated by
179 nockdown diminishes) the ability to generate neurospheres from MNPs, indicating a function in self-re
180                               Using cultured neurospheres from PPT1-KO and wild-type mouse fetuses, w
181 compared FTD-hallmark tau phosphorylation in neurospheres from rTg(tau(P301L))4510 mice and from rTg(
182 pon differentiation, more than twice as many neurospheres from the damaged brain were tripotential, s
183 h the Notch intracellular domain rescued GBM neurospheres from the RA-induced differentiation and ste
184 reater numbers of neurospheres compared with neurospheres from wild-type embryos.
185 ntiated cells (GBMDC) grown in serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro.
186                  Consistently, the mutant DG neurospheres generated fewer NSCs with defects in prolif
187                              We transplanted neurospheres generated from fetal and postnatal intestin
188  cells represent <2% of the cells present in neurospheres generated from postnatal rat brain but >95%
189 l interfering RNA increased the number of WT neurospheres generating differentiated neurons.
190  phenotype defined by glioblastoma invasion, neurosphere growth, and endothelial tube formation was m
191                       In vitro IL-6 enhanced neurosphere growth, self-renewal, and tripotentiality an
192 led that rats transplanted with CNTF-treated neurospheres had a 22% greater striatal volume on the le
193 vely isolated, human CNS stem cells grown as neurospheres (hCNS-SCns) survive, migrate, and express d
194 ted TMZ-sensitization of a TMZ non-responder neurosphere in vitro by treating them with the FDA-appro
195 en fluorescent protein (GFP) and cultured as neurospheres in FGF2-containing medium.
196           GBM-SCs were grown as non-adherent neurospheres in growth factor supplemented serum-free me
197 k genes important in hypoxia, we treated GBM neurospheres in hypoxia and identified monocarboxylate t
198                                 They grew as neurospheres in serum-free medium with epidermal growth
199 adherent in serum-containing media and forms neurospheres in supplemented serum-free media was develo
200 oliferation of NPCs was further found in SVZ neurospheres in tissue culture.
201 but not proliferation or differentiation, in neurospheres in vitro and in newly born SGZ cells in viv
202 ne in three EGFR(+) astrocytes gives rise to neurospheres in vitro, a 20-fold enrichment over unsorte
203  forebrain in vivo, and in adult multipotent neurospheres in vitro, derived from progenitors that exp
204    Using enteric neurons differentiated from neurospheres in vitro, we show that enteric axon growth
205 age of CD44+ cells in glioblastoma multiform neurospheres in vitro.
206  serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro.
207 apitulated all of these findings in cultured neurospheres, in which overexpression and depletion of B
208  each gene in LGE or MGE cells propagated as neurospheres, indicating that these newly identified mol
209                                              Neurospheres infected with lentiviral vectors expressing
210  (NSC) function but the relationship between neurosphere-initiating cells (NICs) and NSCs remains unc
211 The effect of sera on differentiation of NPC neurospheres into neuronal colonies was tested in 72-h-l
212      Obtaining single dissociated cells from neurospheres is difficult using nonenzymatic methods.
213 neurons in 1 d differentiated FMRP-deficient neurospheres is normalized.
214 ation were altered during differentiation of neurospheres isolated from B2BkR knock-out mice.
215                                     Neonatal neurospheres isolated from normal mice expressed a mixtu
216                       Under these conditions neurosphere-like bodies (NLB) developed.
217 tative PCR analysis showed that treatment of neurosphere-like ReN cell aggregate cultures with gamma-
218 ensitive in vitro bioassay for mouse prions; neurosphere lines from other Tg mice overexpressing PrP
219                                              Neurosphere lines from Tg4053 mice provide a sensitive i
220 lf-renewal potential of several glioblastoma neurosphere lines in vitro, and this activity was furthe
221                                              Neurosphere lines isolated from the brains of mice at em
222 osphorylation patterns, the observation that neurosphere lines maintained their cell line-specific-di
223  anti-proliferative actions in GBM stem-like neurospheres mediated, in part, by interactions between
224  not observed in mature hematopoietic cells, neurospheres, mesenchymal stem cells, or hepatocytes.
225 n: more than 80% of the NSCs obtained by the neurosphere method express GD3.
226 r 7 days following a single application with neurosphere method.
227 enotype-specific phosphorylation patterns in neurospheres mimicked those seen in mice, validating use
228                                         This neurosphere model might provide the basis of a human-bas
229            Using patient-derived mutant IDH1 neurosphere models, we showed that PDH activity was esse
230         Neural progenitor cell viability and neurosphere morphology (neurosphere number, size and cha
231 onditioning also modulated alteration in the neurosphere morphology in response to oxidative stress.
232 logical disorders, on the cell viability and neurosphere morphology of NPCs derived from the perivent
233 cells isolated from Sox1 null embryos formed neurospheres normally, but were specifically deficient i
234 ristics of groups of progenitor cells called neurosphere (NS) cells, including individual cell diamet
235 1 of age, hypothalamic NPCs were cultured as neurospheres (NS) and treated with leptin/insulin.
236 for the detection of spikes recorded from 3D neurospheres (NS) with a very low signal-to-noise ratio.
237 lls emerged in primary cultures, they formed neurospheres (NSFCs).
238 r cell viability and neurosphere morphology (neurosphere number, size and chain migration) were asses
239 ration and neurosphere size while decreasing neurosphere numbers, specially in the cultures that were
240 me, on development of neuronal colonies from neurospheres of HNPCs in the presence of Abeta1-40.
241 high yields of single cells from dissociated neurospheres of mouse KT98 and DC115 cell models (passag
242                                    Growth as neurospheres or in co-culture with younger cells did not
243                                              Neurospheres, or neural progenitor and stem cells (NPSCs
244 ith those receiving transplants of untreated neurospheres (P = 0.0003) and a 26% greater striatal vol
245 PCs, namely the chain migration of NPCs from neurospheres, perhaps as a result of its effect on cell
246                  These tumor stem cells form neurospheres, possess the capacity for self-renewal, exp
247  latent neural precursor cells when added to neurosphere preparations from sedentary mice.
248                                           In neurospheres prepared from progenitor cells obtained fro
249                               Notably, GL261 neurospheres produced 3.7-fold more TGF-beta per cell co
250    Similarly, the number and size of primary neurospheres produced from the injured SVZ increased app
251 millions of cortical, hippocampal neurons or neurosphere progenitors from each brain.
252 uld replace the need for ligand in promoting neurosphere proliferation.
253 fferences between neuron differentiation and neurosphere proliferation: adhesion dependence and the d
254 elial cells (hBMEC) or NOTCH ligand with GBM neurospheres promoted GBM cell growth and increased CSLC
255                     GM1 loading of wild-type neurospheres recapitulated the phenotype of beta-gal-/-
256                                      Using a neurosphere recovery assay and xenograft experiments, we
257 ecreased neurosphere formation and inhibited neurosphere recovery.
258                CD24(depleted) cells retained neurosphere regeneration capacity, but following ethanol
259 ation of gliomas from Sulf2(-/-) tumorigenic neurospheres resulted in decreased growth in vivo in mic
260 idative stress increased chain migration and neurosphere size while decreasing neurosphere numbers, s
261                               Using both SVZ neurosphere stem cell and parasagittal brain slice cultu
262  embryonic stem cells, neural stem cells and neurosphere stem/progenitor cells.
263 sistant cancer cells as well as glioblastoma neurosphere stemlike cell cultures derived from patients
264  Thus, transplanted human CNS (hCNS)-derived neurospheres survived robustly in naive and ischemic bra
265                                 Transplanted neurospheres survived robustly in naive and ischemic bra
266 tely 1,400-fold more efficient in generating neurospheres than are GFP-negative cells and, despite th
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 eir small number, give rise to 70 times more neurospheres than does the GFP-negative population.
270 cohort yielded significantly lower number of neurospheres than the WKY cohort (by 69+/-7%; p<0.05).
271 cytes, some of which, when cultured, produce neurospheres that differentiate into neurons and glia.
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                                              Neurospheres were generated from mouse ES cells (ES-NS)
285                                              Neurospheres were injected into the ipsilateral striatum
286 th following early CVB3 infection, surviving neurospheres were readily observed and continued to expr
287                                 Mouse G3 MBs neurospheres were screened against a library of approxim
288 -positive and NG2(+) progenitor cells within neurospheres were shown to preferentially express high l
289          In all, 1.5% of attached cells form neurospheres when transferred to serum-free medium.
290 roliferation of patient-derived glioblastoma neurospheres, whereas a STAT3 inhibitor reversed this ef
291    Here, we demonstrate that cultured murine neurospheres, which comprise neural stem cells and their
292 f function in glioblastoma-derived stem-like neurospheres, whose in vivo growth pattern closely repli
293             Cultures of the SVZ contained 1) neurospheres with a core of Musashi-1-, nestin-, and nuc
294 nsduced neural progenitor cells gave rise to neurospheres with a lower frequency and produced smaller
295     Treatment of cultured embryonic cortical neurospheres with a TLR3 ligand (polyIC) significantly r
296                    Transfection of Cx43-null neurospheres with Cx43 mutants revealed that Cx43 carbox
297  cells and glioblastoma stem cell-containing neurospheres with EGFRvIIIAb-IONPs.
298 ons, Kdm5b-depleted adult NSCs migrated from neurospheres with increased velocity.
299 requirement for MCT4 in vitro, we transduced neurospheres with lentiviruses encoding short-hairpin RN
300 n central nervous system stem cells grown as neurospheres with magnetic nanoparticles does not advers

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