ライフサイエンスコーパス: NPC

1 NPC Neurological Severity Scores (NNSS) were used to com

2 NPCs are built from multiple copies of ~30 different nuc

3 NPCs have been shown to have tissue-specific composition

4 e in southern China and de novo assembled 18 NPC biopsy specimen-derived EBV (NPC-EBV) genomes, desig

5 In this study, we collected 18 NPC biopsy specimens from the Hunan Province in southern

6 igher rate than younger (embryonic day 13.5) NPCs do.

7 apalpha.Kapbeta1 by RanGTP further abrogates NPC barrier function, whereas adding back Kapbeta1 rescu

8 hese results show that Tat adversely affects NPCs and neurogenesis through Notch signaling and point

9 Phylogenetic analysis revealed that all NPC-EBV genomes were distinct from other EBV genomes.

10 o daughter nuclei by linking mitotic DNA and NPC segregation via the mitotic specific chromatin assoc

11 hat HOPX mRNA levels are reduced in OSCC and NPC cell lines and tissues and there is a general reduct

12 is directly coupled to NLS-cargo release and NPC barrier function.

13 ted the association between the two SNPs and NPC risk in 733 patients and 895 controls from a high in

14 static signaling between the vasculature and NPCs, and loss of this function results in escalated Veg

15 ed that nuclear 26S proteasomes crowd around NPCs.

16 o multiple scaffold Nups in vitro and act as NPC-targeting determinants in vivo.

17 rimary mouse and human fetal NPCs as well as NPCs derived from human induced pluripotent stem cells (

18 s, but not during interphase when Gle1 is at NPCs.

19 Proliferation was higher in BERKO NPCs and was inhibited by LY3201.

20 YY1-mediated interactions between NPC regulatory elements are often nested within constitu

21 at the base of looping interactions between NPC-specific genes and enhancers.

22 tion, we provided an artificial link between NPCs and chromatin via Nup133 and histone H1.

23 tin-associated Nup2 might function to bridge NPCs with chromatin during segregation, we provided an a

24 es in man-made molecular filters inspired by NPCs, and their applications in nanotechnology.

25 rough a hindbrain germinal zone populated by NPCs whose peak mitotic activity follows a surge in SVP

26 Niemann-Pick type C (NPC) disease is a fatal neurodegenerative disorder cause

27 orage disorders such as Niemann-Pick type C (NPC) disease, where defects in the endosomal-lysosomal p

28 Niemann-Pick disease type C (NPC) is associated with mutations in NPC1 and NPC2, whos

29 teins revealed that the Niemann-Pick type C (NPC) proteins, which are involved in cholesterol export

30 osomal storage disorder Niemann-Pick type C (NPC), where a defect in intracellular cholesterol transp

31 Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized

32 Nasopharyngeal carcinoma (NPC) is an invasive cancer with particularly high incide

33 cancer.IMPORTANCE Nasopharyngeal carcinoma (NPC) is highly associated with Epstein-Barr virus (EBV)

34 (N) categories and nasopharyngeal carcinoma (NPC) N categories.

35 ment for recurrent nasopharyngeal carcinoma (NPC) remains a clinical dilemma, immunotherapy targeting

36 PIN1 promoter and nasopharyngeal carcinoma (NPC) risk with a small sample size in a low incidence ar

37 ese and Indonesian nasopharyngeal carcinoma (NPC) samples.

38 B-cell lymphomas, nasopharyngeal carcinoma (NPC), and lymphomas that develop in organ transplant rec

39 infection, such as nasopharyngeal carcinoma (NPC), and oral hairy leukoplakia (OHL) lesions that have

40 atients, including nasopharyngeal carcinoma (NPC), breast cancer and hepatocellular carcinoma, and co

41 n cancers, such as nasopharyngeal carcinoma (NPC), Hodgkin's disease, and gastric carcinoma.

42 tory sensory input to neural precursor cell (NPC) turnover in the SVZ but it was not addressed if a r

43 We demonstrate that neural precursor cell (NPC):glioma cell communication underpins this propensity

44 Neural progenitor cell (NPC) culture within three-dimensional (3D) hydrogels is

45 ether disturbance of neural progenitor cell (NPC) differentiation into the oligodendrocyte lineage (O

46 determine whether a neural progenitor cell (NPC) reenters the cell cycle or exits and differentiates

47 (2017) identified a neural progenitor cell (NPC)-specific RNA binding protein that may underlie the

48 of individual human neural precursor cells (NPC) into mature neurons are currently not fully underst

49 ntribution of resident nonparenchymal cells (NPCs) is also evident.

50 oid bodies (EBs) and neural precursor cells (NPCs) during development.

51 nsplantation of neural stem/precursor cells (NPCs) in mice with experimental autoimmune encephalomyel

52 n is restricted to neuronal precursor cells (NPCs) in the human brain.

53 R-19 is enriched in neural progenitor cells (NPCs) and downregulated during neuronal development in t

54 otocol to generate nephron progenitor cells (NPCs) and kidney organoids to facilitate applications fo

55 oth human and mouse neural progenitor cells (NPCs) and led to more severe microcephaly in the mouse f

56 ipotent stem cells, neural progenitor cells (NPCs) and neurons from ASD individuals with early brain

57 eased cell death in neural progenitor cells (NPCs) and neurons.

58 tem cells (ESCs) to neural progenitor cells (NPCs) and recruits the Mediator subunit Med26.

59 of the expansion of neural progenitor cells (NPCs) and their differentiation into neurons is crucial

60 ts HIV infection of neural progenitor cells (NPCs) by a mechanism encompassing NFkappaB/SP1-mediated

61 ent of synapses and neural progenitor cells (NPCs) by microglia is critical for the development and m

62 the HD-iPSC-derived neural progenitor cells (NPCs) demonstrated lower levels of proteasome activity a

63 m cells (iPSCs) and neural progenitor cells (NPCs) derived from individuals with heterozygous 15q13.3

64 The fate of neural progenitor cells (NPCs) during corticogenesis is determined by a complex i

65 Transit-amplifying nephron progenitor cells (NPCs) generate all of the nephrons of the mammalian kidn

66 s a stroke, trigger neural progenitor cells (NPCs) proliferation and migration toward the damaged sit

67 Nephron progenitor cells (NPCs) show an age-dependent capacity to balance self-ren

68 (iPS) cell-derived neural progenitor cells (NPCs) to repair the FTD-associated N279K MAPT mutation.

69 of cultured murine neural progenitor cells (NPCs), which are multipotent stem cells that give rise t

70 multipotent primary neural progenitor cells (NPCs).

71 sport, recent research suggests that certain NPC proteins have additionally acquired the role of affe

72 odel of Parkinson's disease (PD), cografting NPCs with midbrain-derived astrocytes engineered to over

73 e developed a neuropathological comorbidity (NPC) score and compared it to CDR, IQCODE, and NPI score

74 response elements: the nuclear pore complex (NPC) and acyl-CoA dehydrogenase family member-10 (ACAD10

75 However, how nuclear pore complex (NPC) barrier selectivity, Kap traffic, and NLS-cargo rel

76 e key component of the nuclear pore complex (NPC) controlling permeability, selectivity, and the spee

77 The nuclear pore complex (NPC) controls the transport of macromolecules between th

78 g of the capsid to the nuclear pore complex (NPC) is mediated by the capsid protein pUL25 and the cap

79 The nuclear pore complex (NPC) is the principal gateway for molecular exchange bet

80 g model poses that the nuclear pore complex (NPC) is the sole gatekeeper for transit of cellular mate

81 The nuclear pore complex (NPC) mediates nucleocytoplasmic transport through the nu

82 3 ligase Siz2, and the nuclear pore complex (NPC) protein Nup170-physically and functionally interact

83 ans mitosis peripheral nuclear pore complex (NPC) proteins (Nups) disperse from the core NPC structur

84 The nuclear pore complex (NPC) selectively gates the transport of macromolecules b

85 interactions with the nuclear pore complex (NPC), followed by translocation to the nucleus and prefe

86 l, is exclusive to the nuclear pore complex (NPC).

87 tial components of the nuclear pore complex (NPC).

88 oteins (Nups) within nuclear pore complexes (NPC).

89 ranslocation through nuclear pore complexes (NPCs) and retention on nuclear partners.

90 Nuclear pore complexes (NPCs) are approximately 100 MDa transport channels assem

91 Nuclear pore complexes (NPCs) are multiprotein channels connecting the nucleus w

92 meability barrier of nuclear pore complexes (NPCs) controls bulk nucleocytoplasmic exchange.

93 Transport through nuclear pore complexes (NPCs) during interphase is facilitated by the nucleopori

94 ar diffusion through nuclear pore complexes (NPCs) is thought to decrease dramatically beyond a 30-60

95 tightly regulated by nuclear pore complexes (NPCs) made up of nucleoporins (NUPs).

96 biomachines known as nuclear pore complexes (NPCs).

97 f-assembly of nucleobase-peptide conjugates (NPCs), where achiral nucleobases are helically displayed

98 (NPC) proteins (Nups) disperse from the core NPC structure.

99 ion suggesting that the sealing of defective NPCs and nuclear envelope ruptures could proceed through

100 rane seals have been observed over defective NPCs; deletion of CHM7 in these strains leads to a loss

101 At low densities, NPCs moved randomly in an amoeba-like fashion.

102 ASD-derived NPCs display increased cell proliferation because of dys

103 y highlights the utility of iPS cell-derived NPCs to elucidate the role of astrocytes in the pathogen

104 n of RTK and p53 signalling in hiPSC-derived NPCs (iNPCs) recapitulates GTIC properties in vitro.

105 We generated and characterized iPSC derived NPCs and neurons from three SPG11 patients and two age-m

106 The self-assembly of rationally designed NPCs into nanohelices is a promising way to engineer com

107 Niemann-Pick Type C disease (NPC) is a rare metabolic disorder characterized by disru

108 ersies and suggest how molecularly divergent NPCs in different species can perform essentially the sa

109 ted in both 15q13.3 deletion and duplication NPCs.

110 for by both somatic and viral events during NPC pathogenesis.

111 ssembled 18 NPC biopsy specimen-derived EBV (NPC-EBV) genomes, designated HN1 to HN18.

112 clonogenicity, thus depleting the embryonic NPC pool and limiting cortical expansion.

113 certain molecular elements of the endogenous NPC.

114 To enhance NPC migration, we generated a cell-permeable wild-type p

115 m expansion of primary mouse and human fetal NPCs as well as NPCs derived from human induced pluripot

116 are no FDA approved treatments available for NPC patients.

117 mplicates the importance of this complex for NPC binding and genome release.

118 tions, and that the approaches developed for NPC studies are extendable to additional complex systems

119 d inactivating CYLD mutations as drivers for NPC cell growth.

120 e FG Nups are necessary but insufficient for NPC barrier function.

121 ab1/CSN5 can serve as prognostic markers for NPC recurrence; this, in turn, may provide a promising t

122 ach, we bypassed the requirement of Nup2 for NPC segregation.

123 e findings demonstrate a pathogenic role for NPC:glioma interactions and potential therapeutic target

124 a critical role in releasing viral DNA from NPC-bound capsids.IMPORTANCE Herpes simplex virus 1 (HSV

125 Kidney organoids were generated from NPCs within 12 d with high reproducibility using 96-well

126 ective at releasing standalone Kapbeta1 from NPCs.

127 ytic differentiation was not impaired in FTD NPCs derived from one patient carrying the N279K MAPT mu

128 overexpression of FOXO4 but not FOXO1 in HD NPCs dramatically enhanced proteasome activity.

129 Similar to HD NPCs, HD-iPSC-derived neurons showed reduced proteasome

130 When HD NPCs were further differentiated into DARPP32-positive n

131 NFT deposition, vascular lesions, and high NPC scorewere associated with cognitive impairment in a

132 associated Nup complex is distinct from holo-NPCs and that it plays a role in subtelomeric chromatin

133 However, NPCs at high density elongated and aligned their shapes

134 In HSC-NPC co-culture, ConA-induced expression of inflammatory

135 Mouse and human NPCs were infected with EcoHIV (modified HIV virus infec

136 eased HIV production in both mouse and human NPCs.

137 found abnormal expression of miR-19 in human NPCs generated from schizophrenic patient-derived induce

138 l adaption makes ZIKV more virulent to human NPCs, thus contributing to the increased incidence of mi

139 q) of developing neurons to dissect/identify NPC subtypes and critical developmental stages of altern

140 that the injection of this material impacts NPCs proliferation and migration at the subventricular z

141 er (DAPT) significantly rescued Tat-impaired NPC differentiation in vitro and neurogenesis in vivo To

142 Importantly, NPC-derived daughter cells appeared to be latently infec

143 1/CSN5 phenocopied the function of miR-24 in NPC cells after ionizing radiation treatment, resulting

144 ed in a manner opposite to that of miR-24 in NPC tumorigenesis and radioresistance.

145 ie modulation of cancer stem cells (CSCs) in NPC remain unclear.

146 Upon isolation and culture in NPC renewal medium, younger NPCs displayed a higher glyc

147 on contributes to cerebellar degeneration in NPC disease.

148 potential treatments for visceral disease in NPC patients.

149 ts were highly and specifically expressed in NPC and functionally promoted NPC malignant phenotypes.

150 ndicate that GSK3beta is a crucial kinase in NPC physiology and suggest that this molecule plays a ke

151 ial NPC therapeutic by extending lifetime in NPC mice, delaying neurodegeneration, and decreasing vis

152 ociated oncogenic transcriptional network in NPC, which can be exploited for the development of more

153 sequestration in LEs similar to that seen in NPC- and LAMP-deficient cells, we show that the restrict

154 ne niche and results, for the first time, in NPC migration into the stroke site.

155 in, and causes more pronounced cell death in NPCs and neurons, resulting in more severe neuronal loss

156 ontrolled expression of transgenic Dmrta2 in NPCs suppresses differentiation without affecting their

157 parison with MEX1-44, MR-766 grows faster in NPCs and in the developing brain, and causes more pronou

158 small number of CTCF sites arise de novo in NPCs.

159 Conversely, CTCF binding sites in NPCs are largely preexisting in pluripotent stem cells.

160 which Jab1/Csn5 expression is upregulated in NPCs has yet to be determined.

161 R-24 inhibits NPC tumor growth and increases NPC radiosensitivity by directly regulating Jab1/CSN5 an

162 ith Abeta accumulation while also increasing NPC proliferation.

163 sed neuronal differentiation of HIV-infected NPCs in both in vitro and in vivo settings.

164 ology, we show that Atlastins also influence NPC biogenesis and timely exit of secretory cargo from t

165 , our findings indicate that miR-24 inhibits NPC tumor growth and increases NPC radiosensitivity by d

166 es and embedded macromolecules within intact NPCs.

167 structural analysis revealed that interphase NPC assembly proceeds by an asymmetric inside-out extrus

168 ecifically disrupts interactions between key NPC enhancers and their target genes.

169 H1A3 expression and activity in Khdrbs1(-/-) NPCs results in reduced glycolysis and clonogenicity, th

170 s precocious neurogenesis in Dmrta2 knockout NPCs.

171 vely unfolded GLFG repeats as Velcro to link NPC subcomplexes and thus add a new layer of connections

172 ruption of TH action in human and mouse (h,m)NPCs.

173 mrt5) plays an important role in maintaining NPCs in the cell cycle.

174 at A. nidulans cells ensure accurate mitotic NPC segregation to daughter nuclei by linking mitotic DN

175 terestingly, the role of Nup2 during mitotic NPC segregation is independent of its importin alpha- an

176 we report that Nup2 is required for mitotic NPC inheritance in A. nidulans Interestingly, the role o

177 upports the self-renewing potential of mouse NPCs.

178 hanisms underlying this regulation in murine NPCs.

179 engrafted neural stem/progenitor cells (NSC/NPCs).

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

181 on of EBV infection to the aggressiveness of NPC are discussed in this review.

182 V LTR and with the subsequent alterations of NPC neurogenesis.

183 Herein, we review biophysical aspects of NPC architecture and function and cover recent progress

184 Accordingly, some aspects of NPC function have been recapitulated in artificial nanoc

185 tions in the field and biomedical aspects of NPC transport.

186 The centerpiece of NPC transport is the assembly of intrinsically disordere

187 tiation of Th cells, decreased in the CNS of NPC-treated mice, consequently inhibiting the induction

188 is a pivotal, cell-intrinsic determinant of NPC fate, with a high glycolytic flux supporting self-re

189 degeneration is the main clinical feature of NPC disease, and FTY720 accumulates in the CNS and has s

190 and degradability affect the maintenance of NPC stemness in the absence of differentiation factors.

191 ated with, and necessary for, maintenance of NPC stemness.

192 resent previously unrecognized mechanisms of NPC pathogenesis.

193 The pathogenic mechanisms of NPC, particularly those involving epigenetic dysregulati

194 dentify TGF-beta2 as the crucial mediator of NPC immunomodulation.

195 study identifies Sam68 as a key regulator of NPC self-renewal and establishes a novel link between mo

196 nstrated its role in intrinsic resistance of NPC cells to treatment with cisplatin.

197 However, the physiological roles of NPC composition changes and their impacts on cellular pr

198 The scarcity of NPC genomic data hinders the understanding of NPC biolog

199 n the cerebellum at presymptomatic stages of NPC disease represent previously unrecognized mechanisms

200 f NPC1-deficient mice at different stages of NPC disease.

201 Here we review the current status of NPC research with a focus on the functional implications

202 in the NPC scaffold needed for late steps of NPC assembly.

203 ly interact with one another and a subset of NPC components (nucleoporins or Nups).

204 o) predict RV genotype-specific targeting of NPC pathways and cargos.

205 PC genomic data hinders the understanding of NPC biology, disease progression and rational therapy de

206 ey mechanism underlying the vulnerability of NPC cells to THZ1 treatment.

207 ng in high-efficiency production (80-90%) of NPCs from hPSCs within 9 d of differentiation.

208 is approach, the supramolecular chirality of NPCs can be adaptively imparted to metallic nanoparticle

209 ying Smek/Mbd3/NuRD axis-mediated control of NPCs' self-renewal and neuronal differentiation during m

210 The structural details of NPCs vary across species, with many of their constituent

211 Therefore, we quantified differentiation of NPCs into O4(+) cells and measured their maturation via

212 ficantly blocked neuronal differentiation of NPCs, and Mbd3 depletion rescued neurogenesis defects se

213 self-renewal and neuronal differentiation of NPCs.

214 ependent synaptic pruning and elimination of NPCs.

215 cates that METH increases HIV infectivity of NPCs, through the NFkappaB/SP1-dependent activation of t

216 on of Hes1 expression and the maintenance of NPCs during cortical development.

217 differentiation into postmitotic neurons of NPCs derived from embryonic stem cells and in Emx1-cre c

218 a/IRF1 axis, and by modulating properties of NPCs.

219 southern China has a high incidence rate of NPCs.

220 While the primary role of NPCs is to regulate nucleo-cytoplasmic transport, recent

221 in the transcript profiles of young and old NPCs.

222 Older NPCs (postnatal day 0) exit the progenitor niche at a hi

223 isplayed a higher glycolysis rate than older NPCs.

224 ically for periglomerular neurons impacts on NPC-traits in the rostral migratory stream (RMS).

225 wever, in these EBV-associated cancers, only NPC exhibits remarkable ethnic and geographic distributi

226 restricted to members of the inner and outer NPC rings, but it lacks numerous others including cytopl

227 two additional hydrogel systems, permitting NPC-mediated matrix remodelling proved to be a generaliz

228 2i/LIF can abrogate persistent-NPC interactions, recover poorly reprogrammed interactio

229 ng (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome se

230 P-beta-CD) has shown efficacy as a potential NPC therapeutic by extending lifetime in NPC mice, delay

231 sequences from viruses isolated from primary NPC biopsy specimens in this region, revealing whole-gen

232 uence variation in EBV isolated from primary NPC biopsy specimens obtained from the Hunan Province.

233 had more immunologic advantage than primary NPC, especially the Galectin-9/Tim-3 pathway.

234 sphorylate nucleoporin interfaces to promote NPC disassembly and nuclear envelope breakdown.

235 y expressed in NPC and functionally promoted NPC malignant phenotypes.

236 Putative NPC-specific enhancers exhibit strong YY1 signal when en

237 We biochemically reconstituted NPC core protomers and elucidated the underlying protein

238 r cells between paired primary and recurrent NPC from 95 patients and we noted that there was signifi

239 = 0.01) between paired primary and recurrent NPC.

240 a potential salvage treatment for recurrent NPC.

241 with high Galectin-9 expression in recurrent NPC frequently also had high Tim-3 (p = 0.04) and Foxp3

242 Our data suggests that recurrent NPC may had more immunologic advantage than primary NPC,

243 promising therapeutic strategy for reversing NPC radioresistance.

244 ed Jab1/Csn5 expression, thereby sensitizing NPC cells to cisplatin-induced apoptosis both in vitro a

245 Unexpectedly, some NPC interactions around pluripotency genes persist in ou

246 ered via their Rpn9 subunits to two specific NPC locations: binding sites on the NPC basket that refl

247 Gene expression profiling of SPG11-NPCs revealed widespread transcriptional alterations in

248 l, proteomic, and functional analyses of SVZ NPC-secreted factors revealed the neurite outgrowth-prom

249 OCK inhibition decreased invasion toward SVZ NPC-secreted factors.

250 a clinical dilemma, immunotherapy targeting NPC-specific immunosuppression may bring new hope.

251 Tgfb2-/- NPCs transplanted into EAE mice were ineffective in impa

252 oughput chemical screening and observed that NPC cells were highly sensitive to inhibitors of cyclin-

253 Our results show that NPC transplantation, by modulating the excitatory-inhibi

254 in vitro transcriptome analyses showed that NPC-secreted factors inhibit MC differentiation and acti

255 Our findings suggest that NPCs regulate the activity of functional gene groups by

256 Selective binding between DNA and the NPC fibrils was observed with fluorescence polarization.

257 tial relationship between NE budding and the NPC.

258 mutants in both pUL25 and pUL36 dock at the NPC but fail to release DNA.

259 tates Kapbeta1 turnover and occupancy at the NPC in a RanGTP-dependent manner that is directly couple

260 the inner nuclear membrane that encircle the NPC.

261 knowledge gap is how the capsid engages the NPC and what triggers release of the viral genome into t

262 Therefore, we evaluated the NPC and nucleocytoplasmic transport in multiple models o

263 d Rbfox proteins antagonistically govern the NPC-to-neuron transition by regulating neuron-specific e

264 How the NPC assembles into this double membrane boundary has rem

265 To understand how the NPC integrates these functional constraints, we dissecte

266 imulation of differentiation pathways in the NPC decreased glycolytic flux.

267 ckdown reduced the presence of NUP205 in the NPC, and, reciprocally, a NUP205 alteration abrogated NU

268 ing how these nucleoporins assemble into the NPC scaffold imposes a formidable challenge.

269 ayer of connections to current models of the NPC architecture.

270 ly enhance the degenerative phenotype of the NPC cerebellum provides strong support for the notion th

271 CPR5 associates with anchors of the NPC selective barrier to constrain nuclear access of sig

272 nservation suggests that many aspects of the NPC transport mechanism may be understood based on gener

273 Kaps constitute integral constituents of the NPC whose barrier, transport, and cargo release function

274 lly important for a detailed analysis of the NPC, including function, evolution, and assembly.

275 ion structures of the building blocks of the NPC.

276 y intervene to control the plasticity of the NPC.

277 specific NPC locations: binding sites on the NPC basket that reflect its eightfold symmetry and more

278 In total, our findings indicate that the NPC's internal organization consists of multiple dynamic

279 afficking large molecular cargos through the NPC, the processing preferences of individual 2A(pro) pr

280 inner ring complex and its attachment to the NPC coat.

281 addition, whereas targeting of genes to the NPC is independent of transcription, interchromosomal cl

282 ing domain and thus does not localize to the NPC.

283 soluble and membrane proteins transiting the NPC.

284 o stabilize critical interactions within the NPC scaffold needed for late steps of NPC assembly.

285 elatively low sequence conservation; yet the NPC as a whole retains its general architecture and mech

286 Tpr, a component of the NPCs (nuclear pore complexes), facilitates the formation

287 We show that this NPC-localized complex is essential for muscle growth, my

288 Only a few diseases have been attributed to NPC dysfunction.

289 hepatocellular carcinoma, and contributes to NPC's resistance to radiotherapy and cisplatin by regula

290 lower in both MSCs and HSCs when compared to NPCs.

291 at the addition of the Nup210 nucleoporin to NPCs during myoblast differentiation results in assembly

292 des evidence that intrathecally transplanted NPCs interfere with the CNS-restricted inflammation of E

293 urcation and developmental tracks of the two NPC subpopulations, and we captured an early (24 h) tran

294 lity, which may hold a clue in understanding NPC assembly and function.

295 nx1 is essential for maintaining elevated VZ NPC numbers after stroke.

296 estigated the effect of Panx1 deletion in VZ NPCs after focal cortical stroke via photothrombosis.

297 67C > T in PIN1 promoter are associated with NPC risk; as well as the promoter activity is mediated b

298 RPA with NPC N categories resulted in more balanced stage groups

299 es was significantly augmented compared with NPCs alone.

300 d mononuclear cells, and combining them with NPCs and neurons derived from induced pluripotent stem c

301 in the structure and biogenesis of the yeast NPC.

302 n and culture in NPC renewal medium, younger NPCs displayed a higher glycolysis rate than older NPCs.