ライフサイエンスコーパス: NPC

1 NPC disease primarily affects the brain, causing neurona

2 NPCs have a limited lifespan and are depleted near the t

3 poradic NPC cases compared to controls (7.1% NPC/1.7% controls below normal range; OR = 4.5; 95% CI =

4 of hiPSC-derived 3D cultures to model HSV-1-NPC interaction.IMPORTANCE This study employed human ind

5 normal) acquired from 113 tissue sites of 14 NPC patients and 48 healthy subjects during nasopharynge

6 -dimensional (2D) and three-dimensional (3D) NPC cultures was observed, highlighting the potential va

7 tal of 2126 in vivo FP/HW Raman spectra (598 NPC, 1528 normal) acquired from 113 tissue sites of 14 N

8 e of Torsin manipulation represents aberrant NPC intermediates.

9 e adjoining stretches of membrane accumulate NPCs that are associated with the still-intact lamina.

10 Additionally, NPC disease results in sphingolipid accumulation, yet it

11 y behavioral cues to the activation of adult NPCs.

12 that the IMPA1 mutation specifically affects NPC survival and neuronal differentiation.

13 Recently, Hampoelz et al. reported that AL-NPC assembly depends on the coordinated formation, trans

14 wever, cellular mechanisms used to alleviate NPC assembly stress are not well defined.

15 letion partially rescues gene expression and NPC functions.

16 transcriptome' after spinal cord injury and NPC grafting.

17 Only MBIL and NPC found that surgical_margins is a direct risk factor.

18 e extreme longevity of the NPC proteins, and NPC dysfunction in age-related diseases.

19 ignaling rescued enlarged organoid sizes and NPC overproliferation caused by RAB39b mutations.

20 -cell as an expanding infectious center, and NPCs are infected via contact with infected cells far mo

21 t ELA, smaller DG volume, with fewer GNs and NPCs, suggests less neurogenesis and/or more apoptosis a

22 etween the pericentriolar material (PCM) and NPCs.

23 essfully traffic functional antibodies (anti-NPC and anti-pAkt) to cytosol to elicit their bioactivit

24 ance of organ-restricted progenitors such as NPCs, but the chromatin-based mechanisms are incompletel

25 This ensures that both NPCs in interphase and kinetochores in mitosis can gener

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

27 Niemann-Pick type C (NPC) disease is a lysosomal storage disorder arising fro

28 Niemann-Pick type C (NPC) disease is a lysosomal storage disorder characteriz

29 Niemann-Pick type C (NPC) disease is primarily caused by mutations in the NPC

30 we propose that Niemann-Pick disease type C (NPC), a lysosomal storage disorder, may provide new insi

31 In Niemann-Pick type C (NPC), loss of the cholesterol exporter, NPC1, causes cho

32 degeneration in Niemann-Pick disease type C (NPC).

33 responsible for Niemann-Pick disease type C (NPC).

34 the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-

35 lignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).

36 ogical testing for nasopharyngeal carcinoma (NPC) has recently been reinvigorated by the implementati

37 Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer that is consistently

38 ental defects due to neural progenitor cell (NPC) apoptosis, which led to reduction in cortical layer

39 f LIS1 in regulating neural progenitor cell (NPC) daughter cell separation.

40 d a system to induce neural progenitor cell (NPC) development from mouse embryonic stem cell (ESC) li

41 tive, age-depletable neural progenitor cell (NPC) niche, with unique characteristics and culture requ

42 results in loss of nephron progenitor cell (NPC) renewal, a phenotype opposite to WT.

43 VEC) crosstalk with neural progenitor cells (NPC) promoting mutual proliferation, formation of tubula

44 if differentiation of neuroprogenitor cells (NPCs) in BrainPhys medium, previously reported to enhanc

45 rocephaly by killing neural precursor cells (NPCs) and other brain cells.

46 dult mice, quiescent neural precursor cells (NPCs) maintain the highest ROS levels (hiROS).

47 lation of endogenous neural precursor cells (NPCs) may promote cognitive recovery and brain repair, f

48 nal differentiation, neural precursor cells (NPCs), assembled rosettes, and differentiated neuronal c

49 s, Nestin(+)Sox2(+) neural progenitor cells (NPCs) and DCX(+) neuroblasts and immature neurons were d

50 Consistently, neural progenitor cells (NPCs) derived from human induced pluripotent stem cells

51 Higher neuronal progenitor cells (NPCs) differentiation along with better mitochondrial mo

52 osome genes deplete neural progenitor cells (NPCs) during brain development, causing microcephaly.

53 the number of neural stem-progenitor cells (NPCs) during neocortical development, and thus reduced t

54 spinal-cord-derived neural progenitor cells (NPCs) enable the robust regeneration of corticospinal ax

55 iation potential of neural progenitor cells (NPCs) found in the subventricular zone (SVZ) have prompt

56 meobox 2)-positive nephron progenitor cells (NPCs) give rise to all epithelial cell types of the neph

57 Nephron progenitor cells (NPCs) give rise to all segments of functional nephrons a

58 ram is fulfilled by neural progenitor cells (NPCs) of the spinal cord, we analyzed pax6-expressing NP

59 IMPA1-deficient neuronal progenitor cells (NPCs) revealed substantial deficits in proliferation and

60 of ZIKV in infected neural progenitor cells (NPCs), the major cells infected in the fetus.

61 differentiation of neural progenitor cells (NPCs), which resemble neurodevelopmental deficits in KO

62 In neural progenitor cells (NPCs), Ybx1 controls self-renewal and neuronal different

63 clinically relevant neural progenitor cells (NPCs).

64 ighly enriched with neural progenitor cells (NPCs).

65 xperiments of human neural progenitor cells (NPCs).

66 al to proliferating neural progenitor cells (NPCs).

67 Smc5 cKO NPCs formed DNA bridges during mitosis and underwent chr

68 Classifying NPCs on the basis of cellular ROS content identified dis

69 Orf6 localizes at the nuclear pore complex (NPC) and directly interacts with Nup98-Rae1 via its C-te

70 ffold component of the nuclear pore complex (NPC) and has been implicated as a congenital heart disea

71 The intricacy of nuclear pore complex (NPC) biogenesis imposes risks of failure that can cause

72 marker for interphase nuclear pore complex (NPC) biogenesis, is underrepresented relative to FG-nucl

73 membrane fusion during nuclear pore complex (NPC) biogenesis.

74 it is targeted to the nuclear pore complex (NPC) by binding an acidic face of the kinetochore checkp

75 tatic structure of the nuclear pore complex (NPC) continues to be refined with cryo-EM and x-ray crys

76 ings are attributed to nuclear pore complex (NPC) disintegration by nsp1beta, resulting in increased

77 The nuclear pore complex (NPC) employs the intrinsically disordered regions (IDRs)

78 In recent years, the nuclear pore complex (NPC) has emerged as a key player in genome regulation an

79 The Nuclear Pore Complex (NPC) has emerged as an important hub for processing vari

80 een the genome and the nuclear pore complex (NPC) have been implicated in multiple gene regulatory pr

81 Loss of nuclear pore complex (NPC) proteins, transcription factors (TFs), histone modi

82 ity to centrosomal and nuclear pore complex (NPC) proteins-structures where Ca(2+) signaling is large

83 that NUP153 links the nuclear pore complex (NPC) to chromatin architecture allowing genes that are p

84 e such assembly is the nuclear pore complex (NPC), an ~50 MDa assembly comprised of ~30 different pro

85 lly active loci to the nuclear pore complex (NPC), and it also promotes large-scale gene-NPC interact

86 cargo complexes at the nuclear pore complex (NPC).

87 ghtly regulated by the nuclear pore complex (NPC).

88 eus occurs through the nuclear pore complex (NPC).

89 the inner ring of the nuclear pore complex (NPC).

90 Nuclear pore complexes (NPCs) accumulate at TAN lines providing a potential mech

91 Nuclear Pore complexes (NPCs) act as docking sites to anchor particular DNA lesi

92 Nuclear pore complexes (NPCs) are important for cellular functions beyond nucleo

93 Nuclear pore complexes (NPCs) are the main conduits for molecular exchange acros

94 ng to Megator/Tpr at nuclear pore complexes (NPCs) during interphase.

95 Oocytes stockpile nuclear pore complexes (NPCs) in cytoplasmic membrane sheets called annulate lam

96 The interior of nuclear pore complexes (NPCs) is densely filled with FG-nucleoporins that form a

97 Nuclear pore complexes (NPCs) regulate all cargo traffic across the nuclear enve

98 densely packed with nuclear pore complexes (NPCs) that are stockpiled for embryonic development.

99 port (NCT) to bypass nuclear pore complexes (NPCs).

100 earning algorithms Necessary Path Condition (NPC) and Greedy Equivalent Search (GES).

101 ear transport reporter, suggesting conserved NPC regulation by CN.

102 reduction of neurogenic potential in control NPCs-expressing shIMPA1.

103 e inherently more proliferative than control NPCs.

104 When compared with the control NPCs, high-throughput genome-wide translocation sequenci

105 eckpoint protein, MAD1, where it coordinates NPC disassembly with kinetochore assembly.

106 hat conditional Ino80 deletion from cortical NPCs impairs DNA double-strand break (DSB) repair, trigg

107 Exposure of cultured NPCs to hypoxia and sovateltide also showed higher NPC d

108 encing (HTGTS) demonstrates that ASD-derived NPCs harbored elevated DNA double-strand breaks in repli

109 Here, we show that hiPSC-derived NPCs from ASD individuals with macrocephaly display an a

110 and two antibodies were capable of detecting NPC with 99.2% and 98.4% accuracy.

111 ts by rigidly conjugating mEGFP to different NPC proteins.

112 enal agenesis premature NPC differentiation, NPC proliferation, and cell death defects.

113 terious cellular effects caused by disrupted NPC assembly.

114 t of serological markers able to distinguish NPC cases from controls with AUCs of 0.992 (95% confiden

115 between positive and negative signals during NPC maintenance.

116 lular pathways could contribute to effective NPC therapies.

117 d droplets to maintain viability and enhance NPC formation in assembly mutants.

118 the spinal cord, we analyzed pax6-expressing NPCs isolated from regenerating Xenopus tropicalis tails

119 rrently, no FDA-approved therapies exist for NPC and the mechanisms of NPC disease are not fully unde

120 We conclude that EZH2 is required for NPC renewal potential and that tempering of the differen

121 dapted a 13-marker EBV antigen signature for NPC risk identified by proteome arrays to multiplex sero

122 1 during prophase triggers Mad1 release from NPCs and that this is required for kinetochore localizat

123 osphate (RanGTP) promotes their release from NPCs into the nuclear interior.

124 (NPC), and it also promotes large-scale gene-NPC interactions.

125 o hypoxia and sovateltide also showed higher NPC differentiation and maturation.

126 lt hippocampal neurogenesis, recruited hiROS NPCs into proliferation via a transient Nox2-dependent R

127 se data provide an experimental model of how NPCs can facilitate fast passage of cargoes across an or

128 We next demonstrate that co-culturing human NPCs with rodent astrocytes results in mutually synergis

129 Here, we show that (i) NPCs can be efficiently infected by HSV-1, but infection

130 Lytic HSV-1 infections impaired NPC migration, which represents a critical step in neuro

131 implanted into the device and that implanted NPCs in turn extend axons out of the scaffold and into t

132 in rescuing the cholesterol accumulation in NPC and other degenerative diseases.

133 compositional and functional alterations in NPC lysosomes and nature of aberrant cholesterol-mTORC1

134 Fgf20 results in kidney agenesis, defects in NPC proliferation, and cell death.

135 ivated microglia promote PCs degeneration in NPC are not completely understood.

136 an earlier stage and to a greater extent in NPC; therefore, we analyzed the effect of NPC1 deficienc

137 rases EZH1 (enhancer of zeste 1) and EZH2 in NPC maintenance.

138 er function, exacerbating hepatic failure in NPC disease.

139 addition, considerable liver malfunction in NPC disease is common.

140 ime a role for monoamine oxidase A (MAOA) in NPC.

141 Purkinje cells to early neurodegeneration in NPC.

142 e homeostasis and is a targetable pathway in NPC.

143 is downregulated after two weeks, whereas in NPC-grafted mice this transcriptome is sustained.

144 We show that ZIKV spreads cell-to-cell in NPCs as an infectious center and that NPCs are more perm

145 and self-renewal-differentiation choices in NPCs.

146 In contrast, in NPCs derived from these ESC lines we detected 29 RDCs, a

147 viral silencing mechanism is established in NPCs exposed to the antivirals (E)-5-(2-bromovinyl)-2'-d

148 This study shows a novel role of ETBR in NPCs and mitochondrial fate determination in cerebral is

149 SPRY1 expressed in NPCs modulates the activity of FGF signaling and regulat

150 ition, we demonstrate that ZIKV infection in NPCs spreads primarily cell-to-cell as an expanding infe

151 s not prevent the spread of the infection in NPCs.

152 2 is the dominant H3K27 methyltransferase in NPCs and epithelial descendants.

153 that the depletion of centrosome proteins in NPCs prolongs mitosis and increases TP53-mediated apopto

154 cell fate decisions and their regulators in NPCs during regeneration.

155 which modulates renal branching, its role in NPCs is not known.

156 and whether SPRY1 modulates FGF signaling in NPCs and whether FGF8 functions with FGF9 and FGF20 in m

157 deletion promotes PI3K-AKT-mTOR signaling in NPCs of mouse cortex and cerebral organoids.

158 Importantly, ZIKV was able to spread in NPCs in the presence of neutralizing antibody.Importance

159 Herein, we provide evidence that in NPCs infected at an MOI as low as 0.001, HSV-1 can estab

160 y further resolves the NLS-NCs on transit in NPCs and inside the nucleus.

161 nct chromatin-binding patterns of individual NPC components known as nucleoporins (Nups).

162 he susceptibility and fate of HSV-1-infected NPCs are largely unexplored.

163 e expression can be detected in the infected NPCs; (iii) a viral silencing mechanism is established i

164 ological nuclear transport pathway in intact NPCs in cells: that is, inert cargoes ranging from small

165 induced pluripotent stem cells (hiPSCs) into NPCs to generate two-dimensional (2D) and three-dimensio

166 eatest effects on TRANK1 expression in iPSC, NPC, and astrocytes.

167 In Ybx1-knockout NPCs, H3K27me3 reduction by PRC2 enzymatic inhibitor or

168 er, in this context, SIX1 failed to maintain NPC stemness.

169 pivotal roles in generating and maintaining NPCs during kidney development, but little is known abou

170 functions with FGF9 and FGF20 in maintaining NPCs.

171 endence on POM121, and a reduction of mature NPCs in Torsin-deficient cells lead us to conclude that

172 MBIL, NPC, and GES all learned that grade and lymph_nodes_posi

173 es not exchange with NPCs even after mitotic NPC breakdown.

174 bouton-like structures that contact mitotic NPCs in the fetal rhesus monkey but not in rat.

175 ection does not result in cell death of most NPCs, even at high multiplicities of infection (MOIs); (

176 Double-mutant NPCs also overexpressed the SIX family member Six1 Howev

177 Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage plane displac

178 Neither GES nor NPC learned that HER2 and ER are direct risk factors.

179 to rapidly elucidate mechanistic aspects of NPC RDC formation.

180 esults provide a metabolic classification of NPC functional states and describe a mechanism linking t

181 herapies exist for NPC and the mechanisms of NPC disease are not fully understood.

182 ts down-regulation enhances the migration of NPC cells.

183 chondrial dysfunction in a neuronal model of NPC.

184 accumulation in multiple cellular models of NPC disease and observed that the activity of sphingosin

185 Thus, distinct modes of NPC division have divergent requirements for Ino80-depen

186 ed sensors that report on the orientation of NPC components by rigidly conjugating mEGFP to different

187 be an important step in the pathogenesis of NPC.

188 NVJs significantly improve the physiology of NPC assembly mutants, despite having only negligible eff

189 Through proteomic profiling of NPC lysosomes, we find pronounced proteolytic impairment

190 contribution of ANXA6 in the progression of NPC disease, double-knockout mice (Npc1(-/-)/Anxa6(-/-))

191 and contacting dendrites at early stages of NPC, when no loss of PCs is detected.

192 ired the excitatory synaptic transmission of NPC-derived neurons.

193 ulti-faceted nature and the slow turnover of NPC components complicates investigations of how individ

194 e Y complex that affect our understanding of NPC structure and assembly.

195 frequency; (iv) HSV-1 impairs the ability of NPCs to migrate in a dose-dependent fashion in the prese

196 The transport conduit of NPCs is highly enriched in disordered phenylalanine/glyc

197 5BVdU plus IFN-alpha; and (v) 3D cultures of NPCs are less susceptible to HSV-1 infection than 2D cul

198 ype and indicate that induced development of NPCs from ESCs provides an approach to rapidly elucidate

199 autonomously prevents the differentiation of NPCs.

200 de a mechanism linking hyperproliferation of NPCs with the pathogenesis of ASD by disrupting long neu

201 n1c locus plays a key role in maintenance of NPCs during neocortical development.

202 ects on the conformation and permeability of NPCs, where transport barriers are viscosified to lower

203 make contact with the soma and processes of NPCs dividing at the ventricle for over 50 mum along the

204 OU3F2 or TRIM8 promoted the proliferation of NPCs, inhibited their neuronal differentiation, and impa

205 ound that metformin enhanced the recovery of NPCs in the dentate gyrus, with sex-dependent effects on

206 outer radial glia cells (oRGs), a subtype of NPCs barely detectable in rodents but abundant in human

207 bility of key genes during the transition of NPCs to neurons to promote differentiation.

208 We show here that trehalose treatment of NPCs infected with recent ZIKV isolates from Panama and

209 to loss of Ino80-mediated HR is dependent on NPC division mode: Ino80 deletion leads to unrepaired DN

210 ONLR-NPC depletion may help explain why ON diseases such as O

211 Early ONLR-NPC loss results in regional dysfunction and hypomyelina

212 In adulthood, ONLR-NPCs may enable glial replacement and remyelination.

213 inducible gene expression, we show that ONLR-NPCs generate macroglial cells for the anterior ON.

214 Only NPC found that invasive is a direct risk factor.

215 nto 3D biomimetic scaffolds and synapse onto NPCs implanted into the device and that implanted NPCs i

216 endothelial cells (ABEC) in mono-culture or NPC co-culture.

217 Packed NPCs sort into a distinct membrane network, while breaks

218 At low passage NPCs (P1 to P3), we observed cell cycle arrest, apoptosi

219 rescuing bilateral renal agenesis premature NPC differentiation, NPC proliferation, and cell death d

220 show that MAOA is down-regulated in primary NPC tissues and its down-regulation enhances the migrati

221 A receded NPC was present in the majority of young patients with c

222 ew advances and outstanding issues regarding NPC structure and function.

223 the activity of FGF signaling and regulates NPC stemness.

224 Moreover, 53BP1 or USP28 deletion restored NPC proliferation and brain size without correcting the

225 igin of selective acetone formation on Cu-SA/NPC is clarified.

226 encapsulated on N-doped porous carbon (Cu-SA/NPC) catalysts for reducing CO(2) to multi-carbon produc

227 ome analysis of OPCs revealed that senescent NPCs induced expression of epigenetic regulators mediate

228 tate but cycled slowly, leading to a smaller NPC pool and formation of fewer nephrons.

229 of chromatin via interactions with specific NPC sub-complexes, and a subset of Polycomb domains is s

230 magnesium levels was observed among sporadic NPC cases compared to controls (7.1% NPC/1.7% controls b

231 neurons, which were derived from late-stage NPCs.

232 Here, we examined the late mitotic stages NPCs in vivo and mouse embryonic fibroblasts (MEFs) in v

233 Surprisingly, NPCs lacking H3K27 trimethylation maintained their proge

234 mid polyplexes can non-virally transfect SVZ NPCs when directly injected in the lateral ventricles of

235 paired DNA breaks and apoptosis in symmetric NPC-NPC divisions, but not in asymmetric neurogenic divi

236 Taiwanese NPC cases (n = 175) and matched controls (n = 175) were

237 amin-associated domains (LADs) revealed that NPC binding sites can be found within LADs, demonstratin

238 These results suggest that NPC pools could be sites of HSV-1 reactivation in the ce

239 ell in NPCs as an infectious center and that NPCs are more permissive to infection by contact with in

240 th single-cell transcriptomics, we find that NPCs place an early priority on neuronal differentiation

241 We found that NPCs cultured in BrainPhys displayed increased expressio

242 Transcriptome analysis showed that NPCs and neurons derived from ID patients have extensive

243 The NPC has also been viewed as a nuclear architectural plat

244 The NPC is a modular assembly of ~500 individual proteins, c

245 ng the thousands of molecules that cross the NPC, even very large (>15 nm) cargoes such as pathogens,

246 Targeted perturbations in the NPC structure revealed a dynamic resilience to damage.

247 formational changes to Nups elsewhere in the NPC.

248 the sensitivity of the PCM pool, but not the NPC pool, to proteasomal degradation.

249 esults suggest that select components of the NPC are flexible and undergo conformational changes upon

250 iew, we discuss non-transport aspects of the NPC focusing on the NPC-genome interaction, the extreme

251 me interaction, the extreme longevity of the NPC proteins, and NPC dysfunction in age-related disease

252 raphy, in vivo conformational changes of the NPC remain under-explored.

253 n binding maps of two core components of the NPC, Nup107 and Nup93, in Drosophila cells.

254 e and versatile toolkit for the study of the NPC.

255 is an essential scaffolding component of the NPC.

256 transport aspects of the NPC focusing on the NPC-genome interaction, the extreme longevity of the NPC

257 hogens, mRNAs and pre-ribosomes can pass the NPC intact.

258 New discoveries have revealed that the NPC has multiple cellular functions besides mediating th

259 Consistent with the idea that the NPC specifically modulates clock function, we found a st

260 mples summarized herein demonstrate that the NPC, which first evolved to enable the biochemical commu

261 54, Nup58, Nup62) when transport through the NPC is perturbed and no conformational changes to Nups e

262 terial infection, acting in part through the NPC, alters core clock gene expression and/or mRNA accum

263 rgetics of large cargo transport through the NPC.

264 ible connector Nups threading throughout the NPC architecture exchange more rapidly.

265 Throughout the NPC, we find a polarized electrostatic potential and a d

266 over that fusing a DNA binding domain to the NPC basket protein Nup1 reduces telomere relocalization

267 ver, MRX-mediated chromatin anchoring to the NPC contributes to chromosome folding and helps to contr

268 ation also impairs the relocalization to the NPC of expanded CAG/CTG triplet repeats.

269 rfaces of the Y complex and Nic96 within the NPC.

270 tion uncovered differential binding of these NPC subunits, where Nup107 preferentially targets active

271 These NPCs generate both forms of macroglia: astrocytes and ol

272 thenticate, bind, and escort NLS-NCs through NPCs while Ran guanosine triphosphate (RanGTP) promotes

273 ial mechanism for linking mechanical cues to NPC function.

274 ommon disease-associated mutation leading to NPC disease.

275 de of cholesterol and the azasterol probe to NPC proteins, demonstrating the structural similarity of

276 hemical and cell biology findings related to NPC, coupled with the rapidly evolving data on COVID-19.

277 PVEC exhibited a 30-fold greater response to NPC than ABEC (411 vs. 13 DEG).

278 Anchorage to NPCs allows SUMO removal by the SENP SUMO protease Ulp1

279 fficient to bypass the need for anchorage to NPCs and the inhibitory effect of poly-SUMOylation on HR

280 on of TREX-2 subunits (GANP, PCID2, ENY2) to NPCs and results in abnormal RNA transcription and expor

281 f Nup1 in the relocation of stalled forks to NPCs and restriction of error-prone recombination betwee

282 report that relocation of arrested forks to NPCs occurred after Rad51 loading and its enzymatic acti

283 poly-SUMOylation which promote relocation to NPCs but impede the resumption of DNA synthesis by homol

284 rly capable of reversibly inducing transient NPC-like cellular and biochemical phenotypes, constitute

285 VLA4+NPC engraftment in 4L;C* brain also led to enhanced expr

286 despite having only negligible effects when NPC biogenesis is unperturbed.

287 1-enriched NE-vacuole contacts increase when NPC assembly is compromised in several nup mutants, incl

288 We propose a model in which NPC biogenesis is carefully controlled to ensure that a

289 While NPC attrition is linked to TP53-mediated cell death in s

290 The majority of children with NPC die in adolescence.

291 , both injury alone and injury combined with NPC grafts elicit virtually identical early transcriptom

292 e found that EZH2 expression correlates with NPC growth potential and that EZH2 is the dominant H3K27

293 opy studies reveal that Vpx interaction with NPC-associated Nup153 is critical for its efficient nucl

294 of PVEC and their important partnership with NPC, underpinning their unique role in maintaining a hea

295 PSCs) to model the interaction of HSV-1 with NPCs, which reside in the neurogenic niches of the CNS a

296 els to examine the interaction of HSV-1 with NPCs.

297 thesized protein that does not exchange with NPCs even after mitotic NPC breakdown.

298 ysical interaction of chromosomal sites with NPCs.

299 CN dephosphorylates human and yeast NPC proteins and promotes accumulation of a nuclear tran

300 provide a comprehensive picture of the yeast NPC component dynamics.