ライフサイエンスコーパス: primary neuron

1 in a variety of cellular systems, including primary neurons.

2 ein mutants to neurotransmitter signaling in primary neurons.

3 scriptionally and/or post-translationally in primary neurons.

4 n cells and enhanced neuronal development in primary neurons.

5 ctive transport of polysomes in dendrites of primary neurons.

6 -related aggregated amyloid-beta peptides in primary neurons.

7 protein translation in 4E-BP1-overexpressing primary neurons.

8 ing expression in transfected cell lines and primary neurons.

9 te uptake into BV2 microglial-like cells and primary neurons.

10 estrates spine dynamics and morphogenesis in primary neurons.

11 ulation of Slick by NFkappaB was verified in primary neurons.

12 r was demonstrated in heterologous cells and primary neurons.

13 ell-based assay and immunolabeling of murine primary neurons.

14 cell types but were not detectable in mouse primary neurons.

15 ated neurodegeneration in Drosophila and rat primary neurons.

16 alized pathway for constitutive autophagy in primary neurons.

17 pressed in several cell types, but not mouse primary neurons.

18 for the induction of long-term depression in primary neurons.

19 etrin-1 increased endogenous JNK activity in primary neurons.

20 lular ratio in differentiated PC12 cells and primary neurons.

21 pitation experiments and coimmunostaining in primary neurons.

22 pe beta-synuclein is neurotoxic for cultured primary neurons.

23 evented MPP(+)-induced dendrite shrinkage in primary neurons.

24 results in mouse cardiomyocytes and cultured primary neurons.

25 glion neurons, validating Slit2 signaling in primary neurons.

26 lpha-syn-expressing HEK293 cells or cultured primary neurons.

27 appears to be necessary for Tau reduction in primary neurons.

28 rther confirmed to regulate Dlg4 splicing in primary neurons.

29 n of Erf led to an increase in the number of primary neurons.

30 ake was analyzed in brain slice cultures and primary neurons.

31 secretory pathway in heterologous cells and primary neurons.

32 MG selectively activated GABAA receptors in primary neurons.

33 sary to enrich dynactin at the distal end of primary neurons.

34 GN) of both transfected HeLa cells and mouse primary neurons.

35 mitochondria, with broken cristae in AbetaPP primary neurons.

36 tiator caspase activated in rotenone-treated primary neurons.

37 antibody to LRP1 suppressed Abeta uptake in primary neurons.

38 -2a cells and dendritic spine development in primary neurons.

39 were also increased from progranulin-treated primary neurons.

40 Halo-tagged SRF molecules in fibroblasts and primary neurons.

41 se deprivation/reoxygenation models in mouse primary neurons.

42 o trigger inflammatory signaling in cultured primary neurons.

43 100 mV intracellular action potentials from primary neurons.

44 ogous end-joining, including in post-mitotic primary neurons.

45 n ectopic expressing systems and in striatal primary neurons.

46 stoma and striatal cell lines, as well as in primary neurons.

47 mediated filopodia formation and dynamics in primary neurons.

48 reatment reduced apoptosis in HSV-2-infected primary neurons.

49 We show here that hD4R is ubiquitinated in primary neurons.

50 he neuronal activity-inducible gene Npas4 in primary neurons.

51 romotes DNA double-strand breaks in cultured primary neurons.

52 ated and regulates endosomal trafficking, in primary neurons.

53 local illumination in both COS7 cells and in primary neurons.

54 al of these findings were confirmed in mouse primary neurons.

55 c loss in a PKA-dependent manner in cultured primary neurons.

56 neuroserpin polymers in both HeLa cells and primary neurones.

57 Abeta42 compared to DMSO (N2a cells: 7-fold; primary neurons: 4-fold; brain lysates: 2-fold) with an

58 In primary neurons, a reduction in the number of gephyrin c

59 oteomic approach to analyze the secretome of primary neurons after acute BACE1 inhibition, and we ide

60 e show that C1q protects immature and mature primary neurons against fAbeta toxicity, and we report f

61 Fingolimod did not protect primary neurons against glutamate excitotoxicity or hydr

62 Z derivatives were assayed for protection of primary neurons against oxygen-glucose deprivation and e

63 AP-4 silencing in mouse primary neurons also resulted in the accumulation of end

64 LRRK2 aggregation and neuronal protection in primary neurons and a Drosophila model of G2019S LRRK2.

65 Using primary neurons and brain slice cultures, we find that o

66 DSCAM partially co-localized with UNC5C in primary neurons and brain tissues.

67 Complementary experiments in mouse primary neurons and C. elegans support the auto-inhibiti

68 study measured HCA1 and HCA2 entry into rat primary neurons and cultured Neuro2A cells.

69 erograde axonal transport of mitochondria in primary neurons and decreases synaptic mitochondrial act

70 unts of free monomers occurs endogenously in primary neurons and erythroid cells as well as neuroblas

71 he ability of SnoN1 to regulate branching in primary neurons and granule neuron migration in vivo.

72 r EF2K degradation mechanism was observed in primary neurons and HEK cells.

73 Importantly, in primary neurons and hippocampal slices, CALHM1 activatio

74 mal lysosomal morphology, including in mouse primary neurons and human stem cell-derived neurons.

75 ckdown of SnoN2 stimulates axon branching in primary neurons and impairs migration of granule neurons

76 ockdown of the transcription factor MEF2A in primary neurons and importantly in the rat cerebellar co

77 crotubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor def

78 duced cleavage by BACE1 in transfected mouse primary neurons and in isogenic human induced pluripoten

79 insenoside, reduced Abeta levels in cultured primary neurons and in the brains of a mouse model of Al

80 We found that in primary neurons and in Ube3A transgenic autism mouse bra

81 The Hap1 knockdown-induced phenotypes in primary neurons and in vivo recapitulate the phenotypes

82 By using in vitro studies in primary neurons and in vivo studies in mice, we have sho

83 protein in heterologous expression systems, primary neurons and in vivo, and suggest a critical role

84 in vitro and cell lines are recapitulated in primary neurons and in vivo, as genetic reduction in Ran

85 cts in CMT2A patient-derived fibroblasts, in primary neurons and in vivo, in motoneurons of a mouse m

86 alpha-secretase processing in HeLa cells and primary neurons and indicate that both APP processing pa

87 range of cell types, including non-dividing primary neurons and induced-pluripotent stem cells (iPS)

88 bditis elegans models, mammalian cell lines, primary neurons and mouse brains, demonstrating that CHC

89 orylated GluA1-containing AMPARs in cultured primary neurons and mouse forebrain.

90 Here we employ cellular models, primary neurons and mouse models to investigate the pote

91 mRNAs for TRAIL, DR5, OPG, and mDcTRAILR2 in primary neurons and of TRAIL and OPG in OPCs.

92 NA expression of these genes was measured in primary neurons and oligodendrocyte progenitor cells (OP

93 receptors after cytokine exposure and OGD in primary neurons and OPCs were similar to those found in

94 Here we use purified proteins, mouse primary neurons and patient-derived induced neurons to s

95 Using primary neurons and PC12 cells, we demonstrate that miR-

96 le it did not affect the viability of murine primary neurons and primary astrocytes.

97 of SEZ6 reduced surface levels of GluK2/3 in primary neurons and reduced kainate-evoked currents in C

98 the formation of DNA double-strand breaks in primary neurons and reduced synaptic and neurite density

99 d with activation of the UPR caused death of primary neurons and reduced the survival of novel Drosop

100 SOCS3, an inhibitor of STAT3 signaling, into primary neurons and SH-SY5Y cells inhibits OSM and IL-6/

101 -43 nuclear export in immortalized cells and primary neurons and strongly potentiated the recruitment

102 es to mitochondria in non-neuronal cells and primary neurons and that it interacts with dynamin-relat

103 2 induce clustering in transfected cells and primary neurons and that these complexes included other

104 ptor agonist, rapidly activates TrkB in both primary neurons and the rodent brain and mimics the phys

105 age internalized alpha-syn seeds in cultured primary neurons and to quantitatively characterize the c

106 ibrils assembled from recombinant protein to primary neurons and transgenic mice.

107 ibrillar alpha-synuclein was internalized by primary neurons and transported in axons with kinetics c

108 Here, we found that SK2 is nuclear in primary neurons and, unexpectedly, overexpressed SK2 is

109 was validated in mouse embryonic stem cells, primary neurons, and APOE3 and APOE4 mice treated with b

110 ns, we used mouse embryonic stem (ES) cells, primary neurons, and APOE3 and APOE4 mice treated with b

111 TBK1 expression in HD models (cells, primary neurons, and Caenorhabditis elegans) increases m

112 ited activity-dependent neurite outgrowth in primary neurons, and CREST associated with the ALS prote

113 ataxin-3-depleted human cell lines and mouse primary neurons, and in vivo in mice.

114 e had lower NOX activity in the brain and in primary neurons, and neurons had normal ROS levels and s

115 Using cultured cell lines, primary neurons, and organotypic brain slices from an AD

116 to the natural tropism of Nipah virus, i.e., primary neurons, and show that while our first-generatio

117 and binding assays in different cell lines, primary neurons, and synaptosomes with C3-RGD mutants.

118 tant constructs in vitro, and in cell lines, primary neurons, and tau P301S mice crossed with beta-ar

119 HCR/A(W1266A) did not enter primary neurons, and the crystal structure of HCR/A(W126

120 In primary neurons, apoE4 interacts with insulin receptor a

121 Furthermore, primary neurons are also compatible with BloC-Printing.

122 r studying oligodendrocyte myelination using primary neurons are limited by the time, cost and reprod

123 from our laboratory demonstrated that aging primary neurons are more vulnerable to glutamate-induced

124 Thus, native mutant htt occurs in brain and primary neurons as a soluble full-length monomer.

125 AMPK regulates tau phosphorylation in mouse primary neurons as well as in vivo, and thus suggest tha

126 DP-43 contains abundant lcn2 and is toxic to primary neurons as well as neurons in cultured brain sli

127 g of apoE4 is impaired in Neuro-2a cells and primary neurons, as shown by measuring fluorescence reco

128 In mixed cerebellar cultures of primary neurons, astrocytes, and microglia, LPS induced

129 ion of alpha-synuclein when overexpressed in primary neurons at supramolecular and cellular scales in

130 ng transient excitotoxicity in rat and mouse primary neurons at the single-cell level using fluoresce

131 tion of C9orf72 expression in cell lines and primary neurons attenuated autophagy and caused accumula

132 Primary neurons, AWC(ON) and AWA, directly detect the fo

133 nted for the remainder of antibody uptake in primary neurons, based on co-staining with internalized

134 In primary neurons, bexarotene ameliorated the damaged dend

135 In primary neurons, bexarotene enhanced the dendritic compl

136 Knockdown of Egr-1 in rat hippocampal primary neurons blocks NMDAR-induced PSD-95 down-regulat

137 s) confirms that these added DA clusters are primary neurons born in the embryo, rather than secondar

138 at TDP-43 localizes on ribosomes not only in primary neurons but also in SH-SY5Y human neuroblastoma

139 bination with OGD and TNF-alpha/IFN-gamma in primary neurons but not in OPC cultures.

140 take of full-length recombinant fibrils into primary neurons, but HJ9.3 blocked neuronal uptake of Ta

141 that BACE1 exits the Golgi in HeLa cells and primary neurons by a pathway distinct from the trafficki

142 This is blocked in cultured cells and primary neurons by heparin, chlorate, heparinase, and ge

143 to safeguard the homeostasis of postmitotic primary neurons by preventing cell cycle re-entry.

144 LPS-induced phagocytosis of primary neurons by primary microglia was also blocked by

145 , overexpression of Egr-1 in rat hippocampal primary neurons causes reduction in PSD-95 protein level

146 etwork activity (over 30 days in vitro) from primary neurons co-cultured with glia grown on ECM coati

147 e cells and in 3-nitropropionic acid-treated primary neurons compared with untreated neurons.

148 roteomic analysis of insoluble proteins in a primary neuron culture model of alpha-synuclein patholog

149 While rodent primary neuron culture models have shown promise, they y

150 ny of the excitogenic mechanisms observed in primary neuron culture, offering a moderate-throughput m

151 been hindered by limitations associated with primary neuron culture.

152 Primary neurons cultured from the brains of neonatal T40

153 al remodeling of spines and defective LTP in primary neuron cultures and hippocampal slices.

154 Also, in vitro studies in the cell lines and primary neuron cultures further established the role of

155 neration of beta-amyloid (Abeta) peptides by primary neuron cultures generated from the Tg2576 AD mou

156 induced up-regulation of FKBP51 in cells and primary neurons, demonstrating functional, disease-relev

157 In CBS heterozygous mice (cbs(+/-)) and primary neurons depleted with either CBS or IL-1R, IL-1b

158 s of these two receptors using N2A cells and primary neurons derived from knockout mice.

159 , rescued the morphological abnormalities of primary neurons differentiated from iPS cells of human H

160 In hippocampal primary neurons, Egr-1 binds to BACE-1 and p35 promoters

161 We verified that reducing BAG3 levels in primary neurons exacerbated pathological tau accumulatio

162 HD model mice and from mutant Htt-expressing primary neurons exhibited a protein import defect, sugge

163 Culturing primary neuron explants on planar microelectrode arrays

164 roperties of DHA-VE were demonstrated in rat primary neurons exposed to amyloid-beta oligomers.

165 ERCaMPs revealed ER calcium depletion in rat primary neurons exposed to various ER stressors.

166 e brains of ApoE4 knock-in (KI) mice, and in primary neurons expressing ApoE4 alleles compared with t

167 or internalization and also inhibited CME in primary neurons expressing mutant huntingtin, showing di

168 human SH-SY5Y neuroblastoma cells and mouse primary neurons expressing mutant LRRK2 variants.

169 Furthermore, knockdown of GAK in rat primary neurons expressing the A53T mutation of alpha-sy

170 ysosome biology and the autophagy pathway in primary neurons expressing the human LRRK2-G2019S or LRK

171 d Dkk1 protein on whole-genome expression in primary neurons, finding a common pathway suggestive of

172 In an attempt to predict primary neuron firing under natural conditions of sensor

173 ivity, we used a recently developed model in primary neurons for inducing alphaSyn pathology.

174 hese activities of CLIP-170 were required in primary neurons for normal dendritic morphology.

175 Using primary neurons from a well-characterized Abeta precurso

176 Moreover, CC and caffeine protected primary neurons from Abeta-induced cell death and suppre

177 7,8-DHF protected primary neurons from Abeta-induced toxicity and promoted

178 eins and defective mitochondrial function in primary neurons from AbetaPP mice compared with wild-typ

179 , here, we asked whether CLR01 could protect primary neurons from Alzheimer's disease-associated syna

180 n, Arf4 overexpression rescues spine loss in primary neurons from an Alzheimer's disease-related apol

181 ary mouse neurons, and Grn-haploinsufficient primary neurons from an FTD mouse model.

182 TTR mRNA and Western blot analysis show that primary neurons from APP23 mice transcribe TTR mRNA, and

183 4-3-3theta overexpression, neurite length of primary neurons from BAC transgenic G2019S-LRRK2 mice re

184 Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in

185 Further, using primary neurons from BACHD mice, for the first time, we

186 ial deficiencies in postmortem HD brains and primary neurons from BACHD mice.

187 dies and altered differentiation of cultured primary neurons from Clcn4(-/-) mice or after mRNA knock

188 capsaicin-induced Ca(2+) influx in cultured primary neurons from dorsal root ganglia (DRG).

189 We use live-cell imaging and RNAi in primary neurons from GFP-LC3 transgenic mice to show tha

190 family members (A, B, and C) protects mouse primary neurons from hypoxia-induced delayed death.

191 Using primary neurons from newborn mice of either sex in a red

192 In contrast, stimulation of primary neurons from rats and SH SY5Y cells with TNF, wh

193 To address this issue, we transduced primary neurons from Sprague-Dawley rats or APP(-/-) mic

194 uced synaptic alterations, and cell death in primary neurons from Tg2576 mice, and we sought to deter

195 nd increased apoptotic neuronal death in the primary neurons from the AbetaPP mice relative to the WT

196 decreased in the hippocampus and in cultured primary neurons from the brains of the humanized mice.

197 th UNC5C in the peripheral area of the GC of primary neurons from the cerebellar external granule lay

198 n this study, using postmortem HD brains and primary neurons from transgenic BACHD mice, we identifie

199 erograde axonal transport of mitochondria in primary neurons from transgenic mice expressing familial

200 In primary neuron-glia co-cultures from P0 mouse hippocampi

201 m-induced dopaminergic neurotoxicity both in primary neuron-glia cultures (at subnanomolar concentrat

202 used in biomedical applications, on cultured primary neurons harvested from postnatal day 0-1 mouse b

203 However, the neuronal derived inputs for primary neurons have not been systematically identified.

204 In primary neurons, HIF-1alpha was stabilised by FG4592 (30

205 g organotypic hippocampal slice cultures and primary neuron hippocampal cultures from Arp2/3 conditio

206 Here, we observed that treatment of human primary neurons (HPNs) with methamphetamine and HIV gp12

207 idate a quantitative assay for pff uptake in primary neurons, implicate lysosomal processing as the m

208 ostsynaptic PSD95 in long-term cultured live primary neurons in 96 well microplates, and uses automat

209 We found that synthetic lcn2 is cytotoxic to primary neurons in a dose-dependent manner, but is innoc

210 f plasticity genes is observed both in mouse primary neurons in culture and in vivo in the mouse sens

211 is study, we investigated the role of tPA on primary neurons in culture and on brain recovery and pla

212 Accordingly, Psidin-deficient primary neurons in culture display growth cones with sig

213 Using rodent primary neurons in culture, we found that inhibition of

214 Altering GSH:GSSG ratios in mouse primary neurons in vitro also induced hyperfusion.

215 recovery after photobleaching experiments in primary neurons, in different conditions of synapse dens

216 In vitro, eIF5A1 overexpression in primary neurons increased cell survival and elongated ne

217 ind that endogenous AMPK activation in mouse primary neurons induced an increase of tau phosphorylati

218 , autophagosome biogenesis and maturation in primary neurons is a constitutive process that is spatia

219 er, evidence showing Parkin translocation in primary neurons is controversial, leaving unanswered que

220 s reveal that Golgi exit of BACE1 and APP in primary neurons is tightly regulated, resulting in their

221 s confirmed by immunofluorescence imaging of primary neurons isolated from the frontal cortex of mous

222 In mouse hippocampal primary neurons, knockdown of BACE-1 almost completely b

223 Also, primary neurons lacking sortilin exhibit significantly i

224 presynaptic and postsynaptic compartments of primary neurons, leading to the suggestion that Abeta-me

225 tients with Kufor-Rakeb syndrome or in mouse primary neurons leads to impaired lysosomal degradation

226 In primary neurons, light-mediated REST inhibition increase

227 Using a rat primary neuron model, time-lapse imaging, immunohistoche

228 In primary neurons, mRNAs are translated in proximal dendri

229 Depletion of COH1 in primary neurons negatively interfered with neurite outgr

230 In cell models or primary neurons, neither oligomers nor fibrils of TauRD

231 tenuated by noncell-autonomous events, since primary neurons obtained from p140Cap(-/-) mice show a s

232 and ubiquitin-positive LB-like inclusions in primary neurons of alpha-Syn-KO, beta-Syn-KO, and triple

233 We cultured primary neurons on N-cadherin-coated micropatterned subs

234 dent mannose 6-phosphate receptor, in rodent primary neurons or patient-derived human fibroblasts.

235 Expression of polyQ-htt in either primary neurons or striatal cells from HD knock-in mice

236 In rat hippocampal primary neurons, overexpression of Egr-1 induces BACE-1

237 Primary neurons, particularly dopaminergic neurons, were

238 Embryonic neuroblasts produce 1,500 primary neurons (per hemisphere) that make up the larval

239 th and truncated recombinant alpha-syn enter primary neurons, probably by adsorptive-mediated endocyt

240 n binding partner recruitment by Set-beta in primary neurons, raising the hypothesis that nuclear Set

241 Knockdown of clusterin in primary neurons reduced Abeta toxicity and DKK1 upregula

242 Here we show that toxin-treated primary neurons release signaling molecules derived from

243 pL2 cells have physiological similarities to primary neurons, representing a novel and advantageous m

244 ipulations increasing neurotransmission from primary neurons rescues aging-associated neuronal defici

245 SK2656157 or overexpression of PERK-K618A in primary neurons rescues the loss of dendritic outgrowth

246 ing Generalised Linear Models, we found that primary neuron responses were poorly predicted by whiske

247 Moreover, TMEM175 deficiency in rat primary neurons resulted in increased susceptibility to

248 Analysis of primary neurons revealed that neurons tolerate only slig

249 vels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal

250 e addition of preformed alpha-syn fibrils to primary neurons seeds formation of insoluble alpha-syn i

251 During BoNT/A challenge using primary neurons, select derivatives protected SNAP-25 by

252 cno mutant primary neurons show a significant reduction of Robo loc

253 06 expression in differentiated rat cortical primary neurons significantly increased secreted levels

254 lin in Chinese hamster ovary 7WD10 cells and primary neurons significantly reduces Abeta production b

255 Our results suggest that in a primary neuron, SNARE/SM protein complexes containing sy

256 HEK293 cells and primary neurons spontaneously internalized Tau of n >/=

257 Furthermore, 7A rescued primary neurons subjected to oxidation, EC50 of 0.04 vs

258 hibitors efficiently blocked neurite loss in primary neurons, suggesting that increased COX activity

259 The toxicity of TRAIL in primary neurons suggests that TRAIL signaling participat

260 uch higher levels of oxidative stress in rat primary neurons than do the oligomers formed initially,

261 ive at inducing intracellular aggregation in primary neurons than unmodified alphaS (alphaSun).

262 are endocytosed into signaling endosomes by primary neurons that activate TrkB-dependent signaling,

263 y embryonic period, neuroblasts generate the primary neurons that constitute the larval brain.

264 Here, we show that primary neurons that express a synapsin-driven Cav-1 vec

265 Primary neurons that were found with accumulated oligome

266 t-generation inhibitors are poorly active in primary neurons, the cholesterol-conjugated compounds ar

267 In this study, we show that in human primary neurons, the combination of HIV proteins and met

268 In primary neurons, they enable regulation of microtubule d

269 Here, we observed that exposure of cultured primary neurons to Abeta trimers isolated from brain tis

270 Here we used mammalian primary neurons to examine the function of the PINK1/Par

271 of the existing culture models using animal primary neurons to investigate HSV-1 infection of the CN

272 e tracking of fluorescent virus particles in primary neurons to measure anterograde and retrograde ax

273 licited by brefeldin A treatment, we exposed primary neurons to three different Parkinson's disease (

274 iate targeting of olfactory sensory neurons (primary neurons), to the posteroventral main olfactory b

275 g antibody with expression of DSCAM shRNA in primary neurons totally abolished Netrin-1-induced JNK a

276 ntity plus Notch-mediated sister fate govern primary neuron trajectories, whereas temporal fate diver

277 assembly assays and TIRF microscopy, and in primary neurons using live-cell imaging, that p150(Glued

278 mutant htt in embryonic HD(140Q/140Q) mouse primary neurons was intact during cell death and when ce

279 ltered by anti-cancer treatments in cultured primary neurons, we discovered that doxorubicin, a commo

280 Following WNV infection of primary neurons, we found that Asyn protein expression i

281 Using these functional assays in primary neurons, we identified several PTMs whose altera

282 Here, using adult mouse primary neurons, we investigate the role of Ca(2+), its

283 Here, using both transformed cell lines and primary neurons, we investigated the functional impact o

284 Using human APP-overexpressing primary neurons, we observed significantly decreased Abe

285 Using rat primary neurons, we observed that gp120 promotes a time-

286 ly encoded voltage indicators in dissociated primary neurons, we show that at small nerve terminals K

287 e observed in mammalian cells, as well as in primary neurons, where alpha-Syn(G51D) was enriched in t

288 f4 knockdown also decreases spine density in primary neurons, whereas Arf4 overexpression promotes sp

289 32 and miR-212 induces apoptosis in cultured primary neurons, whereas their overexpression is neuropr

290 sed microglial phagocytosis of PC12 cells or primary neurons, which was blocked by inhibition of MerT

291 n conditioned media of mutant tau expressing primary neurons, while the secretion of endogenous wild-

292 rotoxicity by treating 4E-BP1-overexpressing primary neurons with alpha-synuclein preformed fibrils,

293 Treatment of cortical cells or primary neurons with fisetin resulted in significant dec

294 Furthermore, a mixed culture assay of primary neurons with HEK293 cells expressing different A

295 enic mouse production, and magnetofection of primary neurons with luciferase reporters and signal tra

296 We found that preincubation of primary neurons with PolyP reduced glutamate-induced and

297 n of dendritic growth; in fact, treatment of primary neurons with Semaphorin 3A rescues Ndr2 knock-do

298 tient fibroblasts expressing mutant PARK9 or primary neurons with silenced PARK9 exhibited increased

299 Finally, we showed that treatment of primary neurons with the ECE2 inhibitor during recycling

300 toxicity that combines the verisimilitude of primary neurons with the flexibility and scalability of