ライフサイエンスコーパス: primary neuron

1 n ectopic expressing systems and in striatal primary neurons.

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

3 mediated filopodia formation and dynamics in primary neurons.

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

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

6 alized pathway for constitutive autophagy in primary neurons.

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

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

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

10 lular ratio in differentiated PC12 cells and primary neurons.

11 pitation experiments and coimmunostaining in primary neurons.

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

13 results in mouse cardiomyocytes and cultured primary neurons.

14 glion neurons, validating Slit2 signaling in primary neurons.

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

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

17 rther confirmed to regulate Dlg4 splicing in primary neurons.

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

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

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

21 MG selectively activated GABAA receptors in primary neurons.

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

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

24 mitochondria, with broken cristae in AbetaPP primary neurons.

25 tiator caspase activated in rotenone-treated primary neurons.

26 antibody to LRP1 suppressed Abeta uptake in primary neurons.

27 -2a cells and dendritic spine development in primary neurons.

28 were also increased from progranulin-treated primary neurons.

29 e-forming alpha-subunit Na(v)1.1 in cultured primary neurons.

30 expression of Bag1-L augmented cell death in primary neurons.

31 ronal and neuronal cells, including in mouse primary neurons.

32 ely 96% reduction of this protein complex in primary neurons.

33 nregulated by tetrodotoxin (TTX) in cultured primary neurons.

34 iod simply by an increase in arbor volume of primary neurons.

35 on and down-regulated by impulse blockade in primary neurons.

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

37 ite outgrowth and morphological effects upon primary neurons.

38 eases BACE1 and elevates Abeta production in primary neurons.

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

40 ated and regulates endosomal trafficking, in primary neurons.

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

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

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

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

45 n cells and enhanced neuronal development in primary neurons.

46 ctive transport of polysomes in dendrites of primary neurons.

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

48 ing expression in transfected cell lines and primary neurons.

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

50 estrates spine dynamics and morphogenesis in primary neurons.

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

52 r was demonstrated in heterologous cells and primary neurons.

53 neuroserpin polymers in both HeLa cells and primary neurones.

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

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

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

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

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

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

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

61 channels leading to caspase-1 activation in primary neurons and astrocytes.

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

63 eriphery of M17 cells or neuronal process of primary neurons and correlated with reduced spine densit

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

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

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

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

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

69 APK-dependent phosphorylation using cultured primary neurons and HEK-TrkB cells, both of which expres

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

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

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

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

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

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

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

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

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

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

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

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

82 In isolated primary neurons and microglia, TNF-alpha-induced TNF-R1

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

84 In vitro studies of primary neurons and mouse embryonic fibroblasts showed t

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

86 ts actively translocating to distal axons in primary neurons and neuronal cell lines.

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

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

89 fects of the M(1) mAChR on APP processing in primary neurons and on the development of amyloid pathol

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

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

92 in the background of FOXO knockdown in both primary neurons and postnatal rat pups in vivo restores

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

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

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

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

97 -43 nuclear export in immortalized cells and primary neurons and strongly potentiated the recruitment

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

99 2 induce clustering in transfected cells and primary neurons and that these complexes included other

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

101 1) to promote inositol phosphate turnover in primary neurons and to increase c-fos and arc RNA expres

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

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

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

105 transfected APP or APP RNA interference into primary neurons and used electrophysiological techniques

106 g TrkB-Fc during CX614 treatment of cultured primary neurons and was blocked by nifedipine, ryanodine

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

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

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

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

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

112 e performed these studies in cultured cells, primary neurons, and mice.

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

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

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

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

117 ll surface levels, both in cell lines and in primary neurons, and the GBP-induced reduction in calciu

118 he factor whose absence induced autophagy in primary neurons, and this activation was mammalian targe

119 In transfected primary neurons, apoE expression increased dramatically

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 c cell death removes an average of 30-40% of primary neurons around the time of hatching.

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

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

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

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

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

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

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

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

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

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

135 In primary neurons, bexarotene ameliorated the damaged dend

136 In primary neurons, bexarotene enhanced the dendritic compl

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

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

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

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

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

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

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

148 anterograde spread using a compartmentalized primary neuron culture system.

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

150 been hindered by limitations associated with primary neuron culture.

151 Primary neurons cultured from the brains of neonatal T40

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

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

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

155 nd current clamp measurements were made from primary neuron cultures of the pleural ganglion (PVC) an

156 Furthermore, treatment of primary neuron cultures with IFNalpha resulted in dose-d

157 xicity while its depletion enhances death in primary neuron cultures.

158 ha did not have a direct antiviral effect in primary neuron cultures.

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

160 ration in Chinese hamster ovary cells and in primary neurons, demonstrating its physiological role in

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

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

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

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

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

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

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

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

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

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

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

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

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

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 of AD patients or healthy controls protected primary neurons from Abeta toxicity.

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

178 7,8-DHF protected primary neurons from Abeta-induced toxicity and promoted

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

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

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

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

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

184 4-3-3theta overexpression, neurite length of primary neurons from BAC transgenic G2019S-LRRK2 mice re

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

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

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

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

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

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

191 Additional neuronal cell lines and primary neurons from Huntington disease mice also showed

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

193 Using primary neurons from mice transgenic or deficient for ap

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

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

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

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

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

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

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

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

202 w levels of neuronal expression of ceacam1a, primary neurons from wild-type and ceacam1a knockout mic

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

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

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

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

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

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

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

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

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

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

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

214 of exon 4 and exon 16 frequently occurred in primary neurons, indicating that newly identified varian

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

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

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

218 ated that HIV-tat-induced apoptosis in human primary neurons is dependent on N-methyl-D-aspartate rec

219 role in promoting growth and regeneration of primary neurons is not well established.

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

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

222 Also, primary neurons lacking sortilin exhibit significantly i

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

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

225 In primary neurons, light-mediated REST inhibition increase

226 diated by macroautophagy in cell culture and primary neuron models of SCA7.

227 In primary neurons, mRNAs are translated in proximal dendri

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

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

230 demonstrating increased neurite outgrowth in primary neurons obtained from LANP null mice, which is a

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 Thereby, the relatively small number of primary neurons of each primary lineage set up the compa

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

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

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

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

238 Primary neurons, particularly dopaminergic neurons, were

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

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

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

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

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

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

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

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

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

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

249 Analysis of primary neurons revealed that neurons tolerate only slig

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

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

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

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

254 06 expression in differentiated rat cortical primary neurons significantly increased secreted levels

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 ockdown decreased insulin receptor levels in primary neurons, suggesting that decreased neuronal surv

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

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

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

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 a small number of divisions and produce the primary neurons that form the functioning larval brain.

266 Here, we show in heterologous cells and primary neurons that stargazin is physiologically S-nitr

267 Primary neurons that were found with accumulated oligome

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

269 In rat hippocampal primary neurons, the knockdown of Sig-1Rs by siRNAs caus

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

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

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

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

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

275 1 expression is critical for the survival of primary neurons under stress conditions including trophi

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

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

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

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

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

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

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

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

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

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

286 In addition, minocycline prevents death of primary neurons when they are cocultured with ts1-infect

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

288 movement of LysoTracker-positive vesicles in primary neurons, where processive bidirectional motility

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

290 32 and miR-212 induces apoptosis in cultured primary neurons, whereas their overexpression is neuropr

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

292 s take up different fates: deep cells become primary neurons while superficial cells stay as progenit

293 Treatment of rat primary neurons with fibrillar amyloid beta1-42 (Abeta)

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

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

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

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