ライフサイエンスコーパス: PC12 cell

1 ignaling as well as the neurite outgrowth of PC12 cells.

2 y and population-level activation of TrkA in PC12 cells.

3 , were sufficient to induce EF2K turnover in PC12 cells.

4 elease under hypoxic stimulation from living PC12 cells.

5 y to reconstitute secretion in permeabilized PC12 cells.

6 recorded single-vesicle release events from PC12 cells.

7 resumably other proteins) forms a complex in PC12 cells.

8 D) in the cytosol and in the mitochondria of PC12 cells.

9 well as after oxygen-glucose deprivation in PC12 cells.

10 els sharply decrease in fully differentiated PC12 cells.

11 E5 potently acidifies recycling endosomes in PC12 cells.

12 iR-29c resulted in a 46 +/- 5% cell death in PC12 cells.

13 participates in insulin signaling pathway in PC12 cells.

14 blocks Ras signaling in rat pheochromocytoma PC12 cells.

15 ation of dopamine to be 0.59 +/- 0.07 muM in PC12 cells.

16 monitoring of exocytotic events from single PC12 cells.

17 in adult rat dorsal root ganglion axons and PC12 cells.

18 teasome activity caused by mutant Twinkle in PC12 cells.

19 se was similarly mutant Twinkle-dependent in PC12 cells.

20 tine-stimulated catecholamine secretion from PC12 cells.

21 aling endosomes in rat embryonic neurons and PC12 cells.

22 aling specificity achieved by NGF and EGF in PC12 cells.

23 ]norepinephrine release from non-transfected PC12 cells.

24 its ability to support neurite outgrowth of PC12 cells.

25 basis of maintenance of neurite outgrowth in PC12 cells.

26 motes H-Ras-dependent neurite outgrowth from PC12 cells.

27 ith intracellular membranes in nematodes and PC12 cells.

28 ted also by the encounter of Atx and CCOX in PC12 cells.

29 s were much less notable in undifferentiated PC12 cells.

30 nt with suppression of caspase 3 activity in PC12 cells.

31 ors Egr-1 and Sp1 in adrenal medulla-derived PC12 cells.

32 fission in control and syt IV overexpressing PC12 cells.

33 ks RhoA suppression of PPARgamma agonists in PC12 cells.

34 l ganglion cell model line RGC5 and neuronal PC12 cells.

35 tion of tyrosine hydroxylase in vitro and in PC12 cells.

36 P analogs may stimulate neurite outgrowth in PC12 cells.

37 th factor (NGF)-induced neurite outgrowth in PC12 cells.

38 phosphorylation of most B'beta substrates in PC12 cells.

39 ces neurite outgrowth and differentiation in PC12 cells.

40 t vesicle exocytosis in permeable and intact PC12 cells.

41 ase-activating polypeptide) elevates cAMP in PC12 cells.

42 han the wild type when each was expressed in PC12 cells.

43 romote neuritogenesis and differentiation of PC12 cells.

44 ranscription and alters TH mRNA stability in PC12 cells.

45 rns differentiation and neurite outgrowth in PC12 cells.

46 ion in undifferentiated rat pheochromocytoma PC12 cells.

47 cantly reduced by FG4592 or Bayer 85-3934 in PC12 cells.

48 bility to induce neuronal differentiation of PC12 cells.

49 measuring the Rexocytosis for populations of PC12 cells.

50 flippase activity, and neurite extension in PC12 cells.

51 a cancer cells, and low adhesion neuron-like PC12 cells.

52 d secondary necrosis, respectively) in these PC12 cells.

53 s is the first description of AR function in PC12 cells.

54 n, proliferation and survival of SH-SY5Y and PC12 cells.

55 o known as CADPS) and ubiquitous Munc13-2 in PC12 cells.

56 nstream activation of PI3-K delta and Rac in PC12 cells.

57 e of the small dense core vesicle subpool in PC12 cells.

58 vation at the growth cone of differentiating PC12 cells.

59 iggered vesicle exocytosis in neuroendocrine PC12 cells.

60 distribution in unstimulated neuroendocrine PC12 cells.

61 ot two, of vesicles stored and released from PC12 cells.

62 s and endocytic structures in neuroendocrine PC12 cells.

63 er release across a single pheochromocytoma (PC12) cell.

64 secretion from individual pheochromocytoma (PC12) cells.

65 secretion from individual pheochromocytoma (PC12) cells.

66 gle vesicles isolated from pheochromocytoma (PC12) cells.

67 ta-treated, differentiated pheochromocytoma (PC12) cells.

68 has internalization in rat pheochromocytoma (PC12) cells.

69 We conducted evaluations in PC12 cells, a model for neuronal development, with each

70 PC12 cells, a model neuroendocrine cell line, express mu

71 In PC12 cells, a small fraction of nitrated Hsp90 was locat

72 In PC12 cells, a well-established model for sympathetic neu

73 f Abeta(1-42) oligomers enter the nucleus of PC12 cells, accumulate as insoluble oligomeric species,

74 n the SN of 22-month-old mutant mice, and in PC12 cells after 48 h transfection of mutant Twinkle.

75 der high-K(+) buffer stimulation from living PC12 cells also demonstrates that SiNW-FETs can serve as

76 ffects on elevated K(+)-induced secretion in PC12 cells, although m-tomosyn-2 was novel in strongly a

77 phorylation by tetrabromo-2-benzotriazole in PC12 cells and by the identity of in vivo and in vitro p

78 es ("closed" vs. "open") of syntaxin-1 using PC12 cells and Caenorhabditis elegans.

79 enhances the outgrowth of neurites from both PC12 cells and chick embryonic dorsal root ganglia (DRG)

80 bited a sialidase activity that desialylated PC12 cells and could be inhibited by Tamiflu, a neuramin

81 -29c down-regulation and DNMT3a induction in PC12 cells and curtailed ischemic cell death (by 64 +/-

82 here PLCbeta1 or C3PO were down-regulated in PC12 cells and find substantial differences in miR proce

83 urs concomitant with evoked release, both in PC12 cells and hippocampal neurons and was abolished upo

84 expression of cathepsin V in neuroendocrine PC12 cells and human neuronal SK-N-MC cells results in p

85 tion-triggered neurotransmitter release from PC12 cells and in the brains of live animals.

86 sphorylate the neurotrophin receptor TrkA in PC12 cells and increase neurite outgrowth from developin

87 yt I-PS binding, we varied the PS content in PC12 cells and liposomes and studied the effects on the

88 nificant decrease in its level of binding to PC12 cells and mouse cortical/hippocampal neurons.

89 ed in synergistic increases in extensions of PC12 cells and neurite densities and protrusions in prim

90 ided by ropinirole, a D2 receptor agonist in PC12 cells and primary cultures of dopamine neurons.

91 eurite elongation and neurite number both in PC12 cells and primary hippocampal neurons.

92 IP(6) intracellular ratio in differentiated PC12 cells and primary neurons.

93 HIF) prolyl hydroxylases (PHD) inhibitors on PC12 cells and primary rat neurons following oxygen-gluc

94 a protein of the predicted size of uORF5 in PC12 cells and rat brains.

95 in cellular models of PD, including neuronal PC12 cells and rat dopaminergic ventral midbrain neurons

96 The sequence GVOGEA bound weakly to PC12 cells and strongly to activated Rugli cells or to a

97 expression suggests that both differentiated PC12 cells and sympathetic neurons require low levels of

98 assist in controlled degradation of both the PC12 cells and the device construct, small PCL capsules

99 es impaired secretion in syntaxin-1-depleted PC12 cells and the lethality and lethargy of unc-64 (C.

100 ion results in the retraction of neurites in PC12 cells and the rupture of neuronal synapses by modul

101 and PC12 surfaces, enabling Gal-3 binding to PC12 cells and their phagocytosis via MerTK.

102 e RhoA-inhibiting properties of ibuprofen in PC12 cells and, like ibuprofen, promotes neurite elongat

103 in-specific, extends to proBDNF expressed in PC12 cells, and implies the presence of interacting part

104 ssion of neuronal differentiation markers in PC12 cells, and Ras-induced focus formation in NIH 3T3 c

105 (alpha3* nAChRs) expressed in HEK293 cells, PC12 cells, and rat cortical neurons.

106 ons, native Ric-3 levels were higher than in PC12 cells, and Ric-3 and alpha7 subunits were found in

107 ve oxygen species formation and apoptosis in PC12 cells; and (3) that acetazolamide, chlorthalidone,

108 PC12 cells are a popular model system to study changes d

109 GF-1-mediated reductions of EF2K activity in PC12 cells are due to decreased EF2K protein levels, and

110 PC12 cells are frequently used as a model secretory cell

111 AP-driven survival and neuritic extension in PC12 cells are inhibited following NF-kappaB pathway blo

112 METHODS AND Using PC12 cells as a model of catecholamine synthesizing neur

113 We used PC12 cells as ATP biosensors by loading them with Fluo-4

114 end of the neurites in differentiated living PC12 cells as well as in cultured hippocampal neurons.

115 onversely, Trib3 knockdown protects neuronal PC12 cells as well as ventral midbrain dopaminergic neur

116 oCl(2) and X/XO induced neurite outgrowth in PC12 cells, as determined by an overexpression of neuron

117 l (Ni(2+)) for their effects on neuronotypic PC12 cells, assessing gene transcription involved in the

118 Biological duplicates were generated from PC12 cells at days 0, 3, 7, and 12 following treatment w

119 ffects against H2O2-induced neurotoxicity in PC12 cells at the concentration of 10 muM, with an incre

120 Ectopic expression of Prx1 in PC12 cells attenuated mutant Htt-induced toxicity.

121 ic nerve endings (cardiac synaptosomes), and PC12 cells bearing a sympathetic neuron phenotype.

122 rements of exocytosis from pheochromocytoma (PC12) cells between two types of electrodes, carbon fibe

123 d-type primary cultured cortical neurons and PC12 cells but failed to reach neurites in cells lacking

124 or control (p < 0.029) in neural MES23.5 and PC12 cells, but without altering GCase activity.

125 xogeneous DA samples that were prepared from PC12 cells by a DA release assay were successfully measu

126 promotes both survival and neuritogenesis in PC12 cells by activating NF-kappaB pathway, most likely

127 HIF-1alpha was stabilised in PC12 cells by all the PHD inhibitors at 100 uM except fo

128 es neurotrophin-induced neurite outgrowth in PC12 cells by altering TrkA endocytic traffic, inhibitin

129 n that helps to drive the differentiation of PC12 cells by inhibiting a nuclease that promotes RNA-in

130 ent neurite outgrowth and gene expression in PC12 cells by sorting NGF and the activated/phosphorylat

131 g, and after single-vesicle fusion events in PC12 cells by TIRF micro-scopy.

132 icantly curtailed the post-OGD cell death in PC12 cells (by 54 +/- 6%; p<0.05) and decreased the post

133 Silencing of lncRNA BC088414 in PC12 cells caused reduced mRNA level of Casp6 and Adrb2,

134 -expressed dopaminergic neuronal SH-SY5Y and PC12 cells, cellular models of PD, than that in non-alph

135 imaging demonstrate that the drug effect on PC12 cell clusters is consistent with previous single-ce

136 aging single vesicle exocytotic release from PC12 cell clusters is presented at cell clusters incubat

137 and beta-amyloid each have toxic effects on PC12 cells, comparable to hydrogen peroxide(.) However o

138 Overexpressing md130A in PC12 cells completely eliminated the reduction in neurot

139 Mouse fibroblasts and neuronal PC12 cells cultured in standard microplates were stained

140 ntly applied to trace dopamine exocytosis in PC12 cells cultured on such mMEA chip.

141 own of Sh3rf2 promotes apoptosis of neuronal PC12 cells, cultured cortical neurons, and C6 glioma cel

142 nd its various products were investigated in PC12 cells, cultured rat basal forebrain cholinergic neu

143 We conclude that Nur77 exacerbates PC12 cell death at least partially by aggravating the mi

144 GD-PLL microcapsule degradation and eventual PC12 cell death following a pre-specified period of time

145 In PC12 cells, deletion of endogenous Rhes decreases autoph

146 Previous experiments in PC12 cells demonstrated that the transcription factor zi

147 ES partially inhibited PC12 cell differentiation and cerebellar granule cell mi

148 ain induced robust ERK activation leading to PC12 cell differentiation by targeting specifically to K

149 sory neurons deprived of NGF and compromises PC12 cell differentiation in response to NGF.

150 ing RNA has an effect on the early stages of PC12 cell differentiation, whereas fully differentiated

151 tutive Ser(779) phosphorylation and enhanced PC12 cell differentiation.

152 /2 signaling critical for cell migration and PC12 cell differentiation.

153 reduces ERK1/2 activation, thereby blocking PC12 cell differentiation.

154 TrkA activation and signaling that augments PC12 cell differentiation.

155 Overexpression of UBXD4 in differentiated PC12 cells (dPC12) increased nAChR cell surface expressi

156 dia-like structures in bovine chromaffin and PC12 cells driving the footprint expansion, suggesting t

157 Sialidase treatment of PC12 cells enabled Gal-3 to bind and opsonize the live c

158 utilizing alpha7 nAChR-selective ligands in PC12 cells endogenously expressing alpha7 nAChRs.

159 inant FKBP chimeric clathrin polypeptides in PC12-cell endosomes.

160 in 3a hinge-loop (Munc18-1(Delta317-333)) in PC12 cells engineered to knockdown Munc18-1/2 markedly p

161 In PC12 cells, epidermal growth factor (EGF) induces transi

162 thrin-coated vesicle fractions isolated from PC12 cells even after clathrin function is acutely inhib

163 PC12 cells exhibit precise temporal control of growth fa

164 PC12 cells express five adenylate cyclase (AC) isoforms,

165 ain reaction approaches, we demonstrate that PC12 cells express the Rxt1/NTT4 gene and protein.

166 apidly stretch-injured rat pheochromocytoma (PC12) cells express cellular zinc ion fluctuations that

167 Furthermore, the release of FM1-43 dye from PC12 cells expressing either human full-length alpha-syn

168 yclase activating peptide-27) stimulation of PC12 cells expressing Galphas and XLalphas endogenously

169 was tested in three different models of HD: PC12 cells expressing mutant Httex1 under the control of

170 compounds for potent rescue of viability of PC12 cells expressing mutant huntingtin protein, followe

171 We report that yeast cells and neuron-like PC12 cells expressing polyQ-expanded huntingtin (htt) fr

172 metric analysis to determine:1) viability of PC12 cells following knock-down with MyD88 siRNA compare

173 lar Abeta, and protects rat pheochromocytoma PC12 cells from Abeta toxicity, without inducing any tox

174 , which inhibits chloride transport, protect PC12 cells from apoptosis.

175 isolated from Echinophora cinerea to protect PC12 cells from H2O2-induced cytotoxicity.

176 wed that during exocytosis in chromaffin and PC12 cells, fusion pores formed by smaller vesicles dila

177 When these constructs were coexpressed in PC12 cells, glutamate application induced a conformation

178 and co-expression of RGS14 and Galpha(i1) in PC12 cells greatly enhances H-Ras(G/V) stimulatory effec

179 pendent, as we observed better inhibition on PC12 cells grown on collagen compared to laminin matrice

180 To enhance PC12 cell growth and to assist in controlled degradation

181 In contrast, overexpressing md130A in PC12 cells had little or no effect on the response to et

182 We show that PC12 cells harbor endogenous androgen receptor (AR), who

183 ion of exocytosis at the surface of a single PC12 cell has also been demonstrated with this system.

184 In this state, PC12 cells have a spherical morphology, resume prolifera

185 inhibited FeSO4-induced oxidative stress in PC12 cells (IC50 of 80-200 nM).

186 mine from nerve growth factor-differentiated PC12 cells in a concentration-dependent manner.

187 Neuronal differentiation of PC12 cells in response to NGF is a prototypical model in

188 nd mode of toxicity on rat pheochromocytoma (PC12) cells in both differentiated and undifferentiated

189 myotoxic (to C2C12 cells) and neurotoxic (to PC12 cells) in a concentration- and time-dependent manne

190 (from processes of neuronally differentiated PC12 cells) in light of the heterogeneous formalism yiel

191 porine-induced apoptosis in undifferentiated PC12 cells, in an endocytosis-dependent manner.

192 zo[a]pyrene (BaP) on neurodifferentiation in PC12 cells, in combination with a glucocorticoid (dexame

193 nAChR agonist-triggered Ca(2+) transient in PC12 cells induces activation of CaMKII, leading to sequ

194 In PC12 cells, inhibition of phosphoinositide-3 kinase (PI3

195 cilium formation, whereas USP21 knockdown in PC12 cells inhibits nerve growth factor-induced neurite

196 fatty acids, the outgrowth of neurites from PC12 cells is greatly enhanced.

197 PC12 cells lacking PKA or PLCgamma-1 show significant re

198 did not inhibit T. cruzi invasion of mutant PC12 cells lacking TrkA or of normal cells lacking Trk r

199 Depletion of SgII expression in PC12 cells leads to a decrease in both the number and si

200 an established cell-based assay employing a PC12 cell line overexpressing truncated exon 1 of Htt wi

201 ression reduced Htt-N63 toxicity in a stable PC12 cell line.

202 e capacity against Abeta-induced toxicity on PC12 cell lines (viability assessed by MTT assay and int

203 eta and alphaS fibril formation and protects PC12 cell lines against Abeta-induced toxicity.

204 nd have used COS-7 cells, stably transfected PC12 cell lines and transgenic Drosophila melanogaster t

205 ire of docking sites and the availability of PC12 cell lines stably transfected with chimeric recepto

206 PC12 cells loaded with Fura-2AM show a rapid increase in

207 cell fluorescence microscopy in dopaminergic PC12 cells loaded with the calcium-sensitive dye Fura-2.

208 However, the active form of CAPS bound to PC12 cell membranes or to liposomes containing PI(4,5)P2

209 iles by short oligo array using an inducible PC12 cell model expressing an N-terminal huntingtin frag

210 Using an inducible PC12 cell model of Huntington's disease (HD), we show th

211 nt TBP-mediated down-regulation of TrkA in a PC12 cell model of SCA17.

212 In this study, we have used the PC12 cell model to elucidate the mechanisms by which sub

213 and isoliquiritigenin increased MMP in both PC12 cell models in a similar range as the positive cont

214 In PC12 cells, native BgtRs trafficked to the cell surface

215 In DA PC12 cells, neither vector decreased expression of rat S

216 proteins remain bioactive as demonstrated by PC12 cell neurite extension in response to released nerv

217 The effects of S-PrP on PC12 cell neurite outgrowth and Schwann cell migration w

218 S-PrP promoted PC12 cell neurite outgrowth.

219 In living PC12 cell neurites, GFP-dynein puncta travel in both the

220 tudy used nerve growth factor differentiated PC12 cells (NGFDPC12 cells) and found that lysosomal mem

221 Culturing PC12 cells on top of the MEAs has been achieved by modif

222 n response to mutant Htt expressed in either PC12 cells or immortalized striatal cells exposed to 3-n

223 and it increased microglial phagocytosis of PC12 cells or primary neurons, which was blocked by inhi

224 Protein extracts from PC12 cells overexpressing the amino-terminal fragment of

225 In rat pheochromocytoma PC12 cells overexpressing Trk (PCtrk cells), Neurotropin

226 s of cellular injury toward undifferentiated PC12 cells (PC12(undiff)).

227 cholera toxin in protein kinase A-deficient PC12 cells promoted neurite outgrowth in a cAMP-independ

228 Interfering with myosin VI function in PC12 cells reduced the density of SGs near the plasma me

229 The effects of syt IV on fusion pores in PC12 cells resembled the effects on fusion pores in pept

230 ifying potassium (GIRK) channels in neuronal PC12 cells, resulting in loss of function.

231 PC/C(Cdh1) by mutant but not wild-type AR in PC12 cells results in enhanced neurite outgrowth which i

232 ng the transcriptome of PACAP-differentiated PC12 cells revealed an increase in the expression of nuc

233 trically analyzed catecholamine release from PC12 cells, revealing that charge neutralization of 5RK

234 Furthermore, in PC12 cells selected for resistance against Abeta, increa

235 PC12 cells showed a similar profile.

236 -mum-wide ultramicroelectrodes from a single PC12 cell showing that the subcellular heterogeneity in

237 scued the inhibition of neurite outgrowth in PC12 cells silenced for RSK2, revealing that PLD1 is a m

238 In neuronal PC12 cells, silencing of ATF4 enhanced cell death in res

239 -I expression ratio and downregulated p62 in PC12 cells, so did FG4592 (30 uM) and DMOG (100 uM) in n

240 was also observed in extracts prepared from PC12 cells stably expressing PC1/3 or PC2.

241 PC12 cells stably overexpressing Numb isoforms lacking t

242 phorylation is AR-dependent, as it occurs in PC12 cells stably transfected with AR but in neither wil

243 Using PC12 cells stably transfected with short-hairpin RNA tar

244 We show that PC12 cells stimulated with nerve growth factor (NGF) exh

245 thermore, CaBP5 expression in NGF-stimulated PC12 cells stimulates neurite outgrowth and dopamine exo

246 harmacological inhibition of PLD1 or RSK2 in PC12 cells strongly impaired neuronal growth factor (NGF

247 Here, we show that in PC12 cells sublethal concentrations of aggregated Abeta(

248 on, and antibody blockade of non-transfected PC12 cells suppressed plasminogen activation.

249 Moreover, it has been shown in PC12 cells that the localization of the major splice for

250 In untransfected SK-N-SH or PC12 cells, the introduction of siRNA(GAPDH) [small inte

251 neurite outgrowth and vesicle exocytosis in PC12 cells, these results suggest that CaBP5 plays a rol

252 With 100 mV steps in PC12 cells, this probe produced DeltaF/F = 26% (4 muM di

253 In PC12 cells, this system significantly improves light-ind

254 Co-exposure of PC12 cells to a mixture of dieldrin and lindane revealed

255 We exposed PC12 cells to chlorpyrifos, diazinon or parathion in the

256 us neurotransmitters and circuits, employing PC12 cells to explore the targeting of neuroactive pepti

257 questions we used amperometry recording from PC12 cells to investigate the kinetics of exocytosis.

258 ted in the 6-hydroxydopamine (OHDA)-lesioned PC12 cells to investigate the mechanisms underlying Nur7

259 ibody blockade, we confirmed that binding of PC12 cells to peptide III-7 was mediated by integrin alp

260 We transiently transfected this vector in PC12 cells to test the effect of several cytokines on p3

261 pecific genes, plays a key role in switching PC12 cells to their differentiated state.

262 PC12 cells transfected with different ALK mutant variant

263 of wtPC12 cells rich in TrkA with high REST PC12 cells transfected with L1CAM documented the transac

264 o differences in either percent viability of PC12 cells transfected with MyD88 compared to negative c

265 PC12 cells transfected with pEGFP-N1 produced, as antici

266 ting XBP1s neuroprotection, we found that in PC12 cells treated with Abeta oligomers, XBP1s prevents

267 ly described a reduction of EF2K activity in PC12 cells treated with NGF or forskolin.

268 ATF4 levels are also upregulated in neuronal PC12 cells treated with the dopaminergic neuronal toxins

269 In PC12 cells, treatment with premiR-29c prevented OGD-indu

270 In PC12 cells, tyrosine phosphorylation of INSR and IRS-1 i

271 monitoring and screening of NA released from PC12 cells under K(+) ion-extracellular stimulation proc

272 poral chemical changes in living colonies of PC12 cells under nerve growth factor (NGF) stimulation f

273 7A reduced ROS production in PC12 cells under oxidizing conditions, IC50 of 0.08 vs 2

274 red from seven different locations on single PC12 cells using alternately constant-potential amperome

275 released from vesicles in NGF-differentiated PC12 cells using carbon-fiber amperometry, and relative

276 of large dense-core vesicles (LDCVs) in live PC12 cells using total internal reflection fluorescence

277 we identified approximately 1200 proteins in PC12 cell vesicle-enriched fractions, with DCV-associate

278 In PC12 cells, vesicles that harbor these different synapto

279 on dopamine release and neurite outgrowth of PC12 cells was analyzed using ELISA and fluorescent labe

280 in both naive and terminally differentiated PC12 cells was shown to be intermediate between NGF and

281 ously shown to activate NGF signaling in rat PC12 cells was used as an NGF signaling agonist, and rec

282 tracellular Ca(2+) rise by these peptides in PC12 cells was: CST-WT > CST-Ser-364 > CST-Val-367.

283 Using exocytosis-incompetent PC12 cells, we demonstrate that footprint enlargement is

284 Using primary neurons and PC12 cells, we demonstrate that miR-132/212 controls cel

285 ysis of nerve growth factor (NGF)-stimulated PC12 cells, we identified a two-dimensional phospho-ERK

286 privation and reoxygenation (OGD/R) model in PC12 cells, we show that 2-day pretreatment with green t

287 First, using dynamic FRET analysis in PC12 cells, we show that CDO occurs following assembly o

288 Dopamine-secreting PC12 cells were housed within newly formulated alginate-

289 mine beta-hydroxylase (DBH) gene expression, PC12 cells were transfected with expression vector for f

290 of DA release from living pheochromocytoma (PC12) cells were performed.

291 ously modified by Cys(85) S-nitrosylation in PC12 cells, which are a well established model system fo

292 hanced surface expression of the receptor in PC12 cells, which endogenously express the A2A receptor.

293 When treated with nerve growth factor, PC12 cells will differentiate over the course of several

294 Depolarization of neuroendocrine PC12 cells with 56 or 95 mm KCl buffers increased peak C

295 wo exocytotic peak populations obtained from PC12 cells with a disk carbon fiber microelectrode and w

296 hrin in DCV biogenesis, we stably transduced PC12 cells with an inducible short hairpin RNA targeting

297 Modulation of PAI-1 levels by incubating PC12 cells with anti-PAI-1 IgG caused a marked decrease

298 nd nonclustered molecules at the membrane of PC12 cells with single-molecule precision.

299 We challenged PC12 cells with small amyloid fibrils composed of either

300 luorescence) imaging of fluorescently marked PC12 cells with sustained protein phosphorylation activi