ライフサイエンスコーパス: nocodazole

1 se and excessive blebbing in the presence of nocodazole).

2 ntaining a mitotic arrest in the presence of nocodazole.

3 sing cells fail to arrest in the presence of nocodazole.

4 isrupted by microtubule depolymerising agent nocodazole.

5 t increase in MT mass in cells released from nocodazole.

6 highly similar to microtubule disruption by nocodazole.

7 following treatment with the spindle poison nocodazole.

8 ules are no longer resistant to low doses of nocodazole.

9 MCAK or Nuf2 or treatment with low doses of nocodazole.

10 confirmed by inhibition with brefeldinA and nocodazole.

11 microtubules are completely depolymerized by nocodazole.

12 easing the G2/M checkpoint arrest induced by nocodazole.

13 in A, or when microtubules were disrupted by nocodazole.

14 ive drugs such as colcemid, vinblastine, and nocodazole.

15 3 cells were treated with 1-butanol, BFA, or nocodazole.

16 xcess thymidine or in mitosis (M phase) with nocodazole.

17 for bulk translocation, we disrupted it with nocodazole.

18 man (RPE1) cells dividing in the presence of nocodazole.

19 n of BIG1 is inferred from its inhibition by nocodazole.

20 raction by a microtubule depolymerizing drug nocodazole.

21 itive to the microtubule depolymerizing drug nocodazole.

22 d microtubules against depolymerization with nocodazole.

23 sister chromatid cohesion and inviability in nocodazole.

24 -depolymerizing agents such as colchicine or nocodazole.

25 tubule drugs, including the reversible agent nocodazole.

26 han that in wild-type cells after exposed to nocodazole.

27 ation of nuclei or the microtubule inhibitor nocodazole.

28 ture Pds1p degradation in cells treated with nocodazole.

29 lay in mitotic exit following the removal of nocodazole.

30 but not in cells arrested in prometaphase by nocodazole.

31 y enhanced resistance to depolymerization by nocodazole.

32 response to the mitotic destabilizing agent nocodazole.

33 ydrocarbon beta-naphthoflavone and the azole nocodazole.

34 in ice-cold conditions or in the presence of nocodazole.

35 ed with the microtubule-depolymerizing agent nocodazole.

36 omosome congression, and sensitized cells to nocodazole.

37 cells treated with the microtubule inhibitor nocodazole.

38 y 50 muM of the microtubule-disrupting agent nocodazole.

39 nd 10 muM), colchicine (10 and 100 muM), and nocodazole (10 and 100 muM) to disturb microtubule netwo

40 presence of cytochalasin D (3 x 10(-7)m) and nocodazole (3 x 10(-6)m), inhibitors of alpha-actin and

41 te cancer cells to paclitaxel (1 mumol/L) or nocodazole (5 mug/mL) inhibited androgen-dependent AR nu

42 yclin that functions in G1/S transition, and nocodazole, a G2/M phase synchronizer, doubles HDR effic

43 yostelium to identify genetic suppressors of nocodazole, a microtubule depolymerizer.

44 MSCs and lymphoblasts from SDS patients with nocodazole, a microtubule destabilizing agent, led to in

45 specific LC1 antisense oligonucleotides and nocodazole, a microtubule disruptor, significantly prolo

46 Applications of 5-hydroxyindole and nocodazole, a microtubule disruptor, significantly slowe

47 Nocodazole, a microtubule inhibitor, did not disperse ag

48 ster chromatid separation in the presence of nocodazole, a microtubule-depolymerizing drug.

49 crotubule destabilizing agents colchicine or nocodazole abrogated vesicular transport but not the flo

50 has been shown that depolymerizing MTs with nocodazole abrogates the stathmin-depletion induced cell

51 es and, on microtubule depolymerization with nocodazole, activate the mitotic checkpoint.

52 Nocodazole activated Plk3 and its activation was blocked

53 Disruption of microtubule networks by nocodazole activates Mps1 and promotes TGF-beta-independ

54 Although the MT depolymerizing agent nocodazole affected dynamic MTs, HIV-1 particles localiz

55 microtubule polymerization by colchicine and nocodazole affected the kinetics of actin coat formation

56 contributed to prometaphase accumulation in nocodazole after partial Mps1 inhibition and was require

57 pening of microtubule dynamics with low dose nocodazole all result in significantly decreased in syna

58 gly, transient but prolonged treatments with nocodazole allow completion of mitosis, but the daughter

59 pulse of the microtubule-depolymerizing drug nocodazole allowed spindle assembly in these td-kip3 doc

60 Treatment of T98G and HCT116 cells with nocodazole alone resulted in a robust mitotic block with

61 ubation of stably transfected SCC cells with nocodazole, an inhibitor of mitosis, caused a slower acc

62 ability, but inhibits Golgi fragmentation by nocodazole and brefeldin A and also halts cells in early

63 also prevented by the microtubule inhibitor nocodazole and by the inhibition of cytoplasmic dynein,

64 by the destabilization of microtubules with nocodazole and by the phosphatidylinositol 3-kinase inhi

65 fects of microtubule-depolymerizing reagent, nocodazole and colchicine, on GLUT4 translocation in 3T3

66 robed trafficking of N in cells treated with nocodazole and cytochalasin D, which depolymerize microt

67 s slipped through mitosis in the presence of nocodazole and exhibited a higher rate of genomic instab

68 gs suggest a re-evaluation of the effects of nocodazole and increased focus on the role of Rho family

69 ntiation, was in fact increased by taxol and nocodazole and normal in DW12.

70 when exposed to microtubule-targeting drugs nocodazole and paclitaxel (Taxol).

71 the differential response of human cells to nocodazole and paclitaxel.

72 istant to the microtubule destabilizing drug nocodazole and persist throughout the cell cycle.

73 mptothecin, yet this mutant was sensitive to nocodazole and phalloidin.

74 ith a microtubule disrupting agent including nocodazole and taxol or release of mitotic shake-off cel

75 icrotubules, is disrupted by the addition of nocodazole and this process is sensed by the cell QCM bi

76 ed to arrest at metaphase in the presence of nocodazole and underwent apoptosis because of activation

77 ted by depolymerization of microtubules with nocodazole and was unaffected by stabilization of microt

78 vel for three antimitotic drugs: paclitaxel, nocodazole, and an inhibitor of kinesin-5 (also known as

79 e microtubules, show enhanced sensitivity to nocodazole, and cannot recover from prometaphase arrest.

80 sence of the microtubule-depolymerizing drug nocodazole, and in cells lacking intermediate filaments.

81 istant to cleavage induced by TRAIL added to nocodazole, and partially blocked the checkpoint abrogat

82 shortened in cells challenged with taxol or nocodazole, and the cells revert to a G2-like state.

83 ule destabilizers, rotenone, colchicine, and nocodazole, and the microtubule stabilizer paclitaxel in

84 ple the reorganizations, we have used taxol, nocodazole, and the specific GSK3-beta inhibitor DW12, t

85 sis, including blebbistatin, hesperadin, and nocodazole, and then assayed for enucleation.

86 We suppressed dynamic instability using nocodazole, and we observed no qualitative change in the

87 ited by nystatin, cytochalasin, latrunculin, nocodazole, and wortmannin, indicating that microtubules

88 ssayed by fractal dimension was inhibited in nocodazole- and cytochalasin-D-treated neural precursor

89 G(1) arrest before the restriction point in nocodazole- and serum-starved synchronized HT29 cells, w

90 The effects of nocodazole are partially rescued using dominant negative

91 in interactions in mammalian cells following nocodazole arrest, and present a bacterial RNA-interacto

92 In contrast, at a G2/M nocodazole arrest, Cdc6 will reload onto chromatin if an

93 Finally, we show that HIV-1 transduction of nocodazole-arrested cells is reduced in cells that expre

94 our methods in a fully automated fashion to nocodazole-arrested HeLa cell lysate where we identified

95 2 from checkpoint complexes in extracts from nocodazole-arrested HeLa cells was inhibited by Polo-lik

96 enhances the activity of APC/C isolated from nocodazole-arrested HeLa cells without disrupting the Ma

97 vity increases during mitosis, especially in nocodazole-arrested mitotic cells, where these kinases e

98 tiation factor 4G1 (eIF4G1) in interphase or nocodazole-arrested mitotic cells.

99 s 50 nM of the drug, while concentrations of nocodazole as high as 50 microM only had a relatively mi

100 After disruption of microtubules with nocodazole, BIG2 and Exo70 were widely distributed in ce

101 number of cells in G1 following release from nocodazole block.

102 onsistently, microtubule depolymerization by nocodazole blocks granule withdrawal, increases their co

103 r, in the presence of a low concentration of nocodazole, BMI-1026 induced excessive membrane blebbing

104 Several pharmacological agents including nocodazole, brefeldin A (BFA), and primary alcohols (1-b

105 onstriction was inhibited in the presence of nocodazole but not taxol, suggesting that intact, but no

106 We show that nocodazole, but not cytochalasin D, affected the distrib

107 s of the microtubule binding drugs taxol and nocodazole by measuring changes in the QCM steady state

108 Microtubule disruption with nocodazole caused a dramatic redistribution of arginase

109 ting a neutrophil's microtubule network with nocodazole causes it to polarize and migrate.

110 Indeed, nocodazole causes the collapse of endolysosomal tubules.

111 epolymerize their microtubule networks after nocodazole challenge.

112 distribution was inhibited by treatment with nocodazole, colcemid, or cytochalasin D, indicating it i

113 At 37 degrees C, the duration of mitosis in nocodazole, colcemid, or vinblastine concentrations that

114 t because the cytoskeletal disrupting agents nocodazole, colchicine, and cytochalasin D are able to r

115 Using this sensor, we followed nocodazole-, colchicine-, and vincristine-induced depoly

116 otubule stability using either paclitaxel or nocodazole compromised the effects of parthenolide.

117 etics of the Deltaf decrease with increasing nocodazole concentrations measured by the EC QCM biosens

118 ounting, the dose curve was shifted to lower nocodazole concentrations, resulting in a more sensitive

119 of CENP-A and Hec1 and SAC override at high nocodazole concentrations.

120 ure to CLCA1 or after a short treatment with nocodazole, consistent with the hypothesis that CLCA1 st

121 reduction in SAC response to Taxol, but not nocodazole, coupled with the reduced binding of BubR1, b

122 ooth muscle to the microtubule depolymerizer nocodazole did not affect the protein-protein interactio

123 cytoskeletal elements with latrunculin B or nocodazole diminishes cavin expression without affecting

124 Nocodazole disassembly or taxol stabilization of the per

125 Reclustering of nocodazole-dispersed Golgi stacks and microtubule/dynein

126 toskeleton was partially diminished by lower nocodazole doses or augmented and stabilized with taxol.

127 of ECs undergoing treatment with increasing nocodazole doses using a fluorescent antibody to alpha-t

128 For all nocodazole doses, t(0.5) was invariant, averaging t(0.5)

129 p < 0.05) after treatment with paclitaxel or nocodazole due to changes in the MTs network.

130 rons with either colchicine, vinblastine, or nocodazole, each of which disrupts microtubules or affec

131 In the presence of nocodazole, ectopic expression of wild type TRF1 but not

132 reatments that altered microtubule assembly (nocodazole), eliminated kinetochore-microtubule attachme

133 inhibition of MTs by low doses of taxol and nocodazole enhance and impair spine formation elicited b

134 polymerization and increases sensitivity to nocodazole following neurite outgrowth.

135 as unaffected or enhanced in the presence of nocodazole for IAV but inhibited for PIV5.

136 pecific disruption of microtubules in AWC by nocodazole generates two AWC(ON) neurons.

137 laments by cytochalasin D or microtubules by nocodazole had no effect on either lipolysis or ERK acti

138 Nocodazole (i) stimulates backness by increasing Rho- an

139 rization induced by dilution in vitro and by nocodazole in cells, suggesting that it acts by protecti

140 bistatin, while basal levels were reduced by nocodazole, indicating that cortactin's movements into a

141 In support, we found that nocodazole induced hMps1 phosphorylation at the previous

142 -depolymerizing agents such as colchicine or nocodazole induced strong activation of MAP kinases incl

143 Furthermore, the nocodazole-induced activation of RhoA and Rho-associated

144 t it has been shown that under conditions of nocodazole-induced arrest p31(comet), a Mad2-binding pro

145 sed global histone acetylation and perturbed nocodazole-induced Brd4 unloading.

146 RhoA/ROCK/MLC signaling pathway in mediating nocodazole-induced cell contractility.

147 d depletion of GEF-H1 in HeLa cells prevents nocodazole-induced cell contraction.

148 elevated ploidy and bypassed the response to nocodazole-induced cessation of DNA replication in a man

149 GEF-H1 is required and sufficient to mediate nocodazole-induced contractility remains unclear.

150 roteins protects microtubules from cold- and nocodazole-induced depolymerization but the molecular an

151 e susceptibility of microtubules to cold and nocodazole-induced depolymerization in tissue-cultured c

152 se in microtubule stability against cold and nocodazole-induced depolymerizing conditions.

153 /-)) keratinocytes are more resistant toward nocodazole-induced disassembly and display increased ace

154 BKV infection of Vero cells is sensitive to nocodazole-induced disassembly of the microtubule networ

155 Using mammalian cells released from nocodazole-induced disassembly, we observed microtubule

156 Moreover, reduced nocodazole-induced expression of anillin, securin, and c

157 ctor, is responsible for the release of this nocodazole-induced G2/M arrest and that this interaction

158 trafficking as revealed by the formation of nocodazole-induced Golgi mini-stacks at ER exit sites.

159 d based on centers of fluorescence masses of nocodazole-induced Golgi ministacks under conventional o

160 Nocodazole-induced Golgi scattering, a microtubule-indep

161 The chemotactic defect stems from dramatic nocodazole-induced imbalance between the divergent, oppo

162 traction caused by laser-induced severing or nocodazole-induced microtubule depolymerization.

163 on was indicated by delayed progression into nocodazole-induced mitotic arrest and was confirmed by a

164 A phospho-mimicking Cdc20 mutant restores nocodazole-induced mitotic arrest in cells depleted of M

165 re impaired in their ability to recover from nocodazole-induced mitotic arrest: a large fraction of +

166 In cells recovering from nocodazole-induced spindle depolymerization and G(2)/M a

167 t of normal spindle formation, recovery from nocodazole-induced spindle disruption was significantly

168 We can rescue nocodazole-induced stiffening with drugs that reduce act

169 Mechanistically, nocodazole-induced upregulation of cyclin B1, anillin, a

170 Nocodazole induces the same responses in differentiated

171 Depolymerization of mitotic spindles by nocodazole inhibited BMI-1026-induced precocious cytokin

172 Cytochalasin D and nocodazole inhibited the uptake by HeLa cells, indicatin

173 Microtubule depolymerization by nocodazole inhibits lamellipodial protrusions and cell-c

174 Nocodazole inhibits the protein turnover of SOCS-1, demo

175 gi fragmentation induced by ilimaquinone and nocodazole is blocked by betagamma inhibition, demonstra

176 Using pharmacological reagents (e.g., nocodazole), live-cell imaging, and flow cytometry analy

177 de exchange activity of XLfc is required for nocodazole-mediated inhibition of convergent extension;

178 sfaction of the MC was prevented with 500 nM nocodazole or 2.5 muM dimethylenastron (an Eg5 inhibitor

179 and to suppression of microtubule flux with nocodazole or antibodies to Kif2a.

180 e Golgi, and disruption of Golgi with either nocodazole or brefeldin A leads to a redistribution of I

181 The response was diminished by nocodazole or by siRNA knockdown of the Opitz syndrome p

182 for 10 minutes in the continuous presence of nocodazole or colcemid treatment to ensure that the cell

183 Treatment of cells with nocodazole or Colcemid, drugs known to inhibit MT polyme

184 ent with the microtubule-depolymerizing drug nocodazole or compromising kinetochore function results

185 kinetics (~21-22 h) as after treatment with nocodazole or Eg5 inhibitors alone.

186 ion of mitosis (DM) is less in Taxol than in nocodazole or Eg5 inhibitors we studied the relationship

187 rogen is prevented by hydroxyurea but not by nocodazole or IB-MECA (cell cycle inhibitors).

188 ed cells were compared to cells treated with nocodazole or latrunculin to identify components associa

189 oked by microtubule-targeting agents such as nocodazole or paclitaxel (Taxol) and is mediated by mito

190 The addition of TRAIL to either nocodazole or paclitaxel (Taxol) reduced levels of the m

191 lted in no centromere resolution when either nocodazole or RNA interference (RNAi) of the kinetochore

192 d for Aurora B-serine 331 phosphorylation in nocodazole or unperturbed early prometaphase.

193 We found that disruption of microtubules by nocodazole or vinblastine treatment, as well as microtub

194 cone, microtubules were depleted with either nocodazole or vinblastine treatment, resulting in an inc

195 tion process is abolished by cytochalasin D, nocodazole, or anti-DYRK3 (dual specificity tyrosine-pho

196 as, if their microtubules are disrupted with nocodazole, or they express mutant proteins that interfe

197 ed microtubule bundles in cells resistant to nocodazole- or cold-treatment-induced depolymerization.

198 Podophyllotoxin and nocodazole, other colchicine site ligands with divergent

199 Treatment with nocodazole, paclitaxel, or 17-AAG induced CIMD in cell l

200 eckpoint (i.e., cold shock or treatment with nocodazole, paclitaxel, or 17-AAG) induced DNA fragmenta

201 At 6 microM nocodazole, partial reversibility of the EC QCM biosenso

202 omosome mis-segregation after treatment with nocodazole, presumably due to the combination of comprom

203 Conversely, destabilizing microtubules with nocodazole prevented undulations but greatly increased t

204 discs with microtubule-destabilizing reagent nocodazole promotes nuclear translocation of Ci155, sugg

205 Furthermore, following exposure to nocodazole, RB-proficient cells arrest with 4 n DNA cont

206 , destabilizing the microtubule network with nocodazole reduces viral exit, revealing a novel microtu

207 f the phenotypes (precocious furrowing after nocodazole release and excessive blebbing in the presenc

208 ynamin 1 in MPCs increased and decreased the nocodazole resistance of microtubules, respectively.

209 ccumulation of detyrosinated Glu tubulin and nocodazole resistance.

210 Nocodazole-resistant microtubules lost upon removal of a

211 his study, we show that ER sliding occurs on nocodazole-resistant MTs that are posttranslationally mo

212 ed dynamic MTs, HIV-1 particles localized to nocodazole-resistant stable MTs, and infection was minim

213 delay; in this study, depolymerization with nocodazole restored Plk1 activity to near normal levels,

214 MT destabilization induced by thrombin or nocodazole resulted in a decrease of LIMK1 colocalizatio

215 w Ca(2+) and suppression of proliferation by nocodazole resulted in modest changes in WST-1 readings,

216 tion of microtubule-dependent transport with nocodazole revealed that DMRIE-C:DNA complexes cannot en

217 Treatment of cells with nocodazole revealed that pseudophosphorylation of T4 at

218 es of cells with vinblastine, colchicine, or nocodazole reversed alpha-synuclein-mediated inhibition

219 Rho-dependent kinase substantially reverses nocodazole's effects on chemotaxis, straightness of migr

220 This effect is consistent with nocodazole's known disruption of intracellular microtubu

221 Unlike disruption of microtubules with nocodazole, selective inhibition of transport by depleti

222 also within the granule matrix and in small nocodazole-sensitive clusters of the cytoskeletal meshwo

223 in a PDZ (PSD95, Dlg, ZO1) domain-dependent, nocodazole-sensitive manner.

224 he cells as free mannose predominantly via a nocodazole-sensitive sugar transporter.

225 PKC-stimulated motility of MCF-10A cells was nocodazole-sensitive, thereby implicating microtubule el

226 cells, microtubules are most often cold- and nocodazole-sensitive.

227 of Rad52 foci in smc6 mutants suppresses the nocodazole sensitivity of these cells, suggesting that t

228 We also found that presynchronization with nocodazole sensitizes cells to the depletion of CENP-E,

229 Disruption of microtubules with nocodazole significantly restricted the transportation o

230 Disruption of microtubules with nocodazole substantially delays HIV-1 uncoating, as reve

231 rotubules in cells continuously treated with nocodazole suggested that VP40 promotes tubulin polymeri

232 This process was disrupted by nocodazole, suggesting an essential role for microtubule

233 tic cells is inhibited by cytochalasin D and nocodazole, suggesting that both the actin and microtubu

234 more sensitive to the spindle-targeting drug nocodazole, suggesting that LCMT-1 and Balpha are import

235 activity, we monitored the lipid profile of nocodazole-synchronized mouse NIH 3T3 fibroblasts during

236 nt during MUG as cells arrest in response to nocodazole, taxol, or monastrol treatments.

237 ary fibroblasts) are continuously exposed to nocodazole, they remain in mitosis for 10-48 hr before t

238 y treating cells with high concentrations of nocodazole to depolymerize the microtubule network.

239 bule binding or treatment of HeLa cells with nocodazole to induce microtubule depolymerization result

240 o knockdown of XLfc abrogates the ability of nocodazole to inhibit convergent extension.

241 Combining PLK1 inhibition with nocodazole (to induce mitotic arrest) had synergistic an

242 ly correlates with the 2AWC(ON) phenotype in nocodazole-treated animals.

243 Smurf2 inactivation prevents nocodazole-treated cells from accumulating cyclin B and

244 Finally, nocodazole-treated cells that recently slipped through m

245 ased co-localization of GLUT4 and F-actin in nocodazole-treated cells upon PDGF stimulation compared

246 tely 50% of the maximal insulin response, in nocodazole-treated cells with disrupted microtubules.

247 DNA-PKcs, that SAF-A interacts with PLK1 in nocodazole-treated cells, and that serine 59 is dephosph

248 siRNA reduced mitotic cell viability and, in nocodazole-treated cells, increased expression of the pr

249 HDAC6 solubility was increased in nocodazole-treated cells, suggesting impaired microtubul

250 cells restored TNF-induced IKK activation in nocodazole-treated cells.

251 A-PKcs prevents inactivation of the APC/C in nocodazole-treated cells.

252 on, comparison of parameters for control and nocodazole-treated Dictyostelium identified the most pro

253 anin slows the rate of spindle shortening in nocodazole-treated mammalian fibroblasts and in untreate

254 leting caspase-9 alone doubled the number of nocodazole-treated, but not Eg5-inhibited, cells that di

255 This interaction was sensitive to nocodazole treatment and decreased after stimulation.

256 Mutant MEFs have a robust SAC in response to nocodazole treatment but an impaired response to Taxol.

257 c stimulation of GLUT4 translocation, and 2) nocodazole treatment disperses GLUT4 vesicles from the p

258 Localization of Cdc23-GFP was disrupted upon nocodazole treatment in the kinetochore mutant okp1-5 an

259 also demonstrate that Golgi dispersion upon nocodazole treatment mainly occurs through a mechanism t

260 Nocodazole treatment of cells infected with filamentous

261 Nocodazole treatment revealed a population of stable ast

262 Interestingly, nocodazole treatment revealed a small variant population

263 After nocodazole treatment to disrupt microtubules, GLUT4 vesi

264 al and insulin-treated cells with or without nocodazole treatment to disrupt microtubules.

265 In addition, subtle nocodazole treatment was able to induce ciliogenesis und

266 Their mobility increased upon nocodazole treatment, arguing that vesicular tethering i

267 cally normal but show delayed recovery after nocodazole treatment, consistent with a subtle disruptio

268 ttered Golgi mini-stacks upon brefeldin A or nocodazole treatment, respectively.

269 cells had a reduced mitotic index following nocodazole treatment, suggesting a failure in a subset o

270 On nocodazole treatment, the OPTN foci were dispersed into

271 Moreover, in prolonged arrest caused by nocodazole treatment, the overall levels of the CDC20-MA

272 spindle-centering defects can be rescued by nocodazole treatment, which depolymerizes astral MTs, or

273 liminates MT repolymerization after standard nocodazole treatment.

274 MT-dependent Golgi stack repositioning after nocodazole treatment.

275 nd PDGF-stimulated GLUT4 translocation after nocodazole treatment.

276 ame spindle pole (syntelic attachment) after nocodazole treatment.

277 Furthermore, colchicine or nocodazole, two inhibitors of intracellular trafficking,

278 cer cell lines to spindle poisons, including nocodazole, vincristine, and Taxol.

279 ey were arrested in prometaphase with taxol, nocodazole, vincristine, or monastrol.

280 This G2/M arrest in response to nocodazole was also abolished by caffeine, suggesting an

281 contrast, the addition of low-dose TRAIL to nocodazole was associated with maximally increased caspa

282 This kinetic change induced by nocodazole was completely rescued by addition of LC1 but

283 This effect of colchicine, vinblastine, or nocodazole was not linked to a disruption of formation o

284 Yet, when nocodazole was withdrawn, Brd4 was reloaded onto chromos

285 estingly, microtubule repolymerization after nocodazole washout allows HIF-1alpha mRNA to reenter act

286 pitalize on this relationship, we utilized a nocodazole washout assay to mimic spindle assembly.

287 In nocodazole washout assays, FAs in arrestin-deficient cel

288 isternae, and delayed Golgi reassembly after nocodazole washout.

289 ng centers during microtubule regrowth after nocodazole washout.

290 fail to reassemble an integral complex upon nocodazole washout.

291 re required for Golgi ribbon formation after nocodazole washout; in vitro, Mena and microfilaments en

292 Using 0.11-50 microM nocodazole, we observed the Deltaf shift values of the b

293 Moreover, U2OS cells treated with nocodazole were found to undergo mitotic catastrophe mor

294 PC remained bound to MTs stabilized with low nocodazole, whereas EB1 did not.

295 Second, the heat increase is blocked by nocodazole, which inhibits DNA replication, mitosis, and

296 phoblastoid cell lines treated with the drug nocodazole, which is known to block cells at the G2/M tr

297 f the kinetochore-microtubule interaction by nocodazole, which is likely attributed to defective kine

298 ate endogenous Plk1, cells were treated with nocodazole, which reduced TNF-induced IKK activation, an

299 ed upon treatment with microtubule inhibitor nocodazole, which was identified as an HBV replication i

300 ivation by microtubule inhibitors benomyl or nocodazole, wild-type Saccharomyces cerevisiae contains