ライフサイエンスコーパス: nocodazole

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

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

3 highly similar to microtubule disruption by nocodazole.

4 following treatment with the spindle poison nocodazole.

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

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

7 confirmed by inhibition with brefeldinA and nocodazole.

8 microtubules are completely depolymerized by nocodazole.

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

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

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

12 3 cells were treated with 1-butanol, BFA, or nocodazole.

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

14 y enhanced resistance to depolymerization by nocodazole.

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

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

17 response to the mitotic destabilizing agent nocodazole.

18 itive to the microtubule depolymerizing drug nocodazole.

19 d microtubules against depolymerization with nocodazole.

20 sister chromatid cohesion and inviability in nocodazole.

21 -depolymerizing agents such as colchicine or nocodazole.

22 tubule drugs, including the reversible agent nocodazole.

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

24 ation of nuclei or the microtubule inhibitor nocodazole.

25 ture Pds1p degradation in cells treated with nocodazole.

26 lay in mitotic exit following the removal of nocodazole.

27 but not in cells arrested in prometaphase by nocodazole.

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

29 ed with the microtubule-depolymerizing agent nocodazole.

30 omosome congression, and sensitized cells to nocodazole.

31 for bulk translocation, we disrupted it with nocodazole.

32 raction by a microtubule depolymerizing drug nocodazole.

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

34 ntaining a mitotic arrest in the presence of nocodazole.

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

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

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

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

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

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

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

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

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

44 Nocodazole, a microtubule inhibitor, did not disperse ag

45 the mitotic spindle checkpoint triggered by nocodazole, a microtubule polymerization inhibitor.

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

47 Moreover, nocodazole, a microtubule-destabilizing agent, enhanced

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

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

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

51 Nocodazole activated Plk3 and its activation was blocked

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 application of an inhibitor of MT assembly (nocodazole), and studied the resulting centrosome displa

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

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

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

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

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

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

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

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

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

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

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

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

89 The effects of nocodazole are partially rescued using dominant negative

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

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

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

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

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

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

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

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

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

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

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

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

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

103 presence of the microtubule-disrupting agent nocodazole but were enhanced in the presence of the micr

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

105 tive to the microtubule-depolymerizing agent nocodazole, but not to the microfilament-depolymerizing

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

107 at low-dose pharmacological agents taxol and nocodazole can be used as a means to modulate myogenesis

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

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

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

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

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

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

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

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

123 Nocodazole disassembly or taxol stabilization of the per

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

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

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

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

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

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

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

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

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

133 polymerization and increases sensitivity to nocodazole following neurite outgrowth.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Nocodazole-induced Golgi scattering, a microtubule-indep

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

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

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

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

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

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

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

166 Nocodazole induces the same responses in differentiated

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

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

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

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

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

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

173 icrotubule disrupting agents, vinblastin and nocodazole, markedly prevented the formation of these in

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

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

176 after exposure to checkpoint stimuli such as nocodazole or anoxia.

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

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

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

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

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

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

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

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

185 ts, as these cells arrest normally following nocodazole or hydroxyurea treatment.

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

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

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

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

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

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

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

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

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

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

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

197 Podophyllotoxin and nocodazole, other colchicine site ligands with divergent

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

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

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

201 ation), S (with thymidine block) and M (with nocodazole) phases of the cell cycle and investigate the

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 without effect, disruption of microtubules (nocodazole) reduced D by half without affecting the mobi

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

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

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 In contrast, alpha-tubulin inhibition by nocodazole showed little effect on PHE-induced tension (

230 of the mitotic poisons paclitaxel (Taxol) or nocodazole significantly increased apoptosis, similar to

231 Disruption of microtubules with nocodazole significantly restricted the transportation o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 cells restored TNF-induced IKK activation 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 nsitive to low temperature, brefeldin-A, and nocodazole treatment and is inhibited by excess free fer

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

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

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

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

261 Nocodazole treatment of cells infected with filamentous

262 Disruption of the microtubule network by nocodazole treatment results in the arrest of cell migra

263 Nocodazole treatment revealed a population of stable ast

264 Interestingly, nocodazole treatment revealed a small variant population

265 After nocodazole treatment to disrupt microtubules, GLUT4 vesi

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

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

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

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

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

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

272 On nocodazole treatment, the OPTN foci were dispersed into

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

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

275 liminates MT repolymerization after standard nocodazole treatment.

276 MT-dependent Golgi stack repositioning after nocodazole treatment.

277 nd PDGF-stimulated GLUT4 translocation after nocodazole treatment.

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

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

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

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

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

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

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

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

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

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

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

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

290 ng centers during microtubule regrowth after nocodazole washout.

291 fail to reassemble an integral complex upon nocodazole washout.

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

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

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

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

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