ライフサイエンスコーパス: tubulin polymerization

1 ively comparing small molecules that perturb tubulin polymerization.

2 g, whereas TOG2 is critical for accelerating tubulin polymerization.

3 ir anticancer activity through inhibition of tubulin polymerization.

4 y in vitro without affecting either actin or tubulin polymerization.

5 droxyl group are essential for inhibition of tubulin polymerization.

6 hat contribute to cold temperature-dependent tubulin polymerization.

7 arrest in the G2/M phase and block in vitro tubulin polymerization.

8 ive than combretastatin A-4 as inhibitors of tubulin polymerization.

9 All were potent inhibitors of tubulin polymerization.

10 with nocodazole suggested that VP40 promotes tubulin polymerization.

11 in the inhibition of cytosolic taxol-induced tubulin polymerization.

12 he cell cycle at 0.1 microM and also affects tubulin polymerization.

13 Taxol and tau reduce MT dynamics and promote tubulin polymerization.

14 bit both protein-tyrosine kinases (PTKs) and tubulin polymerization.

15 in cancer cell cultures and on inhibition of tubulin polymerization.

16 s were also the most potent as inhibitors of tubulin polymerization.

17 s by a mechanism involving the inhibition of tubulin polymerization.

18 s were moderately effective as inhibitors of tubulin polymerization.

19 ound T138067 is an irreversible inhibitor of tubulin polymerization.

20 ible for the functional loss of tau-mediated tubulin polymerization.

21 pounds with known potencies as inhibitors of tubulin polymerization.

22 ermediates proved to be potent inhibitors of tubulin polymerization.

23 tatively similar effects of the two drugs on tubulin polymerization.

24 optosis without affecting paclitaxel-induced tubulin polymerization.

25 promote microtubule assembly as monitored by tubulin polymerization.

26 tubulin complexes that do not participate in tubulin polymerization.

27 thyl-4,8-diazaundecane (IPENSpm) on in vitro tubulin polymerization.

28 hemiasterlin was previously shown to inhibit tubulin polymerization.

29 toxicity is through interference with normal tubulin polymerization.

30 as cytotoxic compounds and as inhibitors of tubulin polymerization.

31 activity of colchicine for the inhibition of tubulin polymerization.

32 ielded highly potent steroidal inhibitors of tubulin polymerization.

33 it has unusual effects on glutamate-induced tubulin polymerization.

34 cule that functions as a potent inhibitor of tubulin polymerization.

35 ivity in the cancer cells, and inhibition of tubulin polymerization.

36 inding, and plausibly prevent or destabilize tubulin polymerization.

37 ubule (MT)/actin binding and facilitation of tubulin polymerization.

38 Fifteen compounds potently inhibited tubulin polymerization.

39 3B3 in addition to its reported targeting of tubulin polymerization.

40 ition assays and led to potent inhibitors of tubulin polymerization.

41 ell-free conditions, TL-77 potently inhibits tubulin polymerization.

42 o tubulin and the capacity of tau to enhance tubulin polymerization.

43 ycine-rich (CAP-Gly) domain that accelerates tubulin polymerization.

44 ch is explained by the fact that it inhibits tubulin polymerization.

45 roximately 5% ON01500, a potent inhibitor of tubulin polymerization.

46 rm stable complexes with tubulin and inhibit tubulin polymerization.

47 decreased sensitivity to paclitaxel-induced tubulin polymerization.

48 their mechanisms of action by inhibition of tubulin polymerization.

49 ON 01910.Na had minimal effects on tubulin polymerization.

50 sphorylation of beta-tubulin by MNB inhibits tubulin polymerization, a function that is conserved for

51 Tubulin polymerization, a primary effect of paclitaxel,

52 that forced expression of survivin-2B blocks tubulin polymerization, ablates mitotic cells, and induc

53 ive EB1, we have measured the MT binding and tubulin polymerization activities of untagged EB1 and EB

54 n-binding natural products to modulate their tubulin polymerization activities.

55 er degree of saturation, which retain potent tubulin polymerization activity but with a distinct SAR

56 The conjugate has little if any intrinsic tubulin polymerization activity in vitro and is >20 time

57 -170 fragment was also characterized for its tubulin polymerization activity in vitro.

58 The tubulin polymerization activity of this new class of mac

59 ion of cytotoxicity in three cell lines with tubulin polymerization activity showed reasonable agreem

60 Epothilones are a new class of nontaxane tubulin polymerization agents that have activity in taxa

61 exo70 itself was also capable of inhibiting tubulin polymerization, although exocyst complex with ex

62 Tubulin polymerization and [(3)H]-T138067 competition as

63 re further evaluated with in vitro assays of tubulin polymerization and [3H]colchicine binding to tub

64 with subtilisin enhances vinblastine-induced tubulin polymerization and abolishes the anion effect.

65 Ps 22 and 27 represent a new potent class of tubulin polymerization and cancer cell growth inhibitors

66 Compounds of this class potently inhibited tubulin polymerization and cancer cell growth, including

67 Compound 10i inhibits purified tubulin polymerization and circumvents drug resistance m

68 proliferative activity and for inhibition of tubulin polymerization and colchicine binding to tubulin

69 comparable to 2EE in its ability to inhibit tubulin polymerization and colchicine binding to tubulin

70 resulting analogues were determined in both tubulin polymerization and cytotoxicity assays, and seve

71 relatives, and effects on both inhibition of tubulin polymerization and cytotoxicity in cancer cell c

72 nd 65a showed vinblastine-like inhibition of tubulin polymerization and cytotoxicity to L1210 leukemi

73 Here we traced the waves of tubulin polymerization and depolymerization that occur a

74 By regulating the rate of tubulin polymerization and depolymerization, cells organ

75 Their mode of action is to inhibit tubulin polymerization and destabilize microtubules.

76 sed cellular structures depends on regulated tubulin polymerization and directional transport.

77 cells revealed that they inhibited in vitro tubulin polymerization and disorganized microtubules in

78 -thiazole (SMART) compounds, which inhibited tubulin polymerization and effectively circumvented MDR.

79 ne derivatives were discovered as novel dual tubulin polymerization and EGFR kinase inhibitors.

80 g may be derived from its dual inhibition of tubulin polymerization and EGFR kinase.

81 rization reveal how GABARAP can both promote tubulin polymerization and facilitate GABA(A) receptor c

82 2 and 17 and were analyzed as inhibitors of tubulin polymerization and for cytotoxicity.

83 respectively), suggesting that its effect on tubulin polymerization and G(2)/M phase arrest is distin

84 ZIP12 knockdown also reduces tubulin polymerization and increases sensitivity to noco

85 gainst human cancer cell lines by inhibiting tubulin polymerization and inducing G2/M cell cycle arre

86 The taxanes affect tubulin polymerization and interfere with mitotic transi

87 P5 was more active as an inhibitor of tubulin polymerization and less active as a cytotoxic ag

88 ent with 3 micromol/L TMS for 24 h inhibited tubulin polymerization and microtubule formation, caused

89 Purified SSRP1 facilitates tubulin polymerization and MT bundling in vitro.

90 parable to currently available modulators of tubulin polymerization and PDI activity.

91 evented the rigidin analogue from inhibiting tubulin polymerization and reduced its toxicity in 2D ca

92 terpenoid Taxol (paclitaxel), which promotes tubulin polymerization and shows remarkable efficacy in

93 The tubulin polymerization and Src kinase signaling inhibito

94 paclitaxel (Taxol) in its ability to enhance tubulin polymerization and stabilize microtubules.

95 They induced inhibition of tubulin polymerization and subsequent G2/M arrest.

96 he compounds were evaluated as inhibitors of tubulin polymerization and the binding of [3H]colchicine

97 riagonorrhoeae and was a potent inhibitor of tubulin polymerization and the binding of colchicine to

98 ivity correlated well with the inhibition of tubulin polymerization and the lengthening of the G2/M p

99 und 1c was found to be a potent inhibitor of tubulin polymerization and to effectively inhibit the bi

100 ex stability and that both the efficiency of Tubulin polymerization and Tubulin stability are drastic

101 molecule scaffold for compounds that inhibit tubulin polymerization and tumor cell growth.

102 sistently abolished their ability to inhibit tubulin polymerization and usually decreased cytotoxicit

103 maintained its mode of action by inhibiting tubulin polymerization and was effective against P-glyco

104 Laulimalide stimulated tubulin polymerization and, although less potent than pa

105 ved from Celosia argentea, are inhibitors of tubulin polymerization and, thus, lead structures for ca

106 verexpress BAX, including G2-M-phase arrest, tubulin polymerization, and BCL-2 phosphorylation.

107 increased inhibitory effects on cell growth, tubulin polymerization, and binding of colchicine to tub

108 et in tubulin, produces robust inhibition of tubulin polymerization, and disrupts the microtubule net

109 dual ligand of tubulin and Hsp27, inhibited tubulin polymerization, and had the potential to be a cl

110 effects on tumor cell growth, inhibition of tubulin polymerization, and induction of cell cycle arre

111 bstituent was more active as an inhibitor of tubulin polymerization, and it was also more cytotoxic t

112 crotubule network disorganization, excessive tubulin polymerization, and mitochondrial fragmentation.

113 ntributors to the GuHCl-induced promotion of tubulin polymerization, and that charge-shielding is lik

114 luating compounds for their ability to alter tubulin polymerization are low throughput, labor intensi

115 colchicine-binding site in tubulin, inhibit tubulin polymerization, arrest cancer cells in G(2)/M ph

116 Fatostatin inhibited tubulin polymerization, arrested cells in mitosis, activ

117 a paclitaxel-like effect, markedly promotes tubulin polymerization, arrests cell cycle at mitosis, a

118 rate (and to a lesser degree, the extent) of tubulin polymerization as assessed by light scattering.

119 Vinblastine promotes tubulin polymerization as measured by turbidity at 400 n

120 olymerization, thus supporting inhibition of tubulin polymerization as the primary mechanism causing

121 ing site in tubulin protein was confirmed by tubulin polymerization assay and molecular modeling.

122 Tubulin polymerization assay was used to assess whether

123 ues was investigated by cell cycle analysis, tubulin polymerization assay, competitive mass spectrome

124 tein was confirmed by molecular modeling and tubulin polymerization assay.

125 munofluorescence microscopy and a cell-based tubulin polymerization assay.

126 In vitro tubulin polymerization assays furthermore showed that Ca

127 Function of the constructs was verified by tubulin polymerization assays.

128 The most cytotoxic compounds inhibited tubulin polymerization at concentrations substoichiometr

129 Several compounds inhibited tubulin polymerization at submicromolar concentration an

130 the colchicine site of tubulin and inhibited tubulin polymerization at submicromolar concentrations.

131 Two new series of inhibitors of tubulin polymerization based on the 2-(alkoxycarbonyl)-3

132 re mandatory to achieve potent inhibition of tubulin polymerization, binding of colchicine to tubulin

133 ves exhibited much better potency to inhibit tubulin polymerization but a decreased activity to inhib

134 onal assays reveal that 21 inhibits not only tubulin polymerization but also the phosphorylation of S

135 otein 27 (Hsp27), and the compound inhibited tubulin polymerization by binding at the colchicine doma

136 and its hydrochloride 1d potently inhibited tubulin polymerization by binding at the colchicine site

137 ors of R2 ribonucleotide reductase (RNR) and tubulin polymerization by binding at the colchicine site

138 disparate peptidic natural products inhibit tubulin polymerization by binding to a region of the tub

139 Ellagic acid decreased tubulin polymerization by cabazitaxel and bound to tubul

140 The inhibition of parasite actin and tubulin polymerization by cytochalasin D and colchicines

141 Furthermore, CopN inhibits tubulin polymerization by sequestering free alphabeta-tu

142 Drugs that enhance or inhibit tubulin polymerization can destroy this dynamic process,

143 ated protein, CLIP-170, in which case higher tubulin polymerization capacity was observed for EB3/CLI

144 independent tubulin-binding domain that has tubulin polymerization capacity.

145 llular variations caused by Taxol, including tubulin polymerization, caspase-3 cleavage, and upregula

146 hibit impaired epothilone- and taxane-driven tubulin polymerization caused by acquired beta-tubulin m

147 Indeed, 4 suppressed tubulin polymerization, caused G(2)/M cell cycle arrest,

148 cted, highly active compounds, inhibition of tubulin polymerization, cell cycle effects, and in vivo

149 a panel of cancer cell lines, inhibition of tubulin polymerization, cell cycle effects, and in vivo

150 aluation of these compounds as inhibitors of tubulin polymerization demonstrated that variation at th

151 n binding activity than noscapine and affect tubulin polymerization differently from noscapine.

152 ability to cause cell cycle arrest, inhibit tubulin polymerization, dissociate mitochondrial-bound h

153 Defects in Tubulin polymerization dramatically affect spindle forma

154 ditional macromolecules in the regulation of tubulin polymerization during neurite formation by N18 c

155 Tubulin polymerization enhancement and cytotoxicity of p

156 t also quantitatively analyzes its impact on tubulin polymerization, facilitating structure-activity

157 n new molecules were effective inhibitors of tubulin polymerization (IC(50) < 5 muM) with seven of th

158 Compound 13 was also a potent inhibitor of tubulin polymerization (IC(50) = 0.46 microM) and of rad

159 Diol 4c weakly inhibited tubulin polymerization (IC50 = 22 microM, versus 1.2 mic

160 ative 5f was shown to act as an inhibitor of tubulin polymerization (IC50, 0.99 muM) by binding to th

161 was supported by (i) in vitro inhibition of tubulin polymerization, (ii) G(2)/M-phase arrest in HeLa

162 A-204197 prevented tubulin polymerization in a dose-dependent manner (IC50

163 found between cytotoxicity and inhibition of tubulin polymerization in the 2-phenyl-1,8-naphthyridin-

164 ng neurulation with concomitant reduction in tubulin polymerization in the neural plate.

165 Compound 6t inhibited purified tubulin polymerization in vitro and in vivo and circumve

166 coral that is extremely potent for inducing tubulin polymerization in vitro and is cytotoxic for can

167 shares with paclitaxel the ability to induce tubulin polymerization in vitro and is most likely cytot

168 logue ER-040798 to tubulin and inhibition of tubulin polymerization in vitro by ER-076349 and ER-0865

169 was shown to be unique in that they promoted tubulin polymerization in vitro, but did not bind compet

170 CDDO inhibits tubulin polymerization in vitro, possibly through intera

171 n both track MT plus ends in vivo and induce tubulin polymerization in vitro.

172 that purified c-Fes also catalyzed extensive tubulin polymerization in vitro.

173 eight recombinant exocyst subunits inhibited tubulin polymerization in vitro.

174 onstant (K(d)) 0.4 +/- 0.1 muM] and inhibits tubulin polymerization in vitro; 4) had no effect upon t

175 was confirmed by use of an in vitro model of tubulin polymerization in which deguelin and a variety o

176 t a method to rapidly quantify the extent of tubulin polymerization in whole cells using flow cytomet

177 The size of these structures and extent of tubulin polymerization in XMCAK-4A extracts indicate tha

178 tosis, as a consequence of the inhibition of tubulin polymerization, in experimental models of diffus

179 bstituents conferring the ability to inhibit tubulin polymerization included E-3'-hydroxy-1'-propenyl

180 eoplastic agents, and in vitro inhibition of tubulin polymerization indicated that aurone 5a disrupte

181 These compounds were found to inhibit tubulin polymerization, indicating that cyclization of t

182 nhibitors of cell growth, and they inhibited tubulin polymerization, indicating that methylation of t

183 ant to paclitaxel-mediated cytotoxicity, and tubulin polymerization induced by paclitaxel is suppress

184 In contrast, the tubulin polymerization induced by Taxol was not further

185 onclude that the electrostatic regulation of tubulin polymerization induced by vinblastine resides pr

186 exo84, an exocyst subunit that did not show tubulin polymerization inhibition activity, did not caus

187 t sec5, sec6, sec15, or exo70 diminished its tubulin polymerization inhibition activity.

188 ed and mechanistically characterized through tubulin polymerization inhibition and assays of binding

189 -triazole family of compounds exhibit potent tubulin polymerization inhibition and broad spectrum cel

190 thylestradiol (51) showed similar or greater tubulin polymerization inhibition than 2-methoxyestradio

191 uirements for antiproliferative activity and tubulin polymerization inhibition.

192 tannol and the cis-stilbene structure of the tubulin polymerization inhibitor combretastatin A-4, the

193 ula 3L, a Caribbean strain that produces the tubulin polymerization inhibitor curacin A and the mollu

194 ylcholinesterase inhibitor donezepil and the tubulin polymerization inhibitor indanocine.

195 e successful synthesis of the drug molecule "tubulin polymerization inhibitor" free from trace metal

196 tal synthesis of bifidenone, a novel natural tubulin polymerization inhibitor, has been achieved in 1

197 xyestradiol, a naturally occurring mammalian tubulin polymerization inhibitor.

198 essfully applied to synthesize highly potent tubulin polymerization inhibitors and can be easily scal

199 trans-stilbenes had little or no activity as tubulin polymerization inhibitors and were relatively in

200 A new series of tubulin polymerization inhibitors based on the 2-aryl/he

201 triles were synthesized stereoselectively as tubulin polymerization inhibitors for potential use in c

202 as potent antiproliferative agents and novel tubulin polymerization inhibitors that act at the colchi

203 sis and biological evaluation of a series of tubulin polymerization inhibitors that contain the 1,2,4

204 yoxylamides have previously been reported as tubulin polymerization inhibitors, although none has yet

205 A novel series of tubulin polymerization inhibitors, based on the 1-(3',4'

206 he one-pot construction of two highly potent tubulin polymerization inhibitors, i.e., 2-(het)aryl-4-a

207 had similar cytotoxicities and potencies as tubulin polymerization inhibitors, the side chain presen

208 anks them among the most potent of the known tubulin polymerization inhibitors.

209 iety for the development of novel and potent tubulin polymerization inhibitors.

210 an activity profile resembling that of known tubulin polymerization inhibitors.

211 site ligands with indole B rings are potent tubulin polymerization inhibitors.

212 promising lead compound for a novel type of tubulin polymerization inhibitors.

213 cancer leads, indicated by their activity as tubulin-polymerization inhibitors, represents a promisin

214 al of the subject compounds exhibited potent tubulin polymerization inhibitory activity as well as cy

215 ell cycle analysis, confocal microscopy, and tubulin polymerization inhibitory activity studies and p

216 ined antiproliferative, tubulin-binding, and tubulin polymerization inhibitory activity.

217 mal growth factor receptor (EGFR) kinase and tubulin polymerization inhibitory properties.

218 Inhibitors of tubulin polymerization interacting at the colchicine bin

219 These peptides inhibit tubulin polymerization into microtubules and, instead, i

220 at of paclitaxel, in that the agent enhanced tubulin polymerization into polymers that were partially

221 The vinblastine effect on tubulin polymerization is also highly pH-dependent betwe

222 Vinblastine-induced tubulin polymerization is electrostatically regulated an

223 es and propose that its action in regulating tubulin polymerization is mediated at centrosomes.

224 ither actin filaments in the growth cone nor tubulin polymerization is required for initial outgrowth

225 Furthermore, its capacity for inhibiting tubulin polymerization makes it a potential lead for can

226 ilipin that inhibited Rac activity, actin or tubulin polymerization, MRLC phosphorylation, or lipid r

227 C constructs and subjected them to cell-free tubulin polymerization, MT-binding, actin-binding, and a

228 comparing the antiproliferative activity and tubulin polymerization of 43 and 54 with epothilone B (2

229 c arrest either by directly interfering with tubulin polymerization or by other mechanisms were ident

230 In the absence of tubulin polymerization or in the presence of high salt,

231 ADPH oxidase fail to induce either actin and tubulin polymerization or NET formation on activation.

232 sistent with the observed slower kinetics of tubulin polymerization, phosphorylated tau is compromise

233 ne analogues 3, 4, 7, 8, 9, and 11 as potent tubulin polymerization promoters and cytotoxic agents wi

234 Tubulin polymerization promoting protein (Tppp) facilita

235 The disordered microtubule associated Tubulin Polymerization Promoting Protein (TPPP/p25) and

236 Tubulin polymerization promoting protein 1 (Tppp1) regul

237 (MT) acetylation via phosphorylation of the tubulin polymerization promoting protein 1 (TPPP1/p25).

238 n sheath progenitor cells (TSPCs) expressing tubulin polymerization promoting protein family member 3

239 Tubulin polymerization promoting protein family member-3

240 y a specific marker for Golgi outposts-TPPP (tubulin polymerization promoting protein)-that we use to

241 well-conserved and less understood family of Tubulin Polymerization Promoting Proteins (TPPP) is also

242 gh transcriptome profiling, we show that the tubulin polymerization-promoting protein (TPPP) ringmake

243 Two of those proteins that contain tubulin polymerization-promoting protein (TPPP)-like dom

244 EBV-miR-BART12 binds to the 3'UTR region of Tubulin Polymerization-Promoting Protein 1 (TPPP1) mRNA

245 se single-cell transcriptomics to identify a tubulin polymerization-promoting protein family member 3

246 athy by inducible expression of alphaSyn and tubulin polymerization-promoting protein p25alpha.

247 Finally, we show in the absence of tubulin polymerization-promoting protein/p25alpha that a

248 on of alpha-synuclein can be promoted by the tubulin polymerization-promoting protein/p25alpha, which

249 covery of polyamine analogues that can alter tubulin polymerization provides a series of promising le

250 ogues by demonstrating a correlation between tubulin polymerization, Raf-1/bcl-2 phosphorylation, and

251 rom spermine and from each other in terms of tubulin polymerization rate, equilibrium levels, and tim

252 0(-6)m), inhibitors of alpha-actin and alpha-tubulin polymerization, respectively.

253 ticancer agent paclitaxel (Taxol) stabilizes tubulin polymerization resulting in arrest in mitosis an

254 ain their mechanisms of action by disrupting tubulin polymerization, similar to their parental ABI an

255 ons where GF-15 had no significant impact on tubulin polymerization, spindle tension was markedly red

256 Taxol not only induces tubulin polymerization, stabilizes microtubules, blocks

257 east cancer alter the dynamic equilibrium of tubulin polymerization, stathmin may play an important r

258 -ylcarbamate+ ++ (SRI 7614), an inhibitor of tubulin polymerization synthesized at Southern Research

259 pounds 3c-e showed more potent inhibition of tubulin polymerization than combretastatin A-4 and stron

260 gn paradigm for small-molecule inhibitors of tubulin polymerization that bind to the colchicine site

261 ides leading to energy deficit, 2) excessive tubulin polymerization that may impede cardiomyocyte vis

262 luated for their inhibitory activity against tubulin polymerization, the binding of [3H]-colchicine t

263 of inhibition of both cancer cell growth and tubulin polymerization, the dimethylamino and bromo cis-

264 n of Raf-1 kinase by paclitaxel is linked to tubulin polymerization; the effect is blunted in paclita

265 d in general with their abilities to inhibit tubulin polymerization, thus supporting inhibition of tu

266 accalonolides AF and AJ were able to enhance tubulin polymerization to the same extent as paclitaxel

267 ase II-mediated DNA relaxation or to inhibit tubulin polymerization was also examined.

268 The inhibition of in vitro tubulin polymerization was comparable to CA-4, consisten

269 In ck2beta(-/-) platelets, tubulin polymerization was disrupted, resulting in an im

270 Employing in vitro and in vivo assays, tubulin polymerization was found to be slowed (but not a

271 Compound 2b inhibited tubulin polymerization, was effective in cells overexpre

272 encies of the new compounds as inhibitors of tubulin polymerization were determined, and the cytotoxi

273 with regard to the impact of condensation on tubulin polymerization were especially striking in the p

274 compounds were all inactive as inhibitors of tubulin polymerization when tested at concentrations of

275 red light activation triggered inhibition of tubulin polymerization, which led to apoptotic cell deat

276 C(50) values of 1.4 microM for inhibition of tubulin polymerization, which ranks them among the most

277 Unexpectedly, 11a only weakly inhibits tubulin polymerization, which suggests that the mode of

278 terfere with taxane chemotherapy by reducing tubulin polymerization while inhibiting P-glycoprotein d

279 XMAP215/Stu2/Alp14 accelerates tubulin polymerization while processively tracking micro

280 ounds 38 and 42-44 were potent inhibitors of tubulin polymerization with activities nearly comparable

281 oxyphenstatin (6a) was a potent inhibitor of tubulin polymerization with activity comparable to that

282 Compounds 44-50 were potent inhibitors of tubulin polymerization, with activity nearly comparable

283 The most active compounds inhibited tubulin polymerization, with IC(50) values of 1.9-8.2 mu

284 on revealed that As(2)O(3) markedly promoted tubulin polymerization without affecting GTP binding to

285 we demonstrated that VP40 directly enhances tubulin polymerization without any cellular mediators.