ライフサイエンスコーパス: tubulin polymerization

1 droxyl group are essential for inhibition of tubulin polymerization.

2 hat contribute to cold temperature-dependent tubulin polymerization.

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

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

5 3B3 in addition to its reported targeting of tubulin polymerization.

6 All were potent inhibitors of tubulin polymerization.

7 with nocodazole suggested that VP40 promotes tubulin polymerization.

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

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

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

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

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

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

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

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

16 s were moderately effective as inhibitors of tubulin polymerization.

17 ound T138067 is an irreversible inhibitor of tubulin polymerization.

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

19 pounds with known potencies as inhibitors of tubulin polymerization.

20 ermediates proved to be potent inhibitors of tubulin polymerization.

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

22 optosis without affecting paclitaxel-induced tubulin polymerization.

23 promote microtubule assembly as monitored by tubulin polymerization.

24 tubulin complexes that do not participate in tubulin polymerization.

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

26 hemiasterlin was previously shown to inhibit tubulin polymerization.

27 toxicity is through interference with normal tubulin polymerization.

28 as cytotoxic compounds and as inhibitors of tubulin polymerization.

29 activity of colchicine for the inhibition of tubulin polymerization.

30 ielded highly potent steroidal inhibitors of tubulin polymerization.

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

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

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

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

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

36 rm stable complexes with tubulin and inhibit tubulin polymerization.

37 decreased sensitivity to paclitaxel-induced tubulin polymerization.

38 their mechanisms of action by inhibition of tubulin polymerization.

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

40 ively comparing small molecules that perturb tubulin polymerization.

41 Fifteen compounds potently inhibited tubulin polymerization.

42 ir anticancer activity through inhibition of tubulin polymerization.

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

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

45 Tubulin polymerization, a primary effect of paclitaxel,

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

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

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

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

50 -170 fragment was also characterized for its tubulin polymerization activity in vitro.

51 The tubulin polymerization activity of this new class of mac

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 2 and 17 and were analyzed as inhibitors of tubulin polymerization and for cytotoxicity.

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

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

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

76 The taxanes affect tubulin polymerization and interfere with mitotic transi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Tubulin polymerization assay was used to assess whether

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

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

110 In vitro tubulin polymerization assays furthermore showed that Ca

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

112 The most cytotoxic compounds inhibited tubulin polymerization at concentrations substoichiometr

113 Several compounds inhibited tubulin polymerization at submicromolar concentration an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Defects in Tubulin polymerization dramatically affect spindle forma

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

134 Tubulin polymerization enhancement and cytotoxicity of p

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

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

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

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

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

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

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

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

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

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

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

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

147 CDDO inhibits tubulin polymerization in vitro, possibly through intera

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

149 eight recombinant exocyst subunits inhibited tubulin polymerization in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 uirements for antiproliferative activity and tubulin polymerization inhibition.

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

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

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

170 xyestradiol, a naturally occurring mammalian tubulin polymerization inhibitor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 Inhibitors of tubulin polymerization interacting at the colchicine bin

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

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

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

190 Vinblastine-induced tubulin polymerization is electrostatically regulated an

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

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

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

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

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

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

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

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

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

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

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

202 Tubulin polymerization promoting protein 1 (Tppp1) regul

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

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

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

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

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

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

209 0(-6)m), inhibitors of alpha-actin and alpha-tubulin polymerization, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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