ライフサイエンスコーパス: microtubule polymerization

1 nts microtubule depolymerization and rescues microtubule polymerization.

2 le rounds of binding and dissociation during microtubule polymerization.

3 vitro, both at steady state and early during microtubule polymerization.

4 ments can be used to monitor the dynamics of microtubule polymerization.

5 taxel binding and reduced paclitaxel-induced microtubule polymerization.

6 irectly to tubulin heterodimers and promotes microtubule polymerization.

7 bility to bind soluble tubulin and stimulate microtubule polymerization.

8 protein complex maintains attachment during microtubule polymerization.

9 other causes cell cycle-specific defects in microtubule polymerization.

10 tion between Shk1 kinase function and active microtubule polymerization.

11 ne does not significantly promote or inhibit microtubule polymerization.

12 protein but also requires C-APC in promoting microtubule polymerization.

13 ound equipotent with paclitaxel in promoting microtubule polymerization.

14 d tubulin, and that a polarized array drives microtubule polymerization.

15 nserved cysteine residue, thereby disrupting microtubule polymerization.

16 with nocodazole or colchicine, inhibitors of microtubule polymerization.

17 exocytosis, and nocodazole, an inhibitor of microtubule polymerization.

18 that these phenotypes result from excessive microtubule polymerization.

19 art of a ring-shaped complex that can induce microtubule polymerization.

20 ole of GTP hydrolysis and calcium cations in microtubule polymerization.

21 tified counteracting factors that facilitate microtubule polymerization.

22 t it interferes as an off-target effect with microtubule polymerization.

23 des, which can serve as potent inhibitors of microtubule polymerization.

24 ends where the motor domain of Kip2 promotes microtubule polymerization.

25 ell death, associated with the inhibition of microtubule polymerization.

26 he homodimer's N-terminal TOG domains during microtubule polymerization.

27 ty of the complexes and rate of tau-promoted microtubule polymerization.

28 o alpha-tubulin and is a potent inhibitor of microtubule polymerization.

29 ite arbor creates a local system for guiding microtubule polymerization.

30 assembly required during mitosis depends on microtubule polymerization.

31 hicine, a tubulin-binding drug that inhibits microtubule polymerization.

32 unction in such processes as axon growth and microtubule polymerization.

33 ed that bind to tubulin directly and enhance microtubule polymerization.

34 a, without affecting Smad-phosphorylation or microtubule polymerization.

35 microtubules, and 4) its ability to promote microtubule polymerization.

36 ding the CPC from spindle regions engaged in microtubule polymerization.

37 nhibited by colchicine, an agent that blocks microtubule polymerization.

38 ck cognate (Hsc) 70 facilitates Tau-mediated microtubule polymerization.

39 tubule poisons, depending on how they affect microtubule polymerization.

40 l concentration of approximately 1 mg/ml for microtubule polymerization, above which the conductivity

41 for the preparation of potent inhibitors of microtubule polymerization acting through the colchicine

42 Lamin B could also function to sequester microtubule polymerization activities within the spindle

43 Depletion of symplekin attenuates microtubule polymerization activity as well as expressio

44 We show that Stu2's microtubule polymerization activity depends on its basic

45 ng oocyte fate maintenance by promoting high microtubule polymerization activity in the oocyte, and e

46 drug taxol, displays no significant in vitro microtubule polymerization activity, thus underscoring t

47 y of DCAMKL1 has no detectable effect on its microtubule polymerization activity.

48 -tau and tau from PHF tangles restores their microtubule polymerization activity.

49 elling at microtubule ends and abrogates its microtubule polymerization activity.

50 p63 restricts Cep57 assembly, expansion, and microtubule polymerization activity.

51 olyketide macrolide that demonstrates potent microtubule-polymerization activity.

52 ic microtubule structures ('straight' during microtubule polymerization and 'curved' during microtubu

53 pectedly, BBIP10 is required for cytoplasmic microtubule polymerization and acetylation, two function

54 All three factors were required for microtubule polymerization and bipolar spindle assembly

55 RP stabilizes mitotic microtubules, promotes microtubule polymerization and bipolar spindle formation

56 rylated MAP2 favours elongation by promoting microtubule polymerization and bundling, whilst branchin

57 ted degradation to increase the stability of microtubule polymerization and cause an extend mitotic p

58 2ME2 inhibits microtubule polymerization and causes cells to arrest in

59 where it is favorably positioned to regulate microtubule polymerization and confer molecular recognit

60 RPOC to achieve site-specific inhibition of microtubule polymerization and control of organelle dyna

61 We further find that vegetal microtubule polymerization and cortical rotation are dis

62 It is also apparent that forces generated by microtubule polymerization and depolymerization are capa

63 Forces generated by microtubule polymerization and depolymerization are impo

64 f tubulin turnover by lowering both rates of microtubule polymerization and depolymerization as well

65 plasmic concentration decreases the rates of microtubule polymerization and depolymerization proporti

66 We show that the rates of both microtubule polymerization and depolymerization scale li

67 he mechanism of action of inhibition of both microtubule polymerization and depolymerization, (ii) ho

68 ich exist in soluble tubulin and at sites of microtubule polymerization and depolymerization.

69 nticancer drugs that act by interfering with microtubule polymerization and dynamics and thereby indu

70 Stathmin is an important regulator of microtubule polymerization and dynamics.

71 izable encephalopathy and drives accelerated microtubule polymerization and enhanced microtubule stab

72 in filament array that specifies anterograde microtubule polymerization and guides these microtubules

73 esponding to the start and end points in the microtubule polymerization and hydrolysis cycles that il

74 etastatin A4 (CA4) phosphate (CA4P) inhibits microtubule polymerization and is toxic to proliferating

75 The novel small molecule PTC596 inhibits microtubule polymerization and its clinical development

76 ng centers, the chromosomes not only promote microtubule polymerization and organization but their at

77 two 4.1 domains critical for its function in microtubule polymerization and organization utilizing do

78 ntify a role for RASSF1A/C in the control of microtubule polymerization and potentially in the mainte

79 expression with RNA interference can induce microtubule polymerization and promote G(2)/M progressio

80 ically, Bora regulates spindle stability and microtubule polymerization and promotes tension across s

81 d with KRAS in lung tumors, is essential for microtubule polymerization and satisfaction of the spind

82 otubule in a stoichiometric ratio, promoting microtubule polymerization and stability.

83 50% or more of the H(2)O with D(2)O promoted microtubule polymerization and stabilized microtubules a

84 Our results unveil that CH-2-102 suppresses microtubule polymerization and subsequently induces G2 p

85 ture provide insight into the role of GTP in microtubule polymerization and the conformational state

86 a demonstrate that NAD(+) and SIRT3 regulate microtubule polymerization and the efficacy of antimicro

87 ution in fission yeast are driven largely by microtubule polymerization and the elongation of the mit

88 Gene silencing of AKAP220 alters the rate of microtubule polymerization and the lateral tracking of g

89 Because previous studies have indicated microtubule polymerization and the microtubule-associate

90 erodimers, Tau uses a conserved mechanism of microtubule polymerization and, thus, regulation of axon

91 was microtubule dependent but independent of microtubule polymerization and/or an interaction with th

92 results suggest EB1 may modulate kinetochore microtubule polymerization and/or attachment.

93 plays an essential role in the regulation of microtubule polymerization, and a similar mechanism may

94 The compound binds to tubulin, inhibits microtubule polymerization, and depolymerizes preformed

95 ith postsynaptic density proteins, regulates microtubule polymerization, and increases dendrite numbe

96 ylates tau on S214, suppresses tau-dependent microtubule polymerization, and inhibits axonal elongati

97 d the sum of the forces generated by dynein, microtubule polymerization, and Ncd, as a function of th

98 bserved gaps in microtubule bundles, reduced microtubule polymerization, and reduced axon numbers, su

99 two tandem repeats are sufficient to mediate microtubule polymerization, and representative patient m

100 pon forces exerted by cortical dynein and by microtubule polymerization, and that these forces are an

101 ionships of analogues of 2, their effects on microtubule polymerization, and their in vitro and in vi

102 lex may explain how the centrosome nucleates microtubule polymerization, and thereby organizes the mi

103 cidate the effects of EB1 and p150(Glued) on microtubule polymerization, and they show that p150(Glue

104 ch, the molecular mechanisms of Tau-mediated microtubule polymerization are poorly understood.

105 We conclude that pushing forces generated by microtubule polymerization are sufficient to promote spi

106 Actin waves also require microtubule polymerization, arguing that positive feedba

107 jor molecular signals that spatially promote microtubule polymerization around chromatin.

108 Centrosome-independent microtubule polymerization around chromosomes has been s

109 associated variant alleles revealed impaired microtubule polymerization, as well as cell migration an

110 ed no hypernucleation effect in the in vitro microtubule polymerization assay, it was more cytotoxic

111 ient zebrafish embryo screening and in vitro microtubule polymerization assay.

112 In vitro microtubule polymerization assays show that Bim1 promote

113 25C-NBF, and DMBMPP were tested in in vitro microtubule polymerization assays showing that they alte

114 ion factor Knot regulate transient surges of microtubule polymerization at dendrite tips; they drive

115 t pole for how anaphase spindle dynamics and microtubule polymerization at kinetochores prevent poten

116 G beta gamma/tubulin complexes might promote microtubule polymerization attenuating further tubulin a

117 The change in free energy for microtubule polymerization attributable to 400 microM di

118 leation to Golgi outposts for net retrograde microtubule polymerization away from nascent dendrite br

119 artments required adenosine triphosphate and microtubule polymerization but did not require added dem

120 cNAcylation of hT40 and hT39 does not affect microtubule polymerization but has opposite effects on h

121 an active mechanochemical process requiring microtubule polymerization but not kinesin-5 activity.

122 Colchicine inhibits microtubule polymerization by binding to tubulin, thus a

123 Inhibition of microtubule polymerization by colchicine and nocodazole

124 Inhibition of microtubule polymerization by colchicine reduced both NO

125 itro, we demonstrate that kinesin-5 promotes microtubule polymerization by increasing the growth rate

126 Inhibition of microtubule polymerization changed the fine-scale distri

127 Their antagonistic effects on microtubule polymerization confer dynamic instability on

128 e ERC could be inhibited by interfering with microtubule polymerization, consistent with a role for u

129 nsistent with a model in which PMS-dependent microtubule polymerization contributes to their maintena

130 administration of colchicine, which prevents microtubule polymerization, could disrupt pressure-stimu

131 ton was not prevented by inhibitors of actin/microtubule polymerization (cytochalasin B, colchicine,

132 ent, allowing chromosome movement coupled to microtubule polymerization/depolymerization and error-co

133 Analysis of in vitro microtubule polymerization/depolymerization showed that

134 ofolate reductase; colchicine, inhibition of microtubule polymerization; dexamethasone, induced nucle

135 rolling the stability of proteins regulating microtubule polymerization during cortical rotation, and

136 In addition, Ensconsin promotes microtubule polymerization during mitosis to control spi

137 could be a key signaling molecule regulating microtubule polymerization during mitosis.

138 Consequently, microtubule polymerization dynamics affect not only stru

139 To probe these mechanisms, we perturbed microtubule polymerization dynamics and opposed motor pr

140 bservations suggest that SPR1 is involved in microtubule polymerization dynamics and/or guidance, whi

141 support a model of spindle assembly in which microtubule polymerization dynamics are not spatially re

142 GTP-dependent microtubule polymerization dynamics are required for cel

143 Microtubule polymerization dynamics at kinetochores is c

144 nstrate that N-glycosylation does not impact microtubule polymerization dynamics but modulates aggreg

145 olymerization assays showing that they alter microtubule polymerization dynamics in a dose dependent

146 Microtubule polymerization dynamics result from the bioc

147 effects of well-characterized inhibitors of microtubule polymerization dynamics.

148 rotubule-associated proteins (MAPs) regulate microtubule polymerization, dynamics, and organization.

149 ere we demonstrate that agents which inhibit microtubule polymerization (e.g., colchicine) and those

150 les (Kinesin-5, Kinesin-14, dynein), promote microtubule polymerization (EB1, Mast/Orbit [CLASP], Min

151 Furthermore, the reduction in microtubule polymerization efficiency in the absence of

152 gation, the mitotic kinesin-5, Eg5, promotes microtubule polymerization, emphasizing its importance i

153 creased diffusivity by ~30%, suggesting that microtubule polymerization enhances random displacements

154 clear movement and the indentation depend on microtubule polymerization from centrosomes behind the n

155 n functions as part of a complex to nucleate microtubule polymerization from centrosomes.

156 ides did not directly inhibit or destabilize microtubule polymerization from pure tubulin in a microt

157 sual pathway for spindle production involves microtubule polymerization from two centrosomes.

158 e drug raises the critical concentration for microtubule polymerization in 2 M glycerol identically i

159 ese results suggest that tivantinib inhibits microtubule polymerization in addition to inhibiting c-M

160 c extract and that it is required for robust microtubule polymerization in an ATP-dependent manner in

161 le alpha/beta-tubulin levels and accelerated microtubule polymerization in fibroblasts from affected

162 ase Ran has recently been shown to stimulate microtubule polymerization in mitotic extracts, but its

163 AJ also distinctly affected microtubule polymerization in that it enhanced the rate

164 gues were synthesized, all of which promoted microtubule polymerization in the absence of GTP.

165 We report that pharmacological inhibition of microtubule polymerization in the NAc inhibited locomoto

166 Translated Msps stimulates microtubule polymerization in the oocyte, causing more m

167 indle organization and for preventing excess microtubule polymerization in these cells.

168 Furthermore, PGJ2 perturbed microtubule polymerization in vitro and decreased the nu

169 Here, we show that EB1 potently promotes microtubule polymerization in vitro and in permeabilized

170 We found that ITCs disrupted microtubule polymerization in vitro and in vivo with the

171 Dppa2 inhibits microtubule polymerization in vitro, and Dppa2 activity

172 nicotinamides were found to be inhibitors of microtubule polymerization in vitro.

173 Moreover, Pin2/TRF1 also promoted microtubule polymerization in vitro.

174 from other species, and is able to nucleate microtubule polymerization in vitro.

175 cells, whereas purified Ensconsin stimulated microtubule polymerization in vitro.

176 microtubule-associated proteins may regulate microtubule polymerization in vivo.

177 s, i.e. the sites where Tau is needed during microtubule polymerization, independently of directed mo

178 In conclusion, the microtubule polymerization inhibitor CH-2-102 conjugated

179 induced by intraventricular injection of the microtubule polymerization inhibitor colchicine.

180 ared from cells arrested at mitosis with the microtubule polymerization inhibitor nocodazole or with

181 trimethoxyphenyl)methanone (CH-3-8), a novel microtubule polymerization inhibitor with little suscept

182 pindle checkpoint triggered by nocodazole, a microtubule polymerization inhibitor.

183 Addition of the microtubule polymerization inhibitors nocodazol or benom

184 In large cells like neurons, how is microtubule polymerization initiated at large distances

185 tail transiently occluding the longitudinal microtubule polymerization interface.

186 neuronal polarization by inducing concerted microtubule polymerization into the axon tip, which prop

187 Microtubule polymerization is initiated from the microtu

188 cytokine secretion by T lymphocytes, whereas microtubule polymerization is required.

189 Microtubule polymerization is severely inhibited in the

190 model where Kip3 directly suppresses spindle microtubule polymerization, limiting midzone length.

191 tubule plus end, where it lies distal to the microtubule polymerization marker EB1 and directly overl

192 luorescent tubulin, we show that substantial microtubule polymerization occurs in neurons grown at re

193 , suggesting that RanBP10 inhibits premature microtubule polymerization of beta1-tubulin and plays a

194 shed by a conditioning lesion that decreased microtubule polymerization of central DRG axons.

195 ment raises the interesting possibility that microtubule polymerization of midzone microtubules is co

196 that inhibit ciliary biogenesis, which block microtubule polymerization or alter centrosome compositi

197 at underlie each family's ability to promote microtubule polymerization or pause.

198 p53 is transcriptionally inactive, increases microtubule polymerization, paclitaxel binding, and sens

199 firmed that CH-2-102 robustly suppresses the microtubule polymerization process by directly interacti

200 tivity as well as expression of the critical microtubule polymerization protein CKAP5 (TOGp).

201 phase spindles, a defect caused by a reduced microtubule polymerization rate and enhanced by centroso

202 We demonstrate that AKAP9 facilitates the microtubule polymerization rate in endothelial cells, in

203 und that tensile force further increased the microtubule polymerization rate.

204 found that they promote intrinsically faster microtubule polymerization rates in cells and in reconst

205 of microtubules, and not due to a change in microtubule polymerization rates.

206 Endothelial cell S1P1/Gi/Rac pathway induces microtubule polymerization, resulting in trafficking of

207 s actin but is not affected by inhibitors of microtubule polymerization, secretory trafficking, or pr

208 In contrast, inhibition of microtubule polymerization selectively prevents the appe

209 cross-linked tubulin indicated inhibition of microtubule polymerization, similar to colchicine.

210 required to counteract Stu2/XMAP215-mediated microtubule polymerization so that spindle elongation te

211 Defects in microtubule polymerization, spindle pole body duplicatio

212 n and myofibroblast differentiation, and (b) microtubule polymerization state controls myofibroblast

213 GTP hydrolysis, protofilament structure and microtubule polymerization state is poorly understood.

214 rentiation of myofibroblasts is regulated by microtubule polymerization state.

215 was not accompanied by gross changes in the microtubule polymerization state.

216 Using a cell-based assay that recognizes microtubule polymerization status to screen for chemical

217 -down of the endogenous TCoB or Pak1 reduced microtubule polymerization, suggesting that Pak1 phospho

218 is is blocked by nocodazole, an inhibitor of microtubule polymerization that also blocks CEDE.

219 y widen the neurite shaft to allow increased microtubule polymerization to direct Kinesin-based trans

220 complex via its N terminus, allowing nuclear microtubule polymerization to occur.

221 rectly phosphorylates stathmin and regulates microtubule polymerization to provide a pro-invasive and

222 ctions, from the nucleation and promotion of microtubule polymerization to the regulation of microtub

223 GTPase-activating protein that acts, during microtubule polymerization, to stimulate GTP hydrolysis

224 vement is similar to the rate of cytoplasmic microtubule polymerization toward the hyphal tip, sugges

225 ndogenous estradiol metabolite that inhibits microtubule polymerization, tumor growth, and angiogenes

226 on of the small GTPase Rac-1 and in enhanced microtubule polymerization upon FcepsilonRI engagement.

227 s of B1 impairs the ability of PTX to induce microtubule polymerization using immunofluorescence micr

228 a competition assay, and their influence on microtubule polymerization was evaluated by measuring th

229 tabilizing proteins all appeared normal, but microtubule polymerization was nevertheless impaired and

230 Finally, C-APC is able to promote microtubule polymerization when stably expressed in APC

231 s microtubules with high affinity and pauses microtubule polymerization, whereas utrophin has no acti

232 hlight a potential new role for PRUNE during microtubule polymerization, which is essential for the c

233 in also reduces the class IV dendrite arbor, microtubule polymerization within dendrites is unaffecte