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

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

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

3 taxel binding and reduced paclitaxel-induced microtubule polymerization.

4 irectly to tubulin heterodimers and promotes microtubule polymerization.

5 protein complex maintains attachment during microtubule polymerization.

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

7 tion between Shk1 kinase function and active microtubule polymerization.

8 ne does not significantly promote or inhibit microtubule polymerization.

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

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

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

12 ound equipotent with paclitaxel in promoting microtubule polymerization.

13 nserved cysteine residue, thereby disrupting microtubule polymerization.

14 with nocodazole or colchicine, inhibitors of microtubule polymerization.

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

16 that these phenotypes result from excessive microtubule polymerization.

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

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

19 assembly required during mitosis depends on microtubule polymerization.

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

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

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

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

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

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

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

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

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

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

30 le rounds of binding and dissociation during microtubule polymerization.

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

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

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

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

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

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

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

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

39 olyketide macrolide that demonstrates potent microtubule-polymerization activity.

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

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

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

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

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

45 2ME2 inhibits microtubule polymerization and causes cells to arrest in

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

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

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

49 Forces generated by microtubule polymerization and depolymerization are impo

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

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

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

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

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

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

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

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

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

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

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

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

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

63 50% or more of the H(2)O with D(2)O promoted microtubule polymerization and stabilized microtubules a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Centrosome-independent microtubule polymerization around chromosomes has been s

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

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

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

90 In vitro microtubule polymerization assays show that Bim1 promote

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

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

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

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

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

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

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

98 Inhibition of microtubule polymerization changed the fine-scale distri

99 Their antagonistic effects on microtubule polymerization confer dynamic instability on

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

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

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

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

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

105 Analysis of in vitro microtubule polymerization/depolymerization showed that

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

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

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

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

110 Consequently, microtubule polymerization dynamics affect not only stru

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

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

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

114 GTP-dependent microtubule polymerization dynamics are required for cel

115 Microtubule polymerization dynamics at kinetochores is c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Dppa2 inhibits microtubule polymerization in vitro, and Dppa2 activity

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

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

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

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

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

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

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

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

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

144 Addition of the microtubule polymerization inhibitors nocodazol or benom

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

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

147 Microtubule polymerization is initiated from the microtu

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

149 Microtubule polymerization is severely inhibited in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 Defects in microtubule polymerization, spindle pole body duplicatio

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

170 rentiation of myofibroblasts is regulated by microtubule polymerization state.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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