ライフサイエンスコーパス: microfilament

1 g of all three Xis protomers to generate the microfilament.

2 clusion of the middle cerebral artery with a microfilament.

3 virus (TBSV)], is inhibited by disruption of microfilaments.

4 acin blocked binding between purified B2 and microfilaments.

5 SMA) mRNA and protein and a dense network of microfilaments.

6 y expressed protein and a major component of microfilaments.

7 keletal components, such as microtubules and microfilaments.

8 al mobility is restricted by direct links to microfilaments.

9 mediating crosstalk between microtubules and microfilaments.

10 Dys-ABD alone associated with actin microfilaments.

11 ortical PAR-3 localization depends on intact microfilaments.

12 ent factor C3 and that uptake requires actin microfilaments.

13 dependent, while cortical anchoring required microfilaments.

14 es was independent of the integrity of actin microfilaments.

15 associated with microtubules and with actin microfilaments.

16 spyA in HeLa cells resulted in loss of actin microfilaments.

17 through preventing cofilin interaction with microfilaments.

18 the CH domain interacted directly with actin microfilaments.

19 rt toward the nucleus using microtubules and microfilaments.

20 ingle-fiber recordings of teased dorsal root microfilaments.

21 icrovilli, and proliferative pericanalicular microfilaments.

22 tivity, and requires intact microtubules and microfilaments.

23 olesale depolymerization of microtubules and microfilaments.

24 g filaments had the same dimensions as actin microfilaments.

25 of the par genes and the presence of intact microfilaments.

26 ins that promote formation of actin/spectrin microfilaments.

27 proteins is implicated in stabilizing actin microfilaments.

28 ulting in the dissociation of caldesmon from microfilaments.

29 ct the function of thin muscle filaments and microfilaments.

30 odies (I-LBs) move in association with actin microfilaments.

31 to be primarily mediated by microtubules and microfilaments.

32 5) an association of the receptor with actin microfilaments.

33 nvolve the assembly and disassembly of actin microfilaments.

34 contained fine fibers the diameter of actin microfilaments.

35 eraction between a3-containing V-ATPases and microfilaments.

36 oclast-selective a3-subunit of V-ATPase, and microfilaments.

37 subunit of vacuolar H+-ATPase (V-ATPase) and microfilaments.

38 ll possible inclusions, none associated with microfilaments.

39 axial strains caused by the sliding of actin microfilaments about the fixed integrin attachments are

40 ducts interacting with both microtubules and microfilaments, Actin-related protein 87C; and (3) gene

41 Experimental depolymerization of microfilaments actually prevents retraction rather than

42 Inhibitors of microfilament and microtubule activity resulted in signi

43 While disruption of the cellular actin microfilament and microtubule by cytochalasin D and noco

44 , required intracellular calcium, and intact microfilament and microtubule cytoskeletons and were ind

45 Coordinated actin microfilament and microtubule dynamics is required for s

46 the WRAMP proteome, including regulators of microfilament and microtubule dynamics, protein interact

47 coordinates cellular dynamics by regulating microfilament and microtubule function.

48 icating that normal interactions between the microfilament and microtubule systems have been signific

49 ed ATP production by mitochondria and abated microfilament and vesicle motility.

50 teins that are emerging as key links between microfilaments and a variety of cellular structures and

51 iginated mostly from the remodeling of actin microfilaments and adhesion complexes, to less extent fr

52 eripheral cytoskeleton, disassembly of actin microfilaments and disaggregation of microtubules all co

53 al proteins are associated with actin in the microfilaments and have a major role in microfilament as

54 inding between the recombinant B-subunit and microfilaments and inhibited osteoclastogenesis in cell

55 Depolymerization of the actin microfilaments and inhibition of the Arp2/3 complex does

56 l injury through disruptive effects on actin microfilaments and microtubule (MT) organization across

57 Shiga toxin also increases the levels of microfilaments and microtubules (MTs) upon binding to th

58 ors of actin and tubulin, we found that both microfilaments and microtubules affect the shape and mot

59 n, although we show that populations of both microfilaments and microtubules are oriented in the dire

60 s may employ unique KCHs to coordinate actin microfilaments and microtubules during cell growth.

61 In this report we examine the role of microfilaments and microtubules during early viral infec

62 its regulatory effect by disorganizing actin microfilaments and microtubules in Sertoli cells so that

63 and suggest that signal integration between microfilaments and microtubules is required for triggeri

64 Simultaneous disruption of microfilaments and microtubules led to more pronounced c

65 mposed of an interconnected network of actin microfilaments and microtubules when mechanical stresses

66 Depolymerization of microfilaments and microtubules, and disintegration of t

67 Projections depended on microfilaments and microtubules, exhibited meandering tr

68 multidomain protein that can associate with microfilaments and microtubules.

69 cleft progression through regulation of both microfilaments and microtubules.

70 MP structure formation, potentially bridging microfilaments and MVBs.

71 Here we determine the importance of microfilaments and myosins for the sustained intercellul

72 an be used for the assembly of ultraflexible microfilaments and network structures.

73 ons with severely disorganized microtubules, microfilaments and neurofilaments, raising the hypothesi

74 hat was dependent on polymerization of actin microfilaments and on a functional cytoskeleton, as indi

75 volved differently in their requirements for microfilaments and the associated myosin motors, in a ma

76 just after GVBD, cortical granules attach to microfilaments and translocate to the cell surface.

77 bunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments, and also between osteoclast formation an

78 tivation stimulates vesicle association with microfilaments, and is a key regulatory step in the coor

79 ect does not require interactions with actin microfilaments, and it is possible that other actions of

80 s that involves integration of microtubules, microfilaments, and membrane traffic to remove apoptotic

81 nd wortmannin, indicating that microtubules, microfilaments, and signal transduction are required for

82 Vacuolar H(+)-ATPase (V-ATPase) binds microfilaments, and that interaction may be mediated by

83 also indicate that microtubules and cortical microfilaments antagonize each other during the preblast

84 tion of TM1 in breast tumors may destabilize microfilament architecture and confer resistance to anoi

85 ; TM1, together with TM2 remarkably improves microfilament architecture.

86 the cell by controlling the extent to which microfilaments are bundled.

87 When LIMKs are inhibited, actin microfilaments are disorganized and microtubules are sta

88 t, but both intermediate filaments and actin microfilaments are involved in dynamic cross-linking org

89 eton with drugs showed that microtubules and microfilaments are involved in the types of mRNA movemen

90 olar material (PCM) fails to assemble, actin microfilaments are not organized into furrows at the syn

91 AJM-1, an apical junction marker, and apical microfilaments are severely affected in the distal sperm

92 protein of muscle thin filaments, and actin microfilaments are the main component of the eukaryotic

93 Microtubules, but not microfilaments, are required for proper MTOC localizatio

94 receptors with F-actin and myosin to form a microfilament array associated with multivesicular bodie

95 These two proteins can generate microfilament arrays that "yield" at a strain amplitude

96 tous nucleation-promoting factor of branched microfilament arrays, is an essential contributor to ske

97 lactide-co-glycolide) copolymer (PLGA) fiber microfilaments as a floating scaffold to generate elonga

98 nuclear envelope motility depended on actin microfilaments as well as tubulin.

99 adaptation required intact microtubules and microfilaments, as well as new protein synthesis, and wa

100 ected pathways are critical for TM1-mediated microfilament assemblies.

101 the microfilaments and have a major role in microfilament assembly and function.

102 ity, our results suggest that alterations in microfilament assembly caused by caldesmon phosphorylati

103 sperm chromatin is blocked by inhibitors of microfilament assembly or disassembly.

104 shRNA (neither of which alter microtubule or microfilament assembly) causes mesenchymal cells to adop

105 sulted in aberrant distributions of cortical microfilaments associated with abnormal and striking mem

106 ociate with the EVH1 domain of Mena, another microfilament-associated protein.

107 opomyosins (TMs), a family of actin-binding, microfilament-associated proteins, is a prominent featur

108 roteins that enhance the depolymerization of microfilaments at their minus, or slow-growing, ends.

109 a suggest that MV homodimerization modulates microfilament attachment at muscular adhesion sites and

110 The primary mechanism of microfilament-based motility does not appear to be throu

111 Transport is dependent on intact microfilaments, because particle movement is inhibited r

112 Both kinases are implicated in microfilament bundle assembly and smooth muscle contract

113 n summary, plastin 3 is a regulator of actin microfilament bundles at the ES in which it dictates the

114 These actin microfilament bundles require rapid debundling to conver

115 entin intermediate filaments, in addition to microfilament bundles, interact with many of the alphavb

116 ce of higher-order actin structures, such as microfilament bundles, is unknown.

117 sed interprocess spacing and haphazard actin microfilament bundles.

118 nisms, while plastid movement is promoted by microfilaments but inhibited by microtubules.

119 nule translocation requires association with microfilaments but not microtubules.

120 s contained disorganized bundles of parallel microfilaments, but anterior F-actin bundles in untreate

121 modification that regulates microtubules and microfilaments, but its effects on intermediate filament

122 be associated with transverse-cortical actin microfilaments, but never with axial actin cables in cot

123 that C. elegans gastrulation requires intact microfilaments, but not microtubules.

124 ters is prevented by the depolymerisation of microfilaments, but not of microtubules.

125 tile granules that are associated with actin microfilaments, but not with microtubules.

126 By contrast, disruption of actin-containing microfilaments by cytochalasin D or microtubules by noco

127 filament rings, and bottleneck suggests that microfilaments can still contract even though they are n

128 Coordinated microtubule and microfilament changes are essential for the morphologica

129 87C; and (3) gene products interacting with microfilaments, chickadee, diaphanous, Cdc42, quail, spa

130 These findings do not support the microfilament-complex model, but instead indicate that t

131 f these complexes is powered by myosin: the "microfilament-complex" model.

132 and animals: a highly sophisticated array of microfilament components, a large family of G-protein-co

133 cles at the nuclear-cytoplasmic junction and microfilament contraction.

134 ere the result of an alteration of the actin microfilaments, converting from their bundled to branche

135 ate that Capu and Spire have microtubule and microfilament crosslinking activity.

136 disrupt the microtubules (thiabendazole) and microfilaments (cytochalasin D and latrunculin B) of the

137 nteraction between both the microtubular and microfilament cytoskeleton and cellular membranes.

138 In response to this cue, the microfilament cytoskeleton polarizes the distribution of

139 In contrast, the microfilament cytoskeleton was enhanced by ROCK II down-

140 g is dependent on the integrity of the actin microfilament cytoskeleton, we sought to determine if ac

141 d actin isoforms that polymerize to form the microfilament cytoskeleton.

142 zation and requires both the microtubule and microfilament cytoskeleton.

143 Uptake was found to be both microtubule and microfilament dependent and required the Rho family of G

144 ug response suggests a maternally inherited, microfilament-dependent organization within the egg cort

145 process involving distinct microtubule- and microfilament-dependent phases and indicate a role for d

146 Finally, the effect of actin microfilament depolymerization on total release is alter

147 olymerizing agent nocodazole, but not to the microfilament-depolymerizing agent cytochalasin B, indic

148 eidispongiolides and sphinxolides are potent microfilament destabilizing agents that represent a prom

149 In contrast, the depolymerization of actin microfilaments did not have any effect on virus binding,

150 dent process, since treatment with the actin microfilament disrupter cytochalasin D prevented iNOS re

151 oxic derivatives, compound 9 did not exhibit microfilament-disrupting activity at 5 microM.

152 rcinoma (HCT-116) cells) but did not exhibit microfilament-disrupting activity at 80 nM.

153 es, whereas treatment with cytochalasin D, a microfilament-disrupting agent, did not alter GFAP mRNA

154 e impaired by microtubule-disrupting but not microfilament-disrupting agents as well as by overexpres

155 Addition of microfilament-disrupting agents led to rapid and extensi

156 association with actin in cells treated with microfilament-disrupting or filament-stabilizing agents

157 e screen, and all compounds were tested in a microfilament disruption assay.

158 ided dramatic protection against PAN-induced microfilament disruption in sense > vector > antisense c

159 roperties with cholesterol removal and actin microfilament disruption.

160 that 7th mutant inhibited the disassembly of microfilaments during mitosis.

161 Accurate regulation of microfilament dynamics is central to cell growth, motili

162 ot impede BKV infection, while inhibition of microfilament dynamics with jasplakinolide results in re

163 sibly stabilized microtubules, blocked actin microfilament dynamics, inhibited cell motility in vitro

164 polymeric actin (F-actin) and is involved in microfilament dynamics.

165 Microfilament-engineered cerebral organoids (enCORs) dis

166 after nocodazole washout; in vitro, Mena and microfilaments enhanced GRASP65 oligomerization and Golg

167 quires the formation of filopodia from actin microfilaments (F-actin) and their engorgement with micr

168 ECM, the attached ECs rearrange their actin microfilaments first into peripheral stress fibers and s

169 e dependence of TMV, PVX, and TBSV on intact microfilaments for intercellular movement led us to inve

170 The entry was dependent on microfilaments for internalization and subsequently bruc

171 he same genus as TMV, did not require intact microfilaments for normal spread.

172 t low temperatures and by drugs that disrupt microfilament formation and endocytosis.

173 ream of Cdc42 in a pathway that may regulate microfilament formation.

174 Agents that impaired microfilament function, including cytochalasin B, cytoch

175 e activity of caldesmon and through this the microfilament functions in cells.

176 binds to free barbed ends, thereby arresting microfilament growth and restraining elongation to remai

177 Inhibition of actin microfilaments had the greatest effect on bulk compressi

178 er form that polymerizes into a thin, linear microfilament in cells.

179 ndent potentiation are controlled by PKA and microfilaments in a convergent manner.

180 yosin in vitro and to tropomyosin-associated microfilaments in a variety of endothelial cell types.

181 Furthermore, microfilaments in BMPCs consisted of atypically thick bu

182 ability barrier, causing disruption of actin microfilaments in cell cytosol, perturbing the localizat

183 c interaction between microtubules and actin microfilaments in cotton fibers.

184 Nomofungin disrupts microfilaments in cultured mammalian cells and is modera

185 nase, or treatment with Y-27632 disassembled microfilaments in normal NIH3T3 and in TM1 expressing ce

186 death, highlighting the importance of actin microfilaments in rituximab/milatuzumab-mediated cell de

187 s study, the involvement of microtubules and microfilaments in the light-driven translocation of arre

188 cells, a shorter CaD isoform co-exists with microfilaments in the stress fibers at the quiescent sta

189 ant transformation, and that TM1 reorganizes microfilaments in the transformed cells.

190 MIPP protein binds to microfilaments in vitro and co-immunoprecipitates with a

191 t- and phototropin-dependent localization to microfilaments in vivo.

192 ed a critical role for microtubules, but not microfilaments, in hTHTR1 trafficking.

193 of CRB3 KD-induced re-organization of actin microfilaments, in which actin microfilaments were trunc

194 tosis via the accumulation of cortical actin microfilaments induced by the ROP2 effector protein RIC4

195 y, disruption of the microtubule but not the microfilament inhibited HPIV-3 release.

196 tyrosine kinase inhibitor (genistein), by a microfilament inhibitor (cytochalasin B), and by incubat

197 as moving particles, a property inhibited by microfilament inhibitors.

198 on with tropomyosin results in disruption of microfilament integrity leading to inhibition of cell mo

199 Along with microtubules and microfilaments, intermediate filaments are a major compo

200 ide, or colchicine was used to disrupt actin microfilaments, intermediate filaments, or microtubules,

201 tin-dependent manner and to cross-link actin microfilaments into higher-order structures has been cor

202 ither through directed transport along actin microfilaments into one daughter cell or through capture

203 hesized that the ability of TM1 to stabilize microfilaments is crucial for tumor suppression.

204 tood how the interaction of microtubules and microfilaments is mediated in this context.

205 bunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments is required for osteoclast bone resorptio

206 y that links the centrosome and the cortical microfilaments is unknown.

207 ing mutant, S381E, was incapable of bundling microfilaments, it retains the ability to bind F-actin.

208 Disrupting microtubules but not microfilaments led to reorganization of ENaC clusters an

209 expression of exogenous K-cyclin results in microfilament loss and changes in cell morphology; both

210 findings suggest that both microtubules and microfilaments may play a role in the effective traffick

211 As microfilament-membrane linkage is critical to this proce

212 bedded in membrane microdomains induce actin-microfilament meshwork formation, anchoring microtubules

213 on, apical recruitment of p150(Glued), actin microfilament meshwork organization, and ultrastructure

214 Both expanded acinar lumina and thickened microfilament meshworks, and both caused homotypic fusio

215 wever, the mechanisms that regulate cortical microfilament (MF) assembly remain poorly understood.

216 Actin microfilament (MF) organization and remodelling is criti

217 at PS1 associates with microtubules (MT) and microfilaments (MF) and that its cytoskeletal associatio

218 ges due to structural modifications in actin microfilaments (MFs) and microtubules (MTs).

219 s elegans, the partitioning proteins (PARs), microfilaments (MFs), dynein, dynactin, and a nonmuscle

220 -bodies and, regardless of size, VRCs, along microfilaments (MFs).

221 bstrate-dependent cultures, entosis requires microfilaments, microtubules and the Golgi complex for c

222 Disruptors of the cytoskeleton (microfilaments, microtubules, and intermediate filaments

223 filaments within the internal cytoskeleton--microfilaments, microtubules, and intermediate filaments

224 We show that microfilaments, microtubules, and the intermediate filam

225 actin and tubulin revealed similar arrested microfilament motility upon challenge.

226 It is clear from endocytosis assays that microfilament motors are functional prior to meiosis, ev

227 chromatin organization, actin filament, and microfilament movement.

228 the presence of an array of bundles of actin microfilaments near the Sertoli cell plasma membrane.

229 With a close examination of the F-actin microfilament network, these findings show that Panx1 ch

230 caused cell retraction and disruption of the microfilament network.

231 N-WASP-mediated actin nucleation of branched microfilament networks is specifically required for the

232 teractions among Cdk1-CycB, microtubule, and microfilament networks.

233 he nucleus, endoplasmic reticulum, and actin microfilaments of the cytoskeleton in response to reduct

234 fic and high-affinity binding, it may form a microfilament on DNA similar to that described for the p

235 oocyte, which is unlikely mediated either by microfilaments or by microtubules, markedly decreases be

236 the embryos with agents that disrupt either microfilaments or microtubules has little, if any, effec

237 Disruption of microfilaments or microtubules with the use of cytochala

238 ukocyte deformability has been attributed to microfilaments or microtubules, but the present studies

239 To investigate how TM1 induces microfilament organization in transformed cells, we util

240 tochalasin D or latrunculin B to disrupt the microfilament organization selectively slowed only trans

241 D1 plays a central role in the regulation of microfilament organization, consequently controlling cel

242 by depolymerizing actin and disrupting actin microfilament organization.

243 initial uptake of Py, both microtubules and microfilaments play roles in trafficking of the virus to

244 s with cytochalasin E, an inhibitor of actin microfilament polymerisation.

245 an cells, myosin-I is excluded from specific microfilament populations, indicating that its localizat

246 rms of the organism induced endothelial cell microfilament rearrangement and subsequent endocytosis.

247 pathway of phosphoinositol 3-kinase controls microfilament rearrangement and translocation of actin-a

248 brane adhesion, probably due to Sertoli cell microfilament redistribution.

249 In summary, CRB3 is an actin microfilament regulator, playing a pivotal role in organ

250 ctivity of CP alpha expand the repertoire of microfilament regulatory mechanisms assigned to CPs.

251 ype also reduce Cdk1-CycB activities and are microfilament-related genes.

252 , whereas completion of the process required microfilament remodeling and ROCK, MLCK, and dynamin II

253 ble actin microfilaments, we show that actin microfilament remodeling is part of fenestra biogenesis

254 dosomal trafficking, because an inhibitor of microfilament reorganization prevented uptake in both ca

255 The motility of P6 along microfilaments represents an entirely new property for t

256 C4 to promote the assembly of cortical actin microfilaments required for localized outgrowth.

257 omitant to increased polymerization of actin microfilaments resulting in decreased G- to F-actin rati

258 on negatively regulated contractility of the microfilament-rich cell cortex during pronuclear migrati

259 late cellularization allows src64-dependent microfilament ring constriction to drive basal closure.

260 e mutant suggests that src64 is required for microfilament ring contraction even in the absence of Bo

261 Our results suggest that src64-dependent microfilament ring contraction is resisted by Bottleneck

262 controlling contraction of the actin-myosin microfilament ring during this process.

263 craps, a mutation in anillin that eliminates microfilament rings, and bottleneck suggests that microf

264 ted of all, hint at an autonomous process of microfilament self-organization driving the formation of

265 icrotubules or cytochalasin D to disassemble microfilaments simplifies the intermediate scattering fu

266 le (microtubule specific) or cytochalasin D (microfilament specific) prevented the effects of CaM-dep

267 ocytes and in 129 CB3 cells treated with the microfilament stabilizer phalloidin.

268 vely controlled conditions, to perturb actin microfilament structure and assembly in an attempt to an

269 nism for phospholipid-induced changes in the microfilament structure and cell function and suggest th

270 Cell morphology and the microfilament structure of untreated sense and antisense

271 se channels requires interactions with actin microfilaments subjacent to the plasma membrane.

272 ession of activity at fertilization requires microfilaments, suggesting that the transporters are in

273 arrays after an initial period of intensive microfilament synthesis, followed by array elongation, p

274 leading to a reorganization of the podocyte microfilament system and consequent proteinuria.

275 Actin is the main component of the microfilament system in eukaryotic cells and can be foun

276 ells, suggesting that a dynamic state of the microfilament system is important for Py infectivity.

277 VASP, an important component of the cellular microfilament system, plays a major role in regulating S

278 crotubules as well as a dynamic state of the microfilament system.

279 by both phospholipase D (PLD) and the actin microfilament system.

280 t, plant and animal cells that confers actin microfilaments their bundled configuration.

281 li cell cytosol, causing truncation of actin microfilament, thereby failing to support the Sertoli ce

282 e that while P6-GFP inclusions traffic along microfilaments, those associated with microtubules appea

283 one, but not TM2, results in re-emergence of microfilaments; TM1, together with TM2 remarkably improv

284 actin filaments, and their organization with microfilaments to establish and maintain cell polarity d

285 V0domains of V-ATPase through the binding of microfilaments to subunitsBandCand preserving the integr

286 veal that SPATA6 is involved in myosin-based microfilament transport through interaction with myosin

287 l phenotype using antibodies to alpha-actin (microfilaments), vimentin and desmin (intermediate filam

288 that rearrangement of both microtubules and microfilaments was necessary for the uptake.

289 f agents that stabilize or disassemble actin microfilaments, we show that actin microfilament remodel

290 ytokinesis defects and disruption of tubulin microfilaments were also observed by immunofluorescence

291 tion of actin microfilaments, in which actin microfilaments were truncated, and extensively branched,

292 ed by centrifugal cosedimentation with actin microfilaments, where bound protein is separated from ac

293 large cytoplasmic inclusions associated with microfilaments, whereas the 125-kDa protein formed few s

294 ofilin to stress fibers and disorganizes the microfilaments, whereas wild type TM1 appears to restric

295 attR recombination site to generate a curved microfilament, which promotes assembly of the excisive i

296 a reduction in formation of microtubules and microfilaments, which are necessary for the development

297 Actin microfilaments, which are prominent in pollen tubes, hav

298 Disruption of actin microfilaments, which causes delocalization of Bifocal b

299 n, resulting in the re-organization of actin microfilaments, which rendered them similar to those in

300 icrotubules with colchicine (Colch) or actin microfilaments with cytochalasin D (CD) dramatically red