ライフサイエンスコーパス: actin polymerization

1 firmed using specific inhibitors of PI3K and actin polymerization.

2 es a dramatic change in cell shape driven by actin polymerization.

3 regulate lamellipodia formation by dendritic actin polymerization.

4 uclei with their accompanying centrosomes or actin polymerization.

5 PER may increase spine morphogenesis through actin polymerization.

6 own molecular mechanism reportedly requiring actin polymerization.

7 tatively with Latrunculin A, an inhibitor of actin polymerization.

8 ess dependent on extracellular calcium and F-actin polymerization.

9 me, across multiple contexts, and depends on actin polymerization.

10 te smoke extract via oxidative disruption of actin polymerization.

11 ulinum toxin substrate 1 GTPase activity and actin polymerization.

12 enance of total actin levels and preserves F-actin polymerization.

13 5)P2 and PI(3)P in a curved vesicle triggers actin polymerization.

14 ile myosin-II activity and not to elevated F-actin polymerization.

15 o hyperactivation of cofilin and inefficient actin polymerization.

16 a permissive open conformation, speeding up actin polymerization.

17 Uptake was dependent on dynamin and actin polymerization.

18 and PI3K are both upstream and downstream of actin polymerization.

19 elated protein 2/3 (Arp2/3) complex-mediated actin polymerization.

20 ange depends on strong synaptic activity and actin polymerization.

21 ependent, Abl/Src tyrosine kinase-mediated F-actin polymerization.

22 negative regulator of RhoGTPase activity and actin polymerization.

23 d that it regulates contraction by mediating actin polymerization.

24 bles microtubular transport, exocytosis, and actin polymerization.

25 tch vector are dependent on formin-regulated actin polymerization.

26 Rho-kinase signaling pathways and stimulated actin polymerization.

27 ctic signal transduction network, as well as actin polymerization.

28 -readout, likely downstream of PCP-regulated actin polymerization.

29 interest as they bind to G-actin and enhance actin polymerization.

30 ffness increases via a process that involves actin polymerization.

31 bited neutrophil migration and intracellular actin polymerization.

32 ion, impairing N-WASP-driven Arp2/3-mediated actin polymerization.

33 domain but not the TOCA1 HR1 domain inhibits actin polymerization.

34 thesis but requires neither microtubules nor actin polymerization.

35 supports memory by directly driving synaptic actin polymerization.

36 g modes are linked to negative regulation of actin polymerization.

37 ation of T cell receptor-driven (TCR-driven) actin polymerization.

38 fectors such as N-WASP that induce localized actin polymerization.

39 bles microtubular transport, exocytosis, and actin polymerization.

40 e actin and formins and optimize the rate of actin polymerization.

41 contractility of smooth muscle by regulating actin polymerization.

42 -regulation of a large number of genes after actin polymerization.

43 ntegrin activation by fibronectin to nuclear actin polymerization.

44 mplexes that activate pathways that catalyse actin polymerization.

45 rs and facilitating Arp2/3-mediated branched actin polymerization.

46 ves stimulation of host processes apart from actin polymerization.

47 myosin polymerization, adhesome assembly and actin polymerization.

48 ed the stability of Pfn1 mRNA and influenced actin polymerization.

49 whose physical properties are influenced by actin polymerization.

50 gnalling complexes (adhesomes) that catalyse actin polymerization.

51 processes such as motor protein walking and actin polymerization.

52 INF2 is a formin protein that accelerates actin polymerization.

53 ndrome protein involved in the regulation of actin polymerization.

54 for investigating the complex regulation of actin polymerization.

55 CLIP-170-mDia1 complexes promoted actin polymerization ~18 times faster than free-barbed-e

56 Stimuli that promote actin polymerization allow for shuttling of MRTFs to the

57 g mechanism for cell protrusion, upregulated actin polymerization alone does not initiate protrusions

58 um and inhibition of the Arp2/3 complex or F-actin polymerization also caused a decrease in the abili

59 n the patients' cells corrected the impaired actin polymerization and AKT regulation.

60 These effects are due to Cyfip1's role in actin polymerization and are reversed by expression of a

61 rate the crucial role of Skap2 in regulating actin polymerization and binding of talin-1 and kindlin-

62 hogenesis, a process that requires extensive actin polymerization and bundling during development.

63 By chemically inhibiting actin polymerization and by knocking out the forked gene

64 The present study examined the role of actin polymerization and c-Jun N-terminal kinase (JNK) p

65 emory consolidation in a manner dependent on actin polymerization and c-Jun N-terminal kinase phospho

66 on effector protein that plays roles in both actin polymerization and caspase-3 activation in intesti

67 Activation of Rac induces actin polymerization and cell extension, whereas activat

68 brane phospholipids in controlling localized actin polymerization and cell protrusion.

69 We define actin polymerization and contractility as target mechani

70 Pak inhibition suppressed actin polymerization and contraction in response to ACh,

71 ldrich syndrome protein (N-WASP) activation, actin polymerization and contraction in response to ACh.

72 axillin Ser273 phosphorylation and inhibited actin polymerization and contraction.

73 The primary drivers of yeast endocytosis are actin polymerization and curvature-generating proteins,

74 rotein-based network of 14 genes involved in actin polymerization and dendritic spine formation (nomi

75 cytoskeleton, which is regulated in part by actin polymerization and depolymerization.

76 lize actin filaments (F-actin) by inhibiting actin polymerization and depolymerization.

77 While other Mena isoforms promote actin polymerization and drive membrane protrusion, we f

78 ed protein kinase 2 (MK2) pathway to promote actin polymerization and endothelial cell migration.

79 method is then used to treat the dynamics of actin polymerization and force generation during endocyt

80 PAK1 signaling to N-WASP-cortactin-mediated actin polymerization and GLUT4 vesicle translocation.

81 e protrusion, we find that Mena11a decreases actin polymerization and growth factor-stimulated membra

82 to IL-20 that manifested as modification of actin polymerization and inhibition of a broad range of

83 d formation, and chemotaxis due to defective actin polymerization and integrin activation.

84 Cycling requires dynamic actin polymerization and is blocked by inhibitors of bot

85 genes.Trio is a RhoGEF protein that promotes actin polymerization and is implicated in the regulation

86 of constitutively active mutant ADF reduces actin polymerization and junctional protein disassembly,

87 t of the abscission checkpoint that favors F-actin polymerization and limits tetraploidy, a starting

88 dulation of myosin-1 dynamics to co-ordinate actin polymerization and membrane reorganization at site

89 on peripheral blood neutrophils, as well as actin polymerization and migration.

90 letal organization by studying the effect of actin polymerization and nuclear rigidity on the diffusi

91 iological processes of antigen presentation, actin polymerization and organization, phagocytosis and

92 lonRI in processes that depend on stimulated actin polymerization and outward trafficking of REs.

93 e mediated by cytoskeletal changes involving actin polymerization and p38 mitogen-activated protein k

94 I3K) activation and linked to an increase in actin polymerization and protrusive activity in fibrobla

95 athways such as PI3 kinase/Akt/PKB to induce actin polymerization and pseudopod formation at the fron

96 BCAP(-/-) pDC had decreased actin polymerization and Rac1 activation and reduced IKK

97 In summary, Rac activation leads to actin polymerization and recruitment of Myo9b, which loc

98 n-binding protein that promotes formin-based actin polymerization and regulates numerous cellular fun

99 Importantly, inhibiting actin polymerization and Rho-associated protein kinase d

100 entration of tight junction proteins through actin polymerization and ROCK-mediated localized contrac

101 at the Drg1-Dvl interaction regulates apical actin polymerization and stability in MCCs.

102 y mDia1 and Fmnl3 as major factors enhancing actin polymerization and stabilizing E-cadherin at epith

103 ci are generated by Arp2/3-mediated branched-actin polymerization and stochastically associate with a

104 complexes in response to ACh, and inhibited actin polymerization and tension development.

105 moting actin depolymerization and localizing actin polymerization and the actin nucleation promotion

106 ctivation of ROCK/MLC signalling, persistent actin polymerization and the disassembly of junctional p

107 imary PIP3-stimulated Rac activator, whereas actin polymerization and the GTPase-activating protein A

108 ely employed tool to measure the kinetics of actin polymerization and the interaction between actin a

109 ral protein A36 beneath the virus, enhancing actin polymerization and the spread of infection.

110 Mechanistically, actin polymerization and turnover have been shown to be

111 ith the important role of Pfn1 in regulating actin polymerization and various fundamental actin-based

112 uration) leads to inhibition of mDia2-driven actin polymerization and, therefore, may contribute to a

113 is consistent with aura function promoting F-actin polymerization and/or stabilization.

114 regulator, by pharmacological inhibition of actin polymerization, and by the expression of PCARE har

115 Indeed, increases in basal Ca(2+), actin polymerization, and IL-6 production are reversed i

116 , impedes PI(3,4,5)P3 signaling, restrains F-actin polymerization, and inhibits podosome formation.

117 cium channels, protein kinase C, Rho-kinase, actin polymerization, and myocardin-related transcriptio

118 ides induce FPR2 homologous desensitization, actin polymerization, and neutrophil reactivation throug

119 Remarkably, amounts and dynamics of actin polymerization are normal.

120 While F-actin polymerizations are initialized from the ventral l

121 These findings establish dynamic FA actin polymerization as a central aspect of mechanosensi

122 Despite the well-established role of actin polymerization as a driving mechanism for cell pro

123 lipodial extensions generated by Rac-induced actin polymerization as a function of its motor activity

124 clear magnetic resonance and the pointed-end actin polymerization assay, we find that leiomodin-2, a

125 well-understood phenomenon that is based on actin polymerization at a cell's front edge and anchorin

126 dimeric capping protein (CAPZ), which blocks actin polymerization at barbed ends.

127 the contribution of myosin contraction, and actin polymerization at bundles' terminals when the prod

128 ds on F-actin, but the mechanisms regulating actin polymerization at cell-cell junctions remain poorl

129 e we investigated a role for formin-mediated actin polymerization at cell-cell junctions.

130 ntiated NB4 cell migration and intracellular actin polymerization at concentrations seen during acute

131 We propose a model in which EVL-mediated actin polymerization at FAs promotes mechanosensing and

132 oduced by dysregulation of Rac1's control of actin polymerization at glutamatergic synapses.

133 tor SopE, we recapitulated Rho GTPase-driven actin polymerization at model phospholipid membrane bila

134 sidues, in particular tyrosine 421, promotes actin polymerization at newly-forming invadopodia, promo

135 tochastic simulations of force generation by actin polymerization at obstacles coated with actin "nuc

136 a length by transporting cargos that control actin polymerization at stereocilia tips.

137 rotein complex, which has been implicated in actin polymerization at synapses, a process thought to b

138 , we identify a FMNL1-dependent mechanism of actin polymerization at the back of the cell that enable

139 abarti et al. demonstrate that INF2 mediates actin polymerization at the endoplasmic reticulum (ER),

140 connect phosphatidylinositol signaling to F-actin polymerization at the podosome.

141 ata, we now propose a molecular mechanism of actin polymerization at the pointed end in the presence

142 Actin polymerization-based protrusion increases tension

143 Here we show that efficient control of actin polymerization-based protrusion requires an additi

144 ncing demonstrated that different degrees of actin polymerization biased cells toward various endoder

145 Inhibition of actin polymerization, but not microtubules, results in T

146 Mechanoactivation of the AT1 R stimulates actin polymerization by a protein kinase C-dependent mec

147 tin filament length regulator that repressed actin polymerization by binding to monomeric actin.

148 setting established that RHAMM stabilized F-actin polymerization by controlling ROCK signaling.

149 otide exchange factor (RhoGEF) Trio promotes actin polymerization by directly activating the small GT

150 Mechanistically, Lpd promotes actin polymerization by interacting with F-actin and the

151 Cells can control actin polymerization by nucleating new filaments or elon

152 confirm this hypothesis for mDia1 dependent actin polymerization by stretching a single-actin filame

153 Inhibition of actin polymerization by these agents enhanced colocaliza

154 Additionally, applied force from actin polymerization can bypass the instability by induc

155 supports a general mechanism where localized actin polymerization can coordinate activation of the co

156 Force produced by actin polymerization can generate traction across the pl

157 t activates the small GTPase, cdc42, and the actin polymerization catalyst, neuronal Wiskott-Aldrich

158 We find that the expression of the actin polymerization complex Arp2/3 is reduced in dysbin

159 the actin-related proteins 2 and 3 (ARP2/3) actin polymerization complex member N-WASP.

160 n-related transcription factor (MRTF), a Rho/actin polymerization-controlled coactivator of serum res

161 atelets were pretreated with an inhibitor of actin polymerization (cytochalasin D [CytoD]).

162 immunodeficiency was marked by a pronounced actin polymerization defect and a strongly reduced motil

163 The regulation of EAAT2 expression involves actin polymerization-dependent activation of the transcr

164 epaired by recruitment of new material in an actin polymerization-dependent manner.

165 ive of involvement in cell-cell adhesion and actin polymerization-dependent processes.

166 Actin polymerization-dependent protrusive activity is re

167 Therefore, actin polymerization-dependent protrusive activity opera

168 ecific mechanosensing is effected through an actin-polymerization-dependent mechanism.

169 at genetic and pharmacological modulation of actin polymerization disrupts nuclear pore integrity, nu

170 essed in podocytes, inhibits nephrin-induced actin polymerization, down-regulates nonmuscle myosin II

171 driven) vs proplatelet branching (Arp2/3 and actin polymerization-driven).

172 high hydraulic resistance, the efficiency of actin-polymerization-driven cell migration decreases con

173 prisingly, a possibility that unextinguished actin polymerization drives neurite outgrowth in the pre

174 ilin isoforms in suppressing formin-mediated actin polymerization during plant innate immunity respon

175 Any disruption to actin polymerization dynamics will render the parasite i

176 can be applied to studying the integrity of actin polymerization dynamics.

177 on of increased coat rigidity and force from actin polymerization enables robust vesiculation even at

178 layed low RhoA activity and low steady-state actin polymerization (even after stimulation of lysophos

179 s singled out the actin cytoskeleton and the actin polymerization factor, the Arp2/3 complex, as top

180 e found to be microtubule associated, making actin polymerization from microtubule-associated platfor

181 ated that N-WASP is required for localized F-actin polymerization, GLUT4 vesicle translocation, and g

182 icate that the cyto-D treatment blocking the actin polymerization has a dominant effect at the large

183 x and branched actin networks soften it, but actin polymerization has no effect on cortex stiffness.

184 uss here the propagation of forces caused by actin polymerization, highlighting simple configurations

185 onsistent with HSPB7's inhibitory effects on actin polymerization, HSPB7 KO mice had longer actin/thi

186 dynamin oligomerization and thus, increases actin polymerization, improved renal health in diverse m

187 Whether talin ABDs regulate actin polymerization in a constitutive or regulated mann

188 to the nuclear periphery driven by nuclear F-actin polymerization in cells with POT1 mutations.

189 cleation-promoting proteins tightly regulate actin polymerization in cells.

190 lves activation of RhoA signaling leading to actin polymerization in dendritic spines.

191 depolymerizing factor (ADF) causes sustained actin polymerization in ECs, whereas EC-targeted overexp

192 and bundled F-actin filaments and inhibited actin polymerization in in vitro actin assays.

193 bl-related gene (Arg) activation, leading to actin polymerization in invadopodia, extracellular matri

194 risingly important role for CRMP-1, EVL, and actin polymerization in maintaining the structural integ

195 sits that attractive guidance cues stimulate actin polymerization in neuronal growth cones whereas re

196 Actin polymerization in PFN1 knockout cells was severely

197 This change triggers otherwise-forbidden actin polymerization in primary cilia, which excises cil

198 1a can dampen membrane protrusion and reduce actin polymerization in the absence of other Mena isofor

199 in signaling, supporting a critical role for actin polymerization in the GPER-induced regulation of h

200 ures that can mitigate the effect of Pfn1 on actin polymerization in vitro As a further proof-of-conc

201 CRC cell viability, survival, migration and actin polymerization in vitro.

202 f MKL1 expression in MZMs led to defective F-actin polymerization, inability to clear ACs, and, event

203 Our results show that myosin II activity and actin polymerization increase cortex tension and intrace

204 These results demonstrate that actin polymerization independently stimulates the dynami

205 Finally, we found that infusion of the actin polymerization inhibitor, latrunculin A, into the

206 Treatment of Cltc knockdown mESCs with actin polymerization inhibitors resulted in a decrease i

207 wth of neuronal processes in the presence of actin polymerization inhibitors.

208 Actin polymerization is a universal mechanism to drive p

209 Rac-dependent actin polymerization is activated by a guanine nucleotid

210 se results indicate that formin-based linear actin polymerization is critical for the formation and m

211 ogether, we propose that NCKAP1-orchestrated actin polymerization is essential for tumor progression

212 Spatial and temporal control of actin polymerization is fundamental for many cellular pr

213 Here, we show that actin polymerization is indeed essential for stabilizing

214 We conclude that actin polymerization is indispensable for neurite elonga

215 an in vitro assay where Arp2/3 complex-based actin polymerization is induced on bead surfaces in the

216 Actin polymerization is involved in endocytosis in varyi

217 Moreover, we found that the region of actin polymerization is located at the base of the endoc

218 hat Drp1 binds actin filaments directly, and actin polymerization is necessary for mitochondrial Drp1

219 Branched actin polymerization is necessary for the biogenesis of

220 Recent studies revealed that actin polymerization is required for initiation of myeli

221 d raise concerns about the interpretation of actin polymerization kinetics based solely on protein de

222 Integrins and actin polymerization largely regulate this transfer.

223 actin-membrane release works in concert with actin polymerization, leading to a comprehensive model f

224 oting invadopodium maturation and consequent actin polymerization, matrix degradation, and invasive m

225 on is in turn impeded by shutting off axonal actin polymerization, mediated by nitric oxide-cyclic GM

226 nase (ERK) promotes motility by signaling in actin polymerization-mediated edge protrusion.

227 s the activities of proteins affecting local actin polymerization, membrane processing, and phosphoin

228 ovide new insights into how Arp2/3-dependent actin polymerization modulates both Kv3.3 activity and i

229 as an effector of WASP-mediated control over actin polymerization, mutations in protein components of

230 from Tmods, acting as powerful nucleators of actin polymerization, not capping proteins.

231 to membrane and microtubule (MT) and promote actin polymerization nucleation.

232 otein coat, membrane tension, and force from actin polymerization on bud formation.

233 bules can influence actin coat formation and actin polymerization on secretory vesicles during exocyt

234 otein surface cell antigen 2 (Sca2) promotes actin polymerization on the surface of the bacterium to

235 external osmotic pressure, and inhibition of actin polymerization on the viscoelastic properties and

236 The LTP deficit was rescued by promoting actin polymerization or by KIBRA expression.

237 and guanylyl cyclases, AprA does not induce actin polymerization or increase the pseudopod formation

238 Drugs inhibiting actin polymerization or myosin IIA activation prevented

239 Although actin polymerization or myosin-II activity individually

240 promoters of myosin light chain, dystrophin, actin polymerization, PAK regulatory genes and oxidative

241 CXCR4-dependent stimulation of the Rac1/PAK actin polymerization pathway, leading to increased spine

242 genes involved in the small GTPase-dependent actin polymerization pathway.

243 findings help explain how distinct, tunable actin polymerization pathways collaborate to form higher

244 its signaling pathway, leading to defective actin polymerization, platelet activation, and shape cha

245 erties of the cell nucleus and how regulated actin polymerization plays a role in maintaining nuclear

246 that the final steps of extravasation, where actin polymerization plays an important role, are impair

247 isplay low endogenous MKL1 and inhibition of actin polymerization promotes mature pluripotency activa

248 th a keratinocyte-restricted deletion of the actin polymerization-promoting molecule, N-WASP, display

249 ners of CRB3 in the testis were the branched actin polymerization protein Arp3, and the barbed end-ca

250 of Arp3 (actin-related protein 3, a branched actin polymerization protein) and palladin (an actin bun

251 that both proteins are involved in explosive actin polymerization, pseudopod formation, and cell migr

252 hanistically, this phenomenon is mediated by actin polymerization, Rac1 activation, and alphaIIbbeta3

253 s in the model: substrate adhesion strength, actin polymerization rate, myosin contractility, and the

254 om 0.5 to 10 pN can drastically speed up the actin polymerization rate.

255 protrusion waves are due to fluctuations in actin polymerization rates and that overexpression of VA

256 rces that drive registry and their effect on actin polymerization rates, we estimate a characteristic

257 in as bait to recruit and phosphorylate host actin polymerization-regulating proteins, including the

258 CA1 spine density and phosphorylation of the actin polymerization regulator cofilin, suggesting that

259 dulating integrin activation and controlling actin polymerization) remain largely unknown.

260 Further, we find that this force-promoted actin polymerization requires torsionally unconstrained

261 Depleting Mena or disrupting actin polymerization resulted in Golgi fragmentation.

262 Spreading-induced nuclear actin polymerization results in serum response factor (S

263 hesions is compromised, leading to excessive actin polymerization, slower adhesion turnover, and defi

264 Here, we show that INF2-mediated actin polymerization stimulates a second mitochondrial r

265 oherent model of the key players controlling actin polymerization, stressing the importance of well-t

266 n assays, live-cell imaging of motility, and actin polymerization studies to confirm a role for CD13

267 an actin anti-capping protein that promotes actin polymerization, switches highly adherent keratocyt

268 o the WRC regulator, Arf1, thereby impairing actin polymerization, synapse formation, and immune cell

269 Jasplakinolide-induced actin polymerization synergizes with TGFbeta to facilita

270 osphate lipid (PI(3,4,5)P3) production and F-actin polymerization take place at integrin-mediated adh

271 nges but less sensitive to the inhibition of actin polymerization than fibroblasts.

272 courses and the effects of interventions on actin polymerization: the surprising increase in the pea

273 atin and functions within the ICB to promote actin polymerization there.

274 he downstream Rho GTPase effectors mediating actin polymerization through Arp2/3 nucleation, Wiskott-

275 We previously showed that actin polymerization through ER-bound inverted formin 2

276 itself was revealed to regulate cytoplasmic actin polymerization through the formin INF2, with downs

277 Phosphorylated Tiam1 promotes stable actin-polymerization through Rac1, thereby maintaining t

278 an act as a "swinging gate" allowing limited actin polymerization, thus making leiomodin a leaky poin

279 , which trigger a Ca(2+) response and induce actin polymerization to form a phagocytic cup for engulf

280 conoid protrusion, microneme secretion, and actin polymerization, to initiate gliding motility.

281 o, we show that actomyosin contractility and actin polymerization together push on the underlying ves

282 anistic analyses in cardiomyocytes confirmed actin polymerization/turnover defects, thereby affecting

283 at CD73-generated adenosine induces cortical actin polymerization via adenosine A1 receptor (A1R) ind

284 Kv3.3 activity and its ability to stimulate actin polymerization via Hax-1.

285 inding partner of podocalyxin that regulates actin polymerization via Rac1 or RhoA, we did not detect

286 Strikingly, inhibition of actin polymerization was found to be sufficient to recap

287 Actin polymerization was required for neurite outgrowth,

288 nd of motion can be generated by spontaneous actin polymerization waves that contribute to dendritic

289 Here, by using surface micropatterns of actin polymerization, we investigate stochastic transpor

290 The deficits in actin polymerization were revealed in reduced phalloidin

291 , K50Q- and K61Q-actin inhibit INF2-mediated actin polymerization when expressed at low levels.

292 Mena interacts with GRASP65 to promote local actin polymerization, which facilitates Golgi ribbon lin

293 f the cytoskeletal protein HS1, along with F-actin polymerization, which resulted in rapid receptor i

294 mplex (WRC) to drive Arp2/3 complex-mediated actin polymerization, which underpins diverse cellular p

295 ells promoted cell migration and decreased F-actin polymerization, while overexpression of ASB13 supp

296 es microtubule organization as inhibition of actin polymerization with a low dose of latrunculin A di

297 Inhibition of actin polymerization with cytochalasin-D, but not inhibi

298 Furthermore, inhibition of actin polymerization with latrunculin A reduces this fir

299 The inhibition of actin polymerization with latrunculin in Rictor KO B cel

300 rts a novel, G-actin-dependent regulation of actin polymerization within spine heads.