ライフサイエンスコーパス: actin stress fiber

1 lls failed to assemble focal adhesions and F-actin stress fibers.

2 t the ability of adenosine to induce loss of actin stress fibers.

3 tely abrogated class I-mediated formation of actin stress fibers.

4 othelial junctions associated with increased actin stress fibers.

5 ransfection of VopL promotes the assembly of actin stress fibers.

6 A reorientation to provide anchor points for actin stress fibers.

7 ress FA proteins and localize at the ends of actin stress fibers.

8 n of VE- and E-cadherin and the formation of actin stress fibers.

9 tant protein slower than the wild type along actin stress fibers.

10 face areas and, unlike control cells, lacked actin stress fibers.

11 to focal adhesions and co-localization with actin stress fibers.

12 focal adhesion complexes, and longitudinal F-actin stress fibers.

13 terior cytoplasm and function to disassemble actin stress fibers.

14 zed by the appearance of alpha-smooth muscle actin stress fibers.

15 d on (beta)ig-h3-coated plates and developed actin stress fibers.

16 ing V12Rac prevented subsequent alignment of actin stress fibers.

17 ptors in the assembly of focal adhesions and actin stress fibers.

18 aling cascades that regulate the assembly of actin stress fibers.

19 activity as measured by the organization of actin stress fibers.

20 mily members, AGAP1 also induced the loss of actin stress fibers.

21 did it appear to affect assembly of alpha-SM actin stress fibers.

22 cytes (HFKs) requires RhoGTP, a regulator of actin stress fibers.

23 kers in muscle Z-disks, focal adhesions, and actin stress fibers.

24 nd its loss is accompanied by an increase in actin stress fibers.

25 as associated with the presence of disrupted actin stress fibers.

26 nd the downregulation of focal adhesions and actin stress fibers.

27 matrix deposition, cell-matrix adhesion, and actin stress fibers.

28 nal domain and affect formation of host-cell actin stress fibers.

29 the force-sensitive accumulation of zyxin on actin stress fibers.

30 mellipodia formation and reorganization of F-actin stress fibers.

31 erance of filamentous actin and formation of actin stress fibers.

32 e formation of prominent focal adhesions and actin stress fibers.

33 heterogeneously express alpha-smooth muscle actin stress fibers, a marker of myofibroblast different

34 but lose the planar polarity of their basal actin stress fibers, a phenotype it shares with Dystroph

35 transformed NIH3T3 results in restoration of actin stress fibers accompanied by a loss of cytoplasmic

36 olocalization of caspase 8 and EC MLCK along actin stress fibers after TNF-alpha.

37 ee clones expressing rPLD1-V5 failed to form actin stress fibers after treatment with LPA.

38 adaptation: cell elongation and formation of actin stress fibers aligned to the flow direction.

39 , and reduced RhoA-GTP, phospho-cofilin, and actin stress fibers, all of which were reversed by shRNA

40 misdirected protrusions and the formation of actin stress fibers anchored in streak-like focal adhesi

41 eveloped myofibroblastic features, including actin stress fibers anchored to paxillin-containing foca

42 growth factor, an increase in contractile F-actin 'stress' fibers and blocks invasive growth in thre

43 ia induction but also for the RhoA-regulated actin stress fiber and focal adhesion complex formation

44 PA (20 microM) and S1P (1 microM) stimulated actin stress fiber and focal adhesion formation, increas

45 in the RhoA(-/-) cells resulted in a loss of actin stress fiber and focal adhesion similar to that of

46 as 2.2 times slower than the wild type along actin stress fibers and 1.5 times slower within focal ad

47 a decrease in focal adhesion sites, reduced actin stress fibers and a collapse of microtubule struct

48 An adhesive phenotype is developed with actin stress fibers and activation of focal adhesion kin

49 tility which is accompanied by a decrease in actin stress fibers and an increase in adherence junctio

50 ng the dynamic disassembly and reassembly of actin stress fibers and associated focal adhesions to th

51 reases beta-catenin level, which decreases F-actin stress fibers and attenuates plasma membrane resea

52 terization showed that MCP compounds restore actin stress fibers and cause flat reversion in NIH 3T3

53 We show that IpaA-induced loss of actin stress fibers and cell rounding do not require vin

54 eased contractility, account for the loss of actin stress fibers and cell rounding observed in cells

55 ished by the ability of p114RhoGEF to induce actin stress fibers and cell rounding.

56 ibronectin and alpha-SMA in animals, whereas actin stress fibers and contractility are both induced i

57 iveness by regulating the proper assembly of actin stress fibers and contractility through a ROCKII/L

58 ice lacking these miRNAs, due to disarray of actin stress fibers and diminished migratory activity of

59 In addition, ACK2 dissolves actin stress fibers and disassembles focal complexes but

60 RSK2 appears to affect integrins by reducing actin stress fibers and disrupting focal adhesions.

61 These effects are accompanied by loss of actin stress fibers and electrophysiologic changes.

62 T) destabilization promotes the formation of actin stress fibers and enhances the contractility of ce

63 Depletion of Rnd3 promoted prominent actin stress fibers and enlarged focal adhesions.

64 how that Nf1-deficient astrocytes have fewer actin stress fibers and exhibit increased cell motility

65 osphopeptide analogs of HSP20 led to loss of actin stress fibers and focal adhesion complexes as demo

66 Expression of Hax-1 reduces the formation of actin stress fibers and focal adhesion complexes in Galp

67 n3, but not cten, augmented the formation of actin stress fibers and focal adhesions and enhanced cel

68 ing arg-/- fibroblasts have more prominent F-actin stress fibers and focal adhesions and exhibit incr

69 beta(1) integrin to promote the formation of actin stress fibers and focal adhesions in fibronectin (

70 Myocilin transduction resulted in a loss of actin stress fibers and focal adhesions in TM cells in c

71 ro, and diverts its normal localization from actin stress fibers and focal adhesions in vivo.

72 The presence of actin stress fibers and focal adhesions was determined b

73 ng to reduced Rho-GTPase activity, decreased actin stress fibers and focal adhesions, and reduced mot

74 cells exhibited a decrease in the number of actin stress fibers and focal adhesions, leading to enha

75 gh the mutant cells exhibited alterations in actin stress fibers and focal adhesions, no other phenot

76 d human TM cells, induced a dramatic loss of actin stress fibers and focal adhesions.

77 two proteins; and ultimately disassembly of actin stress fibers and focal adhesions.

78 p27(-/-) cells have increased numbers of actin stress fibers and focal adhesions.

79 ither Sema3d or Sema3e demonstrate a loss of actin stress fibers and focal adhesions.

80 Activation of v-Src elicited a loss of actin stress fibers and focal contacts.

81 blasts by oncogenic Src causes disruption of actin stress fibers and formation of invasive adhesions

82 F-actin organization disruption with loss of actin stress fibers and formation of membranous F-actin

83 eport that UNC-45a is a dynamic component of actin stress fibers and functions as a myosin chaperone

84 gulates the formation of focal adhesions and actin stress fibers and hence plays an important role in

85 A pathway, producing enhanced development of actin stress fibers and impaired migration of cancer cel

86 ions for the assembly of focal adhesions and actin stress fibers and in the phosphorylation of focal

87 The collapse of actin stress fibers and increased trypsin sensitivity fr

88 fibroblasts, Shroom readily associates with actin stress fibers and induces bundling, Apxl is found

89 EPLIN increases the number and size of actin stress fibers and inhibits membrane ruffling induc

90 There was also loss of wide F-actin stress fibers and large focal adhesions.

91 olves mechanosensitive targeting of zyxin to actin stress fibers and localized recruitment of actin r

92 tat3 caused the rearrangement of cytoplasmic actin stress fibers and microtubules in both DU145 and P

93 NMU independently induced actin stress fibers and MLC phosphorylation in TM cells,

94 ulted in cell shape changes and decreases in actin stress fibers and MLC phosphorylation.

95 reated cells had a more extensive network of actin stress fibers and more numerous focal adhesion pla

96 creased intracellular calcium, and decreased actin stress fibers and myosin light chain phosphorylati

97 interfering RNA (siRNA) caused a decrease in actin stress fibers and myosin light chain phosphorylati

98 vitro, dominant negative N19RhoA reduced EC actin stress fibers and prevented ECs from contracting a

99 endent cation/Ca(2+) influx, thickening of F-actin stress fibers and reinforcement of focal adhesion

100 T also produced a marked increase in central actin stress fibers and significantly altered VE-cadheri

101 al Src in Myc-deficient cells led to loss of actin stress fibers and surface fibronectin, indicating

102 tion, leading to the association of Fas with actin stress fibers and the adaptor protein TRIP6.

103 nculin treatment triggered a coupled loss of actin stress fibers and the colocalized, long-lived CaMK

104 generate cellular actin structures, such as actin stress fibers and the cytokinetic actomyosin contr

105 formation of contractile smooth muscle alpha-actin stress fibers and the deposition of collagen type

106 -in signaling as measured by cell spreading, actin stress-fiber and focal adhesion formation, and foc

107 n, migration, tube formation, formation of F-actin stress fiber, and in vivo Matrigel angiogenesis.

108 impaired organization of focal adhesions and actin stress fibers, and an irregular cell shape.

109 cellular and nuclear membranes, contractile actin stress fibers, and focal adhesion dynamics; 3) str

110 maintaining optimal FAs, for organization of actin stress fibers, and for cell migration and spreadin

111 g to actinomyosin contractility, assembly of actin stress fibers, and formation of focal adhesions.

112 ells of the aorta, spleen, and eye occurs in actin stress fibers, and is necessary for normal cell fu

113 l polarization, a reduction in the number of actin stress fibers, and less punctate labeling of focal

114 h depolymerization of initially high-tension actin stress fibers, and reinforcement of an initially l

115 eins strongly bind F-actin, are localized to actin stress fibers, and synergistically enhance STARS-d

116 es with myosin phosphorylation, formation of actin stress fibers, and the appearance of paracellular

117 expressing the GEF-deficient F1685A mutant: Actin stress fibers are decreased and cell migration is

118 Actin stress fibers are required for HSC contraction, an

119 ells, leading to reduced focal adhesions and actin stress fibers as well as altered morphology.

120 TGF-beta induced actin stress fibers as well as lamellipodia within the l

121 meshwork cells, and there was a decrease of actin stress fibers, as well as a decrease in focal adhe

122 in the developing mammary gland compromised actin stress fiber assembly and inhibited cell contracti

123 otile cells by unknown mechanisms to control actin stress fiber assembly, contractility, and focal ad

124 Here we identified a novel actin stress fiber-associated protein, LIM and calponin-

125 change their form and function by assembling actin stress fibers at their base and exerting traction

126 2CLP monolayers had fewer actin stress fibers before stretch, a more robust stretc

127 The role of the MDV US3 protein in actin stress fiber breakdown was investigated by visuali

128 ncogenic H-RasV12 contributes to the loss of actin stress fibers by inducing cytoplasmic localization

129 ll metastasis is unclear, but disassembly of actin stress fibers by platelet-derived growth factor an

130 ive Src in metastatic UMUC-3 cells decreases actin stress fibers, cell migration, and metastasis, whi

131 evelopment of thrombin-induced transcellular actin stress fibers, cellular contractions, and paracell

132 escent dextran and in formation of increased actin stress fibers compared to RhoA-transfected cells,

133 ent changes in cell morphology, decreases in actin stress fiber content and in focal adhesions and ad

134 y staining was used to determine filamentous actin stress fiber content, whereas Western blot analysi

135 matrix deposition, involves formation of an actin stress fiber contractile apparatus that radiates f

136 ells (HSCs) and is necessary for assembly of actin stress fibers, contractility, and chemotaxis.

137 tly with actin filaments and functions as an actin stress fiber cross-linking protein that promotes t

138 We have examined the ability of actin stress fiber disassembly to induce lens cell diffe

139 riggers actin depolymerization, resulting in actin-stress-fiber disassembly through p53-dependent Rho

140 nce microscopic evidence of both cytoplasmic actin stress fiber dissolution and strong augmentation o

141 ial for down-regulation of Rho signaling and actin stress fiber dissolution.

142 family GTPase-activating protein, regulates actin stress fiber dynamics via hydrolysis of Rho-GTP.

143 ality is characterized by a decrease in long actin stress fibers, enhanced sensitivity to actin depol

144 igration, tube formation, and formation of F-actin stress fiber, even in the absence of VEGF-A(165) s

145 grin prevented damage-induced decreases in F-actin stress fibers, focal adhesions, and active beta1-i

146 cell morphology and reversible decreases in actin stress fibers, focal adhesions, and adherens junct

147 sible changes in cell shape and decreases in actin stress fibers, focal adhesions, and protein phosph

148 cific inhibitor (Y-27632)-induced changes in actin stress fibers, focal adhesions, and protein phosph

149 ed protein kinases (MAPKs) in 4-HNE-mediated actin stress fiber formation and barrier function in lun

150 tion was associated with mild increases in F-actin stress fiber formation and causally linked to p38

151 this beneficial effect in part by preventing actin stress fiber formation and claudin 18 disorganizat

152 le depolymerization results in Rho-dependent actin stress fiber formation and contractile cell morpho

153 VASP at Ser-239 is accompanied by increased actin stress fiber formation and enhanced endothelial tu

154 xanox, a compound that is known to attenuate actin stress fiber formation and FGF1 release, was able

155 IGPR-1 activity also modulates actin stress fiber formation and focal adhesion and redu

156 ree to which G1 phase progression depends on actin stress fiber formation and imposition of cellular

157 MLCK) through integrin beta1 is required for actin stress fiber formation and proliferative growth.

158 utant protein in Nf1(-/-) astrocytes rescued actin stress fiber formation and restored cell motility

159 Acute hypoxia enhanced actin stress fiber formation and RhoA activity in both i

160 zyxin using siRNA inhibited thrombin-induced actin stress fiber formation and SRE-dependent gene tran

161 othelial migration include the disruption of actin stress fiber formation and the decreased expressio

162 ion, myosin light chain phosphorylation, and actin stress fiber formation as well as inter-endothelia

163 e find that the ability of NET1 to stimulate actin stress fiber formation does not correlate with its

164 uced myosin light chain phosphorylation, and actin stress fiber formation due to JAM-C knockdown.

165 MCP1 also stimulated F-actin stress fiber formation in a delayed manner in HASM

166 factor in vitro and its ability to stimulate actin stress fiber formation in cells.

167 human homolog, zebrafish Arhgef11 stimulated actin stress fiber formation in cultured cells, whereas

168 permeabilities induced by PMA, and increased actin stress fiber formation in epithelial and endotheli

169 ulation failed to induce RhoA activation and actin stress fiber formation in human pulmonary arterial

170 an increase in paracellular permeability and actin stress fiber formation in lung microvascular endot

171 ermore, constitutively active EhRho1 induces actin stress fiber formation in mammalian fibroblasts, t

172 Firm adhesion to both ligands and actin stress fiber formation required both Syk and Rho a

173 200RhoGAP in Swiss 3T3 fibroblasts inhibited actin stress fiber formation stimulated by lysophosphati

174 e of PKD as a regulator of RhoA activity and actin stress fiber formation through phosphorylation of

175 ced, and G protein-coupled receptor-induced, actin stress fiber formation was completely blocked.

176 ROCK-mediated cytoskeleton re-organization (actin stress fiber formation) following LPA stimulation,

177 horylation and NO bioavailability, increased actin stress fiber formation, and a lack of distinct cel

178 ix contraction by preventing cell spreading, actin stress fiber formation, and activation of focal ad

179 arcoma HT1080 cells enhanced cell spreading, actin stress fiber formation, and adhesion to extracellu

180 WAVE2 interaction, G-actin polymerization, F-actin stress fiber formation, and HASMC migration.

181 h WAVE2, affecting G-actin polymerization, F-actin stress fiber formation, and HASMC migration.

182 of HTM cells with CTGF for 24 hours induced actin stress fiber formation, and increased MLC phosphor

183 n, disruption of interendothelial junctions, actin stress fiber formation, and increased permeability

184 MCP1-induced HASMC G-actin polymerization, F-actin stress fiber formation, and migration.

185 expression, increased RhoA activity, induced actin stress fiber formation, and produced an amplified

186 horylation, increased RhoA activity, induced actin stress fiber formation, and produced an irreversib

187 ppressed myosin light chain phosphorylation, actin stress fiber formation, and the increased endothel

188 njury induced increases of NO production and actin stress fiber formation, both of which were markedl

189 integrin cluster formation is independent of actin stress fiber formation, but requires active (high-

190 MEKK1-driven JNK activation is required for actin stress fiber formation, c-Jun phosphorylation and

191 other G-protein receptor-coupled agonists on actin stress fiber formation, cell shape change, and ROS

192 l) reduced constitutive alphaSMA expression, actin stress fiber formation, contraction, and nuclear S

193 y employing integrin alpha9beta1, abolishing actin stress fiber formation, inhibiting YAP and its tar

194 SnoN exhibited an increase in cell motility, actin stress fiber formation, metalloprotease activity,

195 tion of Pak1 suppressed MCP1-induced HASMC F-actin stress fiber formation, migration, and proliferati

196 k1 signaling and, thereby, decreased HASMC F-actin stress fiber formation, migration, and proliferati

197 activation and resulted in decreased HASMC F-actin stress fiber formation, migration, and proliferati

198 rther show that mTOR-dependent regulation of actin stress fiber formation, motility, and proliferatio

199 of lamellipodia, DeltaN-Ect2 DH/PH enhanced actin stress fiber formation, suggesting that C-terminal

200 nt resulted in a decrease of G-actin and the actin stress fiber formation, the effects seen upon FDH

201 JNK is involved in transcription-independent actin stress fiber formation, which needs also the activ

202 ctor kinases ROCK1 and -2, which all prevent actin stress fiber formation.

203 the ability of full-length NET1 to stimulate actin stress fiber formation.

204 in alveolar epithelial cells, which requires actin stress fiber formation.

205 ontacts, a loss of VE-cadherin, and aberrant actin stress fiber formation.

206 creasing its dependence on ERK signaling and actin stress fiber formation.

207 eficent cells restored the G protein-induced actin stress fiber formation.

208 phorylation by myosin light chain kinase and actin stress fiber formation.

209 The ability of LMP1 to induce actin stress-fiber formation, a Rho GTPase-mediated phen

210 ads to the stimulation of ROCK, which causes actin stress-fiber formation.

211 tal reorganization with filamentous actin (F-actin) stress fiber formation.

212 was associated with lack of thrombin-induced actin-stress fiber formation and a reduced endothelial c

213 Prolonged FlnB loss, however, promotes actin-stress fiber formation following plating onto an i

214 Loss of actin stress fibers has been associated with cell transf

215 trained and isotropic cells, which lack long actin stress fibers, have more deformable nuclei than el

216 d reinforcement and gradual reorientation of actin stress fibers; however, the mechanism by which cel

217 sion of ARHI also disrupted the formation of actin stress fibers in a FAK- and RhoA-dependent manner.

218 ion/inactivation of cofilin and formation of actin stress fibers in a ROCK-dependent manner.

219 g, focal adhesion density, and the number of actin stress fibers in a substrate-dependent manner.

220 developed to describe the reorganization of actin stress fibers in adherent cells in response to div

221 small GTPase Rho regulates the formation of actin stress fibers in adherent cells through activation

222 et cells upon cell contact induces a loss of actin stress fibers in cells and promotes the reorganiza

223 yamine depletion caused the disappearance of actin stress fibers in cells transfected with empty vect

224 Experimental disassembly of actin stress fibers in cultured lens epithelial cells wi

225 pastatin prevented VEGF-induced increases in actin stress fibers in endothelial cells and angiogenesi

226 rcomeres are the tension-generating units of actin stress fibers in endothelial cells.

227 ation of an elaborate fibronectin matrix and actin stress fibers in fibrin-embedded tumor cells.

228 triggered changes in cell shape and reduced actin stress fibers in HTM cells but did not exert signi

229 Both the actin stress fibers in lens epithelial cells and the cor

230 Significantly, short-term disassembly of actin stress fibers in lens epithelial cells by cytochal

231 bundled actin filaments and associated with actin stress fibers in microinjected cells.

232 factor beta (TGF-beta)-mediated induction of actin stress fibers in normal and metastatic epithelial

233 Reinforcement of actin stress fibers in response to mechanical stimulatio

234 Rho-GTP loading in vivo and the formation of actin stress fibers in response to serum or LPA stimulat

235 ain of Daam1 and was localized with Daam1 to actin stress fibers in response to Wnt signaling in mamm

236 rphological change and enhanced formation of actin stress fibers in squamous cancer cells.

237 protein occludin and decreased the number of actin stress fibers in the absence of cell death.

238 pha-actinin with phosphoinositides regulates actin stress fibers in the cell by controlling the exten

239 nexpectedly, deletion of Rac1 also abolished actin stress fibers in the cells without detectable alte

240 d this was again dependent on the absence of actin stress fibers in the cells.

241 e demonstrate that adenosine induces loss of actin stress fibers in the LX-2 cell line and primary HS

242 and E-cadherins, as well as the formation of actin stress fibers in these cells.

243 e-stranded DNA in vitro and microtubules and actin stress fibers in whole cells.

244 lated myosin light chain colocalization with actin stress fibers increased in endothelial monolayers

245 Our results demonstrate that disassembly of actin stress fibers induced lens cell differentiation, a

246 oA in myosin light chain phosphorylation and actin stress fiber induction but sensitized the cells to

247 We further demonstrate that loss of actin stress fibers is due to a cyclic adenosine monopho

248 ch promotes formation of focal adhesions and actin stress fibers, is inhibited upon initial cell atta

249 FA6R regulated ARF6 localization and thereby actin stress fiber loss.

250 ed myocilin phenotypes including the loss of actin stress fibers, lowered RhoA activities and comprom

251 e-dimensional VIC hydrogels, suggesting that actin stress fibers mediate TNF-alpha-induced effects.

252 er cells and evaluated the effect of this on actin stress fibers, migration using Transwells, and lun

253 denatured collagen possess a well-defined F-actin stress fiber network, a spread morphology, and the

254 stent with these findings, the high level of actin stress fibers normally present in MEFs was conside

255 Loss of actin stress fibers occurs via the A2a receptor at adeno

256 eted of RhoA showed no significant change in actin stress fiber or focal adhesion complex formation i

257 e presence of lovastatin exhibited a loss of actin stress fiber organization concomitant with a marke

258 Changes in filamentous actin stress fiber organization were visualized with Ale

259 pyrophosphate to the culture medium restored actin stress fiber organization while selectively facili

260 tin (Eln(-/-)), we show that elastin induces actin stress fiber organization, inhibits proliferation,

261 l velocity, induced elongation, and promoted actin stress fiber organization.

262 /3, or alter the proportion of smooth muscle actin stress fiber-positive fibroblasts.

263 Incorporation of NM-II into actin stress fiber provides a traction force to promote

264 oma, with reduced ASAP3 expression had fewer actin stress fiber, reduced levels of phosphomyosin, and

265 Thickening of actin stress fibers reflects a cellular adaptation to me

266 sts to uniaxial cyclic stretch results in an actin stress fiber reinforcement response that stabilize

267 L) protein, and causes a significant loss in actin stress fibers, reminiscent of what is observed wit

268 Zyxin-null fibroblasts also show deficits in actin stress fiber remodeling and exhibit changes in the

269 integrin expression, RhoGTPase activity and actin stress fiber remodeling.

270 fluence integrin-dependent cell motility and actin stress fiber remodeling.

271 lin-2-expressing HeLa cells showed a loss of actin stress fibers, Rhophilin-1 expression had no notic

272 While some Drf1 +/- lines had fewer actin stress fibers, several Drf1 +/- and -/- cells were

273 but not EGF or IGF-1 causes a rapid loss of actin stress fibers (SFs) and focal adhesions (FAs), whi

274 Actin stress fibers (SFs) are load-bearing and mechanose

275 Actin stress fibers (SFs) play an important role in many

276 and podocyte GR knockout mice showed similar actin stress fiber staining patterns in unstimulated con

277 xhibited an unusual polygonal arrangement of actin stress fibers that indicated a profound change in

278 erase each inhibited collagen I induction of actin stress fibers that mediate cell retraction and eac

279 logical changes, including the disruption of actin stress fibers, the loss of focal adhesion sites, m

280 ounding is caused by the depolymerization of actin stress fibers, through the unique mechanism of cov

281 at allows it to guide microtubule ends along actin stress fibers to focal adhesions, promoting disass

282 ng revealed that SHP-2 was co-localized with actin stress fibers to the cell peripheral at low cell d

283 gged cytoskeletal proteins, we observed that actin stress fibers undergo local, acute, force-induced

284 ubule-associated formin, mDIA2, localized to actin stress fibers upon treatment with TGF-beta, and pa

285 Disruption of actin stress fibers using any of these redifferentiation

286 s rapidly (10 min) induced the appearance of actin stress fibers via a Rho-mediated pathway.

287 Enhanced formation of actin stress fibers was also observed in the Ikkbeta(-/-

288 regions suggested that the disassembly of F-actin stress fibers was not simply caused by Rho sequest

289 Association of uPAR with actin stress fibers was visualized when FITC-labeled uPA

290 e important role of Rac1 in the formation of actin stress fibers, we examined the effect of adenosine

291 ntrols, the cell migration was retarded, the actin stress fibers were fewer and shorter, and the tryp

292 EGFP-tagged FERM subdomains colocalize with actin stress fibers when expressed in COS cells.

293 GFP fusion expressing this domain decorates actin stress fibers when expressed in MDCK cells.

294 s in cell morphology and the accumulation of actin stress fibers, whereas Maf1 overexpression suppres

295 TGF-beta promotes association of mDia2 with actin stress fibers, which further drives stress fiber f

296 domain but did not maintain the formation of actin stress fibers, which indicated that Rho had been i

297 on of the C3aR caused transient formation of actin stress fibers, which was not PT-sensitive, but dep

298 ed (NP) surface coated with FN, showed clear actin stress fibers with anchoring spots of phosphorylat

299 ies with RhoA and Rho kinase, colocalizes on actin stress fibers with RhoA and MBS, and is associated

300 semaphorin 3C, and exhibited disorganized F-actin stress fibers within the aorticopulmonary septum.