ライフサイエンスコーパス: actin stress fiber

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

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

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

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

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

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

7 othelial junctions associated with increased actin stress fibers.

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

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

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

11 expression by siRNA caused disappearance of actin stress fibers.

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

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

14 oliferative, with mature alpha-smooth muscle actin stress fibers.

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

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

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

18 terior cytoplasm and function to disassemble actin stress fibers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 stiffness was accompanied by the presence of actin stress fibers and accumulation of the inactive, ph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 ion molecules was accompanied by increased F-actin stress fibers and increased endothelial barrier pe

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

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

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

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

83 t a starved adhesion phenotype consisting of actin stress fibers and large peripheral focal adhesion.

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

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

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

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

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

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

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

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

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

93 phosphor mutants had defects in alleviating actin stress fibers and rescuing the reduced invasivenes

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

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

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

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

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

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

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

101 oblasts formed alphaSMA (alpha-smooth muscle actin) stress fibers and expressed myofibroblast-specifi

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

103 s to one with increased cytoplasm, extensive actin stress fibers, and actomyosin-dependent flattening

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

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

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

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

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

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

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

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

112 Poorly developed filamentous actin stress fibers are found only in cells on 3-um netw

113 Actin stress fibers are required for HSC contraction, an

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

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

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

117 IGPR-1 activation stimulated actin stress fiber assembly and cross-linking with vincu

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

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

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

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

122 2CLP monolayers had fewer actin stress fibers before stretch, a more robust stretc

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

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

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

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

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

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

129 riented basement membrane (BM) fibrils and F-actin stress fibers constrain follicle growth, promoting

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

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

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

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

134 HPKs by inhibiting the actomyosin machinery (actin stress fibers, contractility, and stiffness).

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

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

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

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

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

140 Actin stress fiber dynamics are required for thrombin-in

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

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

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

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

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

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

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

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

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

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

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

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

153 ocked N-WASP effects in P aeruginosa-induced actin stress fiber formation and increased paracellular

154 wnregulation attenuated P aeruginosa-induced actin stress fiber formation and prevented paracellular

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 200RhoGAP in Swiss 3T3 fibroblasts inhibited actin stress fiber formation stimulated by lysophosphati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 eficent cells restored the G protein-induced 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 ads to the stimulation of ROCK, which causes actin stress-fiber formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 ed cell spreading while reducing contractile actin stress fibers in normal and breast cancer cells an

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

229 Reinforcement of actin stress fibers in response to mechanical stimulatio

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

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

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

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

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

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

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

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

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

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

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

241 sion in cultured ECs led to increased radial actin stress fibers, increased adherens junction width a

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

243 EGF-induced endothelial cell signaling for F-actin stress fiber inducing endothelial barrier dysfunct

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

245 we describe that IL-9 profoundly reduced the actin stress fibers, inhibited contractility, and reduce

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

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

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

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

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

251 s show that YAP activation is dependent on F-actin stress fiber mediated nuclear pore opening, howeve

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 along the cell long axis (i.e., alignment of actin stress fibers) or at different angles (90 degrees

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

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

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

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 IL-17A increased the actin stress fibers, promoted cellular contractility, an

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

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

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

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

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

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

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

271 helial cell cultures and explants results in actin stress fiber reorganization, stimulation of focal

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

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

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

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

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

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

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

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

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

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

282 dynamic shortening of myosin IIA-associated actin stress fibers to drive rapid fibronectin fibrillog

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

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

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

286 Disruption of actin stress fibers using any of these redifferentiation

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

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

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 tinal epithelial tight junction and within F-actin stress fibers where it is critical for barrier int

294 othelial cells increased focal adhesions and actin stress fibers whereas FOXC2-KD increased focal adh

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

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

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.