ライフサイエンスコーパス: stress fiber

1 mechanical information along the length of a stress fiber.

2 tic Kelvin-Voigt element that represents the stress fiber.

3 ontractile actomyosin bundles called ventral stress fibers.

4 n muscle Z-disks, focal adhesions, and actin stress fibers.

5 studied remodeling of contractile actomyosin stress fibers.

6 loss is accompanied by an increase in actin stress fibers.

7 st cancer cells and induces the formation of stress fibers.

8 s similar to those of in vivo myofibrils and stress fibers.

9 ytes required the induction of RhoA-mediated stress fibers.

10 ation for mechanics of contractile rings and stress fibers.

11 ociated with the presence of disrupted actin stress fibers.

12 downregulation of focal adhesions and actin stress fibers.

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

14 ied by alpha-smooth muscle actin (alpha-SMA) stress fibers.

15 ential role in structures from sarcomeres to stress fibers.

16 main and affect formation of host-cell actin stress fibers.

17 es, in which alpha-SMA was incorporated into stress fibers.

18 recruit nonmuscle myosin II and mature into stress fibers.

19 rce-sensitive accumulation of zyxin on actin stress fibers.

20 gen I and alpha-smooth muscle actin-positive stress fibers.

21 of RhoA and formation of focal adhesions and stress fibers.

22 odia formation and reorganization of F-actin stress fibers.

23 es surrounding the endoplasm, adhesions, and stress fibers.

24 ze, transient traction forces, and decreased stress fibers.

25 stimulates formation of focal adhesions and stress fibers.

26 in contributes to the assembly of functional stress fibers.

27 activation of RhoA, and to the formation of stress fibers.

28 n of G-actin and disrupting the formation of stress fibers.

29 of filamentous actin and formation of actin stress fibers.

30 ation of prominent focal adhesions and actin stress fibers.

31 ns from this preferred level destabilize the stress fibers.

32 as lamellar meshes, filopodial bundles, and stress fibers.

33 chains highly reminiscent of mammalian cell stress fibers.

34 scently tagged Tpm3.1 recovers normally into stress fibers.

35 eorganization of the actin cytoskeleton into stress fibers.

36 nical sensing is dependent on RhoA-regulated stress fibers.

37 l decrease in the number and total length of stress fibers.

38 of ECs reduced TNFalpha-induced increases in stress fibers.

39 ation of contractile acto-myosin bundles, or stress fibers.

40 the appearance of alpha-smooth muscle actin stress fibers.

41 of Rho kinase or nonmuscle myosin attenuated stress fiber accumulation and abrogated LR asymmetry of

42 ritically to the mechanochemical behavior of stress fibers, actin arcs, and cortical actin-based stru

43 tion: cell elongation and formation of actin stress fibers aligned to the flow direction.

44 ugh increased cell adhesion, elongation, and stress fiber alignment.

45 ected protrusions and the formation of actin stress fibers anchored in streak-like focal adhesions.

46 ed by KAI1/CD82, consistent with the loss of stress fiber and attenuation in cellular retraction.

47 oor formations of actin cortical network and stress fiber and by aberrant dynamics in actin organizat

48 o1 in endothelial cells leads to deficits in stress fiber and cellular orientation in response to she

49 RhoA signaling controls stress fiber and focal adhesion formation and cell motil

50 RhoA(-/-) cells resulted in a loss of actin stress fiber and focal adhesion similar to that of C3 to

51 is associated with a significant increase of stress fiber and gap formation in EC.

52 initial stretch increases the tension in the stress fiber and suppresses myosin detachment.

53 rease in focal adhesion sites, reduced actin stress fibers and a collapse of microtubule structures.

54 dynamic disassembly and reassembly of actin stress fibers and associated focal adhesions to the acti

55 beta-catenin level, which decreases F-actin stress fibers and attenuates plasma membrane resealing.

56 n responses occurred for all orientations of stress fibers and cellular protrusions relative to the s

57 ctin and alpha-SMA in animals, whereas actin stress fibers and contractility are both induced in cult

58 pears to underlie its ability to localize to stress fibers and decrease cell migration.

59 ppears to affect integrins by reducing actin stress fibers and disrupting focal adhesions.

60 chicine, resulted in a formation of numerous stress fibers and expression of myofibroblast differenti

61 Similar configurations were observed in stress fibers and filopodia, suggesting that nanoscopic

62 Palladin coexists with alpha-actinin in stress fibers and focal adhesions and binds to both acti

63 t not cten, augmented the formation of actin stress fibers and focal adhesions and enhanced cell moti

64 sts that the mechanical coupling between the stress fibers and focal adhesions leads to a complex, dy

65 of SM alpha-actin induction on formation of stress fibers and focal adhesions, filamentous to solubl

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

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

68 that UNC-45a is a dynamic component of actin stress fibers and functions as a myosin chaperone in viv

69 PS, GR knockout podocytes demonstrated fewer stress fibers and impaired migration compared to wild ty

70 way, producing enhanced development of actin stress fibers and impaired migration of cancer cells.

71 , is a component of alpha-actinin containing stress fibers and inhibits migration.

72 ilaments and higher order structures such as stress fibers and lamellipodia are fundamental for cell

73 ed the appearance of actin-rich protrusions, stress fibers and large basal focal adhesions, while inc

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

75 mechanosensitive targeting of zyxin to actin stress fibers and localized recruitment of actin regulat

76 PDGF also induces stress fibers and loss of cell-cell contacts of epicardi

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

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

79 d intracellular calcium, and decreased actin stress fibers and myosin light chain phosphorylation, wi

80 ering RNA (siRNA) caused a decrease in actin stress fibers and myosin light chain phosphorylation.

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

82 in the Cutando et al. article) in cerebellar stress fibers and the activation of microglia, raising p

83 leading to the association of Fas with actin stress fibers and the adaptor protein TRIP6.

84 treatment triggered a coupled loss of actin stress fibers and the colocalized, long-lived CaMKII tra

85 ate cellular actin structures, such as actin stress fibers and the cytokinetic actomyosin contractile

86 ion of contractile smooth muscle alpha-actin stress fibers and the deposition of collagen type I, whi

87 This leads to the disassembly of the stress fibers and the observed fluidization.

88 by reinforcing the cross-linking of lamellar stress fibers and the stability of nascent focal adhesio

89 CAFs to phorbol esters reduced the number of stress fibers and triggered the appearance of individual

90 factor, an increase in contractile F-actin 'stress' fibers and blocks invasive growth in three-dimen

91 ss path, i.e., a percolating path of axially stressed fibers and cross-links, we demonstrate that the

92 ration, tube formation, formation of F-actin stress fiber, and in vivo Matrigel angiogenesis.

93 lar and nuclear membranes, contractile actin stress fibers, and focal adhesion dynamics; 3) structura

94 a major upstream regulator of RhoA activity, stress fibers, and focal adhesion formation in keratinoc

95 Dorsoventral polarity, stress fibers, and focal adhesions are markedly attenuat

96 ining optimal FAs, for organization of actin stress fibers, and for cell migration and spreading.

97 of myosin phosphatase, promoted assembly of stress fibers, and increased the formation of plasma mem

98 rization, a reduction in the number of actin stress fibers, and less punctate labeling of focal adhes

99 l contact and an elevation of cellular RhoA, stress fibers, and other indicators of contractile signa

100 lymerization of initially high-tension actin stress fibers, and reinforcement of an initially low-ten

101 tion, and indicators of contractility (i.e., stress fibers, arcs, and focal adhesions) and are primed

102 Importantly, stress fibers are critical for several endothelial cell

103 ssing the GEF-deficient F1685A mutant: Actin stress fibers are decreased and cell migration is inhibi

104 While it is well established that stress fibers are mechanosensitive structures, physical

105 anging from contractile lamellar networks to stress fibers are observed in adherent cells.

106 The model is based on the assumptions that stress fibers are pre-extended to a preferred level unde

107 Contractile actomyosin bundles, stress fibers, are crucial for adhesion, morphogenesis,

108 in structures, such as contractile rings and stress fibers, are poorly understood.

109 hanges manifest themselves as alterations in stress fiber arrangement rather than cortical cytoskelet

110 45a knockout cells display severe defects in stress fiber assembly and consequent abnormalities in ce

111 As myosin II activity drives stress fiber assembly and enhanced tension at adhesions

112 e developing mammary gland compromised actin stress fiber assembly and inhibited cell contractility t

113 pha-actinin 1 activity selectively inhibited stress fiber assembly at adhesions but retained a contra

114 We propose that stress fiber assembly at the adhesion site serves as a s

115 on dynamics and force transmission, impaired stress fiber assembly impeded focal adhesion composition

116 rks is unaffected, whereas tension-dependent stress fiber assembly is abrogated.

117 of either protein produces graded changes in stress fiber assembly, traction force generation, cellul

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

119 MM), two distinct pools of SMM, diffuse, and stress-fiber-associated, were visualized by immunocytoch

120 ar cells polarized rightward and accumulated stress fibers at an unbiased mechanical interface betwee

121 on of the transverse arc and radial (dorsal) stress fibers at the leading lamella of migrating renal

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

123 As stress fibers build and tension increases, myosin band s

124 occurred in expanding or contracting intact stress fibers but over much longer timescales.

125 vented actin polymerization and formation of stress fibers by reducing the activation of RhoA and pho

126 up-regulated formation of actin cytoskeleton stress fibers, caused redistribution of more F-actin fib

127 c in metastatic UMUC-3 cells decreases actin stress fibers, cell migration, and metastasis, while Cav

128 ment of thrombin-induced transcellular actin stress fibers, cellular contractions, and paracellular g

129 Instead, we found that a subset of stress fibers continuously elongated at their attachment

130 Stress fibers-contractile actomyosin bundles-are importa

131 th actin filaments and functions as an actin stress fiber cross-linking protein that promotes the mat

132 pidly accumulates at sites of strain-induced stress fiber damage and is essential for stress fiber re

133 ong cytoskeletal changes: disorganization of stress fibers, decreased number of focal adhesions, and

134 as been observed that CDR formation leads to stress fibers disappearing near the CDRs.

135 mammalian cells results in cell rounding and stress fiber disruption, a phenotype that is rescued by

136 r down-regulation of Rho signaling and actin stress fiber dissolution.

137 d phosphorylation of VASP, and thereby halts stress fiber elongation and ensures their proper contrac

138 revented damage-induced decreases in F-actin stress fibers, focal adhesions, and active beta1-integri

139 distinguished by the initial geometry of the stress fiber-focal adhesion system, and by the external

140 the mechanochemistry governing force in the stress fiber-focal adhesion system.

141 Finally, we measured resting stress fibers, for which the model predicts constant act

142 While conventional basal stress fibers form only past a threshold shear stress of

143 tent in HLFs, but inhibited TGF-beta-induced stress fiber formation and activation of serum response

144 hoA and its downstream effector ROCK mediate stress fiber formation and cell contraction through thei

145 es in mouse embryonic fibroblasts, including stress fiber formation and cell migration, it's deletion

146 to activate RhoA and activated RhoA leads to stress fiber formation and cell spreading.

147 eases outflow facility, whereas S1P promotes stress fiber formation and contractility in cultured tra

148 xcessive migratory response through enhanced stress fiber formation and disruption of endothelial cel

149 Moreover, C4a increased stress fiber formation and enhanced endothelial permeabi

150 IGPR-1 activity also modulates actin stress fiber formation and focal adhesion and reduces ce

151 tured mouse podocytes with Bis-T-23 promoted stress fiber formation and focal adhesion maturation in

152 bers, we examined the effect of adenosine on stress fiber formation and found that adenosine inhibits

153 leted cells display substantial decreases of stress fiber formation and impaired cell migration and s

154 ning protein (Radil) to inhibit Rho-mediated stress fiber formation and induces junctional tightening

155 ed keratocyte contractility, as indicated by stress fiber formation and matrix compaction and alignme

156 th actin stress fibers, which further drives stress fiber formation and myofibroblast differentiation

157 tor, SMI formin homology 2 domain, inhibited stress fiber formation and myofibroblast differentiation

158 the decrease in the E-cadherin abundance and stress fiber formation by TGF-beta, gene ontology analys

159 Because stress fiber formation can be modified by substrate stif

160 RhoA and RhoB maximized the hypoxia-induced stress fiber formation caused by RhoB/mammalian homolog

161 PAR1 wildtype strongly induced RhoA-mediated stress fiber formation compared with mutant receptor.

162 increasing stiffness raised mDia1-nucleated stress fiber formation due to Rho activation.

163 VEGF(164), play a crucial role in transient stress fiber formation during osteoblast mechanotransduc

164 Prolonged FlnB loss, however, promotes actin-stress fiber formation following plating onto an integri

165 MCP1 also stimulated F-actin stress fiber formation in a delayed manner in HASMCs, as

166 othelial resistance changes and cytoskeletal stress fiber formation in both human umbilical vein endo

167 rease in paracellular permeability and actin stress fiber formation in lung microvascular endothelial

168 , constitutively active EhRho1 induces actin stress fiber formation in mammalian fibroblasts, thereby

169 dium or exogenous VEGF significantly induces stress fiber formation in osteoblasts that is comparable

170 A key mediator of steady flow-induced stress fiber formation is Src that regulates downstream

171 cesses within 3-D matrices, without inducing stress fiber formation or collagen reorganization.

172 a fluid shear stress-mediated mechanism for stress fiber formation that involves a TXNIP-dependent v

173 KD as a regulator of RhoA activity and actin stress fiber formation through phosphorylation of rhotek

174 mplex with RhoA and switch Rho function from stress fiber formation to membrane ruffling to confer an

175 nistically, LPP increased focal adhesion and stress fiber formation to promote endothelial cell motil

176 the S435E rhotekin mutant displayed enhanced stress fiber formation when expressed in serum-starved f

177 mediated cytoskeleton re-organization (actin stress fiber formation) following LPA stimulation, but d

178 lectrical resistance, increased actinomyosin stress fiber formation, and alterations in tight junctio

179 a formation, cell spreading, focal adhesion, stress fiber formation, and compaction, whereas Par1b de

180 2, affecting G-actin polymerization, F-actin stress fiber formation, and HASMC migration.

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

182 M cells with CTGF for 24 hours induced actin stress fiber formation, and increased MLC phosphorylatio

183 ruption of interendothelial junctions, actin stress fiber formation, and increased permeability in co

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

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

186 induced increases of NO production and actin stress fiber formation, both of which were markedly redu

187 farnesylation leading to RhoA-ROCK-mediated stress fiber formation, but membrane dynamics is reliant

188 in cluster formation is independent of actin stress fiber formation, but requires active (high-affini

189 tective effect was associated with increased stress fiber formation, cell-matrix, and cell-cell adhes

190 uced constitutive alphaSMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3

191 ion, serum response factor response element, stress fiber formation, ERK1/2 phosphorylation, and beta

192 o ECM stiffening including cell spread area, stress fiber formation, focal adhesion maturation, and i

193 oying integrin alpha9beta1, abolishing actin stress fiber formation, inhibiting YAP and its target ge

194 tor, thrombin, exaggerated AJ disruption and stress fiber formation, leading to an irreversible incre

195 f Pak1 suppressed MCP1-induced HASMC F-actin stress fiber formation, migration, and proliferation.

196 naling and, thereby, decreased HASMC F-actin stress fiber formation, migration, and proliferation.

197 tion and resulted in decreased HASMC F-actin stress fiber formation, migration, and proliferation.

198 ncluding extension of cellular processes and stress fiber formation, occurred predominantly in the st

199 ulted in a decrease of G-actin and the actin stress fiber formation, the effects seen upon FDH expres

200 ally, steady flow increased Src activity and stress fiber formation, whereas it decreased TXNIP expre

201 Ectopic expression of hCDC14A induced stress fiber formation, whereas stress fibers were dimin

202 oblasts that is comparable with PFSS-induced stress fiber formation, whereas VEGF knockdown abrogates

203 ensor that regulates Src kinase activity and stress fiber formation.

204 ole for beta-arrestin in RhoA activation and stress fiber formation.

205 ooth muscle actin (alpha-SMA) expression and stress fiber formation.

206 inase blocked both TGFbeta- and FGF2-induced stress fiber formation.

207 nd found that adenosine inhibits HGF-induced stress fiber formation.

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

209 abrogated cell proliferation, migration and stress fiber formation.

210 eolar epithelial cells, which requires actin stress fiber formation.

211 s, a loss of VE-cadherin, and aberrant actin stress fiber formation.

212 ion of the myosin regulatory light chain and stress fiber formation.

213 nfected with scAAV2.dnRhoA showed diminished stress fiber formation.

214 extension followed by abrupt retractions and stress fiber fracture.

215 ch-induced JNK activation slowly subsides as stress fibers gradually reorient perpendicular to the st

216 d and isotropic cells, which lack long actin stress fibers, have more deformable nuclei than elongate

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

218 MLK3 silencing increased focal adhesions and stress fibers in breast cancer cells.

219 revealed dispersed, shorter and disoriented stress fibers in Cdc42-null NCCs.

220 induced the formation of focal adhesions and stress fibers in cells in which the RhoA signaling pathw

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

222 neration and proper alignment of contractile stress fibers in migrating cells.

223 own to be under mechanical stress, including stress fibers in migratory distal tip cells and the prox

224 Reinforcement of actin stress fibers in response to mechanical stimulation depe

225 gical change and enhanced formation of actin stress fibers in squamous cancer cells.

226 en expression, and inhibits the formation of stress fibers in TGF-beta1 treated HSCs.

227 g protein h3/acidic calponin associates with stress fibers in the absence of stimulation but is targe

228 nded DNA in vitro and microtubules and actin stress fibers in whole cells.

229 myosin light chain colocalization with actin stress fibers increased in endothelial monolayers treate

230 including RhoA activation, alphaSMA-positive stress fibers, increased fibronectin fibrillogenesis, an

231 iety of settings, including various types of stress fibers, individual filaments throughout the cell,

232 its polarized orientation but altered the FA/stress fiber interface in a linear manner, consistent wi

233 e membrane and C terminus demarcating the FA/stress fiber interface.

234 capable of targeting migfilin to actin-rich stress fibers, is the predominant driver of migfilin loc

235 ia, fail to migrate into the wound, and form stress fiber-like arrays of actin at the free edges of c

236 egulated ARF6 localization and thereby actin stress fiber loss.

237 cilin phenotypes including the loss of actin stress fibers, lowered RhoA activities and compromised c

238 Stress fiber maturation additionally requires ADF/cofili

239 nsional VIC hydrogels, suggesting that actin stress fibers mediate TNF-alpha-induced effects.

240 ls and evaluated the effect of this on actin stress fibers, migration using Transwells, and lung meta

241 distinguishable by their denser actomyosin (stress fiber) network.

242 Stress fibers newly formed near the leading edge are enr

243 use this method to demonstrate that ventral stress fibers of U2OS-cells are typically under higher m

244 f RhoA showed no significant change in actin stress fiber or focal adhesion complex formation in resp

245 under higher mechanical tension than dorsal stress fibers or transverse arcs.

246 ell contractility, as evidenced by decreased stress fiber organization and collagen contraction with

247 lated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exhibited reduced contract

248 ence of lovastatin exhibited a loss of actin stress fiber organization concomitant with a marked accu

249 Changes in filamentous actin stress fiber organization were visualized with AlexaFluo

250 osphate to the culture medium restored actin stress fiber organization while selectively facilitating

251 city, induced elongation, and promoted actin stress fiber organization.

252 in ppET-1 mRNA content, ET-1 secretion, and stress fiber organization.

253 (>7-fold) secretion of ET-1 while enhancing stress fiber organization.

254 opic by examining the role of tropomyosin in stress fiber organization.

255 sion of smooth muscle alpha-actin (alphaSMA) stress fibers, plays a central role in wound healing and

256 The increased stress fibers present increased replenishment of the G-a

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

258 bution of active myosin II from junctions to stress fibers, reduced tension on VE-cadherin and loss o

259 ha-Actinin and Ena/VASP proteins bind to the stress fiber reinforcement domain of zyxin.

260 uniaxial cyclic stretch results in an actin stress fiber reinforcement response that stabilizes the

261 in kinase-dependent zyxin phosphorylation or stress fiber remodeling in cells exposed to uniaxial cyc

262 ent of both groups of proteins to regions of stress fiber remodeling.

263 rin expression, RhoGTPase activity and actin stress fiber remodeling.

264 ced stress fiber damage and is essential for stress fiber repair and generation of traction force.

265 ir stress transmission function, followed by stress fiber repair that restores this capability.

266 organization of actin from cortical actin to stress fibers, resulting thereby in formation of leaky e

267 reorganization of the lamellar network into stress fibers results in moderate changes in cellular te

268 Their formation of stress fibers results in the release of myocardin-relate

269 The recruitment of LIMCH1 into contractile stress fibers revealed its localization complementary to

270 Actin stress fibers (SFs) are load-bearing and mechanosensitiv

271 Stress fibers (SFs) are often the most prominent cytoske

272 The assembly and mechanics of actomyosin stress fibers (SFs) depend on myosin regulatory light ch

273 2), localizes specifically to FAs and dorsal stress fibers (SFs) in fibroblasts.

274 Actomyosin stress fibers (SFs) play key roles in driving polarized

275 tributions of the branched actin network and stress fibers (SFs).

276 docyte GR knockout mice showed similar actin stress fiber staining patterns in unstimulated condition

277 ng cells, inducing a light-dependent loss of stress fibers that is characteristic of cAMP action.

278 Actin recruitment to stress fibers that maintain the cell shape under flow ma

279 rix, MIIA was strongly assembled in oriented stress fibers that MIIB then polarized.

280 erior accumulation of more stable NMIIB-rich stress fibers, thus strengthening cell polarity.

281 the cause for the asymmetric response of the stress fiber to the CS and SC maneuvers.

282 ell junctions, HGF attenuates the linkage of stress fibers to cell-to-cell junctions with concomitant

283 trate junctions, HGF augments the linkage of stress fibers to cell-to-substrate junctions with no app

284 biomechanical model to probe the response of stress fibers to the two maneuvers.

285 ytoskeletal proteins, we observed that actin stress fibers undergo local, acute, force-induced elonga

286 arcs, which serve as precursors for ventral stress fibers, undergo lateral fusion during their centr

287 associated formin, mDIA2, localized to actin stress fibers upon treatment with TGF-beta, and paclitax

288 s, zyxin is recruited to focal adhesions and stress fibers via C-terminal LIM domains and modulates c

289 The loss of pMLC along the stress fibers was comparable to that induced by Y-27632

290 rtant role of Rac1 in the formation of actin stress fibers, we examined the effect of adenosine on st

291 anization in standard 3-D matrices; however, stress fibers were consistently expressed within compres

292 C14A induced stress fiber formation, whereas stress fibers were diminished in hCDC14A(PD) cells.

293 , the cell migration was retarded, the actin stress fibers were fewer and shorter, and the trypsiniza

294 ilin-mediated disassembly of non-contractile stress fibers, whereas contractile fibers are protected

295 with cortactin, CTTNBP2NL is associated with stress fibers, whereas CTTNBP2 is distributed to the cor

296 n, triggering the development of a transient stress fiber, which orchestrates cellular repulsion.

297 nker found in the lamellar actin network and stress fibers, which are critical for mechanosensing of

298 eta promotes association of mDia2 with actin stress fibers, which further drives stress fiber formati

299 an increasingly strong pulling force through stress fibers with a positive feedback loop on very stif

300 e gaps, fibroblasts develop thick peripheral stress fibers, with a concave curvature.

301 oteins alpha-actinin and VASP to compromised stress fiber zones.