ライフサイエンスコーパス: stress fiber

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

2 mechanical information along the length of a stress fiber.

3 in contributes to the assembly of functional stress fibers.

4 chains highly reminiscent of mammalian cell stress fibers.

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

6 eorganization of the actin cytoskeleton into stress fibers.

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

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

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

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

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

12 (ZYX), and produced profoundly disorganized stress fibers.

13 ontractile actomyosin bundles called ventral stress fibers.

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

15 studied remodeling of contractile actomyosin stress fibers.

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

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

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

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

20 ociated with the presence of disrupted actin stress fibers.

21 downregulation of focal adhesions and actin stress fibers.

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

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

24 ential role in structures from sarcomeres to stress fibers.

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

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

27 recruit nonmuscle myosin II and mature into stress fibers.

28 sed percentages of fibroblasts with alphaSMA stress fibers.

29 myosin, as a stable component of contractile stress fibers.

30 ssion by siRNA caused disappearance of actin stress fibers.

31 ative, with mature alpha-smooth muscle actin stress fibers.

32 lpha-SMA expression and alpha-SMA-containing stress fibers.

33 ation for mechanics of contractile rings and stress fibers.

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

35 Disrupting stress fibers abolishes differences in cell stiffness, c

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

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

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

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

40 opodia (fascin), lamellipodia (fimbrin), and stress fibers (alpha-actinin).

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

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

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

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

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

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

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

48 ess was accompanied by the presence of actin stress fibers and accumulation of the inactive, phosphor

49 nd in vivo is associated with the absence of stress fibers and an order of magnitude decrease in nucl

50 ff-target staining that occur along immature stress fibers and cell boundaries and choosing metrics t

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

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

53 MP distribution changed from primarily basal stress fibers and cytoplasm in undifferentiated cells to

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

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

56 wing F-actin to interact with myosin to form stress fibers and enhance the contraction induced by met

57 formed alphaSMA (alpha-smooth muscle actin) stress fibers and expressed myofibroblast-specific ECM g

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

59 ercellular filopodia that radiate from basal stress fibers and extend penetrating neighboring cell co

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

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

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

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

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

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

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

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

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

69 lecules was accompanied by increased F-actin stress fibers and increased endothelial barrier permeabi

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

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

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

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

74 arved adhesion phenotype consisting of actin stress fibers and large peripheral focal adhesion.

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

76 tin fibers drastically reduces the amount of stress fibers and mature focal adhesions to result in th

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 hor mutants had defects in alleviating actin stress fibers and rescuing the reduced invasiveness in t

83 Cells on soft (1 kPa) gels formed fewer stress fibers and retained a more dendritic morphology,

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

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

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

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

88 nder starving conditions, the maintenance of stress fibers and the large adhesion phenotype required

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

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

91 ver, the relationship between BM fibrils and stress fibers and their respective impact on elongation

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

93 co-localized with myosin II motor domains in stress fibers and was enriched at the ends of myosin II

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

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

96 ne with increased cytoplasm, extensive actin stress fibers, and actomyosin-dependent flattening again

97 ght junction proteins, increased endothelial stress fibers, and decreased microvessel density in the

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

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

100 s reversible glomerular dysfunction, loss of stress fibers, and foot process effacement.

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

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

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

104 -smooth muscle actin and depolymerization of stress fibers, and reduces the expression of profibrotic

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

106 pomyosin filaments, loss of force-generating stress fibers, and severe defects in cell morphology.

107 confinement induces remodeling of actomyosin stress fiber architecture.

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

109 Importantly, stress fibers are critical for several endothelial cell

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

111 Poorly developed filamentous actin stress fibers are found only in cells on 3-um networks.

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

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

114 shapes, sizes, and orientations, as well as stress-fiber arrangements within the cells with remarkab

115 c forces, we found that the number of apical stress fibers (aSFs) anchored to adherens junctions scal

116 45a knockout cells display severe defects in stress fiber assembly and consequent abnormalities in ce

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

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

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

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

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

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

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

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 Moreover, they also orient stress fibers, by acting locally and in parallel to Fat2

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

128 d basement membrane (BM) fibrils and F-actin stress fibers constrain follicle growth, promoting its a

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

130 Stress fibers-contractile actomyosin bundles-are importa

131 y inhibiting the actomyosin machinery (actin stress fibers, contractility, and stiffness).

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

133 ty of cellular structures such as filopodia, stress fibers, cytokinetic rings, and focal adhesions.

134 ooth muscle actin and its incorporation into stress fibers, cytoskeletal changes, collagen-1 producti

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

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

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

138 Actin stress fiber dynamics are required for thrombin-induced

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

140 ver, had broad morphologies, formed abundant stress fibers, exhibited greater levels of alpha-smooth

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 N-WASP effects in P aeruginosa-induced actin stress fiber formation and increased paracellular permea

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

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

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

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

160 lation attenuated P aeruginosa-induced actin stress fiber formation and prevented paracellular permea

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

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

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

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 indeed substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-en

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

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

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

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

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

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

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

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

175 biting PKCepsilon enhances RhoA activity and stress fiber formation, a phenotype also observed in TGF

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

177 2, affecting G-actin polymerization, F-actin stress fiber formation, and HASMC migration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 abrogated cell proliferation, migration and stress fiber formation.

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

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

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

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

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

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

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

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

205 IL-17R, followed by PKCalpha activation and stress fiber formation.

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

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

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

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

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

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

212 distribution of intercellular filopodia and stress fibers in follicle cells.

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

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

215 and Tmod3, as key components of contractile stress fibers in non-muscle cells.

216 l spreading while reducing contractile actin stress fibers in normal and breast cancer cells and stro

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

218 5-HT(2A) activation gave rise to stress fibers in these cells and was also required for t

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

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

221 n cultured ECs led to increased radial actin stress fibers, increased adherens junction width and inc

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

223 nt mice, the absence of Synpo caused loss of stress fibers, increased the number and size of focal ad

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

225 duced endothelial cell signaling for F-actin stress fiber inducing endothelial barrier dysfunction.

226 cribe that IL-9 profoundly reduced the actin stress fibers, inhibited contractility, and reduced the

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

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

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

230 egulated ARF6 localization and thereby actin stress fiber loss.

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

232 Stress fiber maturation additionally requires ADF/cofili

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

234 that YAP activation is dependent on F-actin stress fiber mediated nuclear pore opening, however the

235 Sarcomeres arise from muscle stress fibers (MSFs) that are translocating on the top (

236 fluctuations of cells' actomyosin cortex and stress fiber network in detail.

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

238 ebrates to create new structures such as the stress fibers, new cell types such as endothelial cells,

239 Stress fibers newly formed near the leading edge are enr

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

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

242 the cell long axis (i.e., alignment of actin stress fibers) or at different angles (90 degrees or 45

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

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

245 (>7-fold) secretion of ET-1 while enhancing stress fiber organization.

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

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

248 anges within the cells, including increasing stress-fiber polarization and cell elongation; and 2) en

249 IL-17A increased the actin stress fibers, promoted cellular contractility, and incr

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

251 oretical modeling using discrete anisotropic stress fibers recapitulates experimental results and rev

252 down of CAP1 in cancer cells led to enhanced stress fibers, reduced cell motility and invasion into M

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

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

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

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

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

258 cell cultures and explants results in actin stress fiber reorganization, stimulation of focal adhesi

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

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

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

262 changes in the actin cytoskeleton including stress fiber (SF) reinforcement and realignment.

263 copy of the actin cytoskeleton revealed that stress fibers (SFs) are integrated into an isotropic net

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

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

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

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

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

269 nto diverse load-bearing networks, including stress fibers (SFs), muscle sarcomeres, and the cytokine

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

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

272 sm by which these LIM domains associate with stress fiber strain sites (SFSS) is not known.

273 resence of the perinuclear actin cap (apical stress fibers), such as those encountered in cells subje

274 t as a persistent cue for the orientation of stress fibers that are the main effector of elongation.

275 We also modeled contractile stress fibers that bind the discrete adhesions.

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

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

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

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

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

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

282 ic shortening of myosin IIA-associated actin stress fibers to drive rapid fibronectin fibrillogenesis

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

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

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

286 rized) cells with strong focal adhesions and stress fibers; very soft substrates give a less develope

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

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

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

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

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

292 al cells increased focal adhesions and actin stress fibers whereas FOXC2-KD increased focal adherens

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

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

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

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

297 G also increases the number and thickness of stress fibers, which are sensitive to blebbistatin, sugg

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.