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1 traction, owing to defective epidermal actin stress fibre.
2 effect on the ability of RhoE to disassemble stress fibres.
3  membrane domains close to the ends of actin stress fibres.
4 round up, and disassemble F-actin-containing stress fibres.
5 orylation consistent with formation of actin stress fibres.
6 adherin junctions without formation of actin stress fibres.
7 ons and the bundling of actin filaments into stress fibres.
8  actin cytoskeleton and the disappearance of stress fibres.
9 ecretion and contraction of actomyosin-based stress fibres.
10 mulates the bundling of actin filaments into stress fibres [3], Rac reorganises actin to produce memb
11 s matrix, mutant cells exhibited contractile stress fibre accumulation, increased focal adhesions, an
12  of RhoA effectors in the formation of actin stress fibres, activation of transcription by serum resp
13 taining smaller cell area with reduced actin stress fibre alignment across a range of physiological a
14 ated the formation and organisation of actin stress fibres and actin expression in trophoblast outgro
15 t the DIX domain mediates targeting to actin stress fibres and cytoplasmic vesicles in vivo.
16 ell line showed abnormal clustering of actin stress fibres and decreased formation of adherens juncti
17 s that rapidly propagate across the cell via stress fibres and drive increased actin flow.
18 ibodies against PtdInsP2 inhibit assembly of stress fibres and focal adhesions.
19 ipodia and focal complexes, and Rho-mediated stress fibres and focal adhesions.
20 he formation of Rho-induced actin-containing stress fibres and focal-adhesion complexes, to which the
21 of the ROCK target LIM kinase restores actin stress fibres and inhibits the motility of Ras-transform
22 ts of RhoA to promote the formation of actin stress fibres and integrin-based focal adhesions.
23                                 Furthermore, stress fibres and intermediate filaments modulate the me
24  by considerable reduction of actin filament stress fibres and junctional F-actin in cultured endothe
25 n 2 using siRNA leads to the accumulation of stress fibres and loss of protrusive and retractile acti
26 cluding reduced NO activity, prominent actin stress fibres and poorly developed cellular junctions.
27 , activated mNET1 induces formation of actin stress fibres and potentiates activity of the transcript
28  of IFT80-deficient OPCs by disrupting actin stress fibres and promoting cilia formation and Hh-Gli s
29 ed to induce association of v-Src with actin stress fibres and redistribution to sites of focal adhes
30 podin in kidney podocytes causes the loss of stress fibres and the formation of aberrant non-polarize
31 lei, absence of alpha-smooth muscle actin or stress fibres, and a corresponding reduction in migrator
32 ficient than FGF1 and FGF2 in inducing actin stress fibres, and the specific p38 inhibitor SB202190 c
33 as a regulator of stress fibre mechanics, as stress fibres are fluid-like without flow reversal in it
34 , which functions to antagonise RhoA-induced stress fibre assembly.
35 adhesion complexes, to which the ends of the stress fibres attach.
36  Using a physical model, we demonstrate that stress fibres behave elastic-like, even at timescales ex
37  showed that ANG II increased the density of stress fibres by 23%, while ADO decreased the density of
38  23%, while ADO decreased the density of the stress fibres by 45%.
39  proline-rich actin-binding protein, induces stress fibres by blocking the Smurf1-mediated ubiquitina
40            We show that synaptopodin induces stress fibres by competitive blocking of Smurf1-mediated
41 fish ZF4 cells, Afp18(G) depolymerizes actin stress fibres by mono-O-GlcNAcylation of RhoA at tyrosin
42 g of TPMalpha but not TPMbeta causes loss of stress fibres by promoting Smurf1-mediated ubiquitinatio
43 hoE correlates with its activity in inducing stress fibre disruption and inhibiting Ras-induced trans
44 e artefacts at the cellular level, impacting stress fibre dynamics and actin cytoskeleton architectur
45 s as a conserved mechanism for regulation of stress fibre dynamics and cell motility in a cell type-s
46 ncy range of 0.01-10 Hz caused spreading and stress fibre formation (optimum 0.1 Hz) that persisted a
47 for a stiff matrix in stimulating spreading, stress fibre formation and growth.
48             The repression of Rho- dependent stress fibre formation by ERK-MAP kinase signalling cont
49                               Stimulation of stress fibre formation by LPA and PA was sensitive to ge
50 st, elevated cell contractility due to actin stress fibre formation dampens aromatase transcription.
51 id not stimulate PLD activity, but did cause stress fibre formation in a manner that was insensitive
52 ning this effect revealed that PGI2 reversed stress fibre formation in adherent platelets, reduced pl
53 errant membrane ruffling and defective actin stress fibre formation in cells.
54                                              Stress fibre formation is a RhoA dependent process and w
55       In PAE cells, the stimulation of actin stress fibre formation was a consequence of PA generatio
56                    LPA also stimulated actin stress fibre formation, but was inhibited by butan-1-ol;
57 kinase, two Rho effectors required for actin stress fibre formation.
58 g in activation of transcription factors and stress fibre formation.
59 rin junctions, but in association with actin stress fibre formation.
60 hibitor, U0126, had no effect on FGF-induced stress fibre formation.
61 o reduced cell spreading, focal adhesion and stress fibre formation.
62  other unidentified effector is required for stress fibre formation.
63 ntractile proteins and their localisation to stress fibres in HASMCs.
64 of c-Cbl restores Nck1 protein abundance and stress fibres in synaptopodin knockdown cells.
65 containing the SH3 domain 2 of Nck1 restores stress fibres in synaptopodin-depleted podocytes through
66 ation of contractile actin-myosin-containing stress fibres in the cell body and at the rear.
67 ransforming growth factor-beta induces actin stress fibres in trabecular meshwork cells, indicating t
68 ey no longer regulate the formation of actin stress fibres in transformed cells.
69                        Synaptopodin restores stress fibres in tropomyosin-deficient human MDA-MB 231
70 , Rho mediates the formation of cytoskeletal stress fibres induced by lysophosphatidic acid, while Ra
71 ised on fibronectin micropatterns to control stress fibre location, yielded a recovery time constant
72          We identify zyxin as a regulator of stress fibre mechanics, as stress fibres are fluid-like
73                                   Actomyosin stress fibres, microtubules and intermediate filaments h
74 stable AJs and redistributed to radial actin stress fibres of remodelling focal AJs.
75 of RuRuPhen causes rapid disruption to actin stress fibre organisation, compromising actomyosin contr
76 t dramatically suppressed cell spreading and stress fibre organization, while knockdown of KCC2 showe
77 , but elevates non-canonical Hh-Galphai-RhoA-stress fibre signalling by increasing Smo and Galphai bi
78 21, and by sequestering residual TRIM21 on a stress-fibre subset that is insensitive to substrate sti
79 tribution to sites of focal adhesions at the stress fibre termini.
80  resulted in alterations in the detection of stress fibres that correlated with the ability of CT694
81                       The effects of PGI2 on stress fibres were mimicked by the adenylyl cyclase acti
82            PAK stimulates the disassembly of stress fibres, which has been shown to accompany formati
83 gradation is triggered by the disassembly of stress fibres, which releases the PFK-targeting E3 ubiqu
84 ation of filopodia is accompanied by loss of stress fibres (whose formation is mediated by Rho).