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1 atrunculin A or by inhibiting myosin II with blebbistatin).
2 d by myofilament Ca(2+) desensitization with blebbistatin.
3 ted by myofilament Ca2+ desensitization with blebbistatin.
4 on, but failing to move into lamellipodia in blebbistatin.
5 d in cells treated with the motor inhibitor, blebbistatin.
6 with ML7 and myosin II ATPase activity with blebbistatin.
7 was blocked by inhibition of myosin II with blebbistatin.
8 ed by treatment with the myosin II inhibitor blebbistatin.
9 ly 90% at 40 microM actin in the presence of blebbistatin.
10 P(i) release was blocked in the presence of blebbistatin.
11 he inhibition of myosin ATPase activity with blebbistatin.
12 determinant of the potency of compounds like blebbistatin.
13 assembly induced by the myosin II inhibitor, blebbistatin.
14 till present when active force is blocked by Blebbistatin.
15 stabilized by either lattice compression or blebbistatin.
16 acted collagen fibrils, which was blocked by blebbistatin.
17 cle types and in the presence and absence of blebbistatin.
18 activation and were abolished or reversed by blebbistatin.
19 the actomyosin inhibitors cytochalasin D and blebbistatin.
20 low myosin affinity and water solubility of blebbistatin.
21 identical inhibitory properties to those of blebbistatin.
22 rdered lipids, was also reduced by Lat B and blebbistatin.
23 +/- 15 years) using the dye Di-4-ANBDQBS and blebbistatin.
24 NM II or treatment with the myosin inhibitor blebbistatin.
25 interference (RNAi) and the myosin inhibitor blebbistatin.
26 ay were not significantly altered by binding blebbistatin.
27 d after injection of the myosin II inhibitor blebbistatin.
28 lowing inhibition of myosin II function with blebbistatin.
29 -1)) was reduced slightly in the presence of blebbistatin (0.38 +/- 0.03 microM(-1) s(-1)), while man
30 (3 to 30 micromol/L) and myosin II inhibitor blebbistatin (1 to 10 micromol/L) inhibited CyPA secreti
31 The negative inotropic agents BDM (5 mm) or blebbistatin (10 microM) decreased cell shortening and N
34 ma invasion we blocked glioma migration with blebbistatin, a blocker of myosin kinase II, which is ne
36 ated in porcine TM and CB cells treated with blebbistatin, a cell-permeable, specific inhibitor of my
39 he MEA-SICM setup to visualize the effect of blebbistatin, a myosin II inhibitor, on the morphodynami
40 tility-previously assumed-was verified using blebbistatin, a myosin-II ATPase inhibitor that permitte
41 screen on human motor neurons and identified blebbistatin, a non-muscle myosin II inhibitor, as the m
42 dividing normal rat kidney (NRK) cells with blebbistatin, a potent inhibitor of the nonmuscle myosin
44 Consistent with this, embryos treated with Blebbistatin-a small molecule inhibitor for myosin II ac
46 rements of single ATP turnovers to show that blebbistatin also stabilizes the SRX in both fast and sl
50 to a virion surface protein and by the drugs blebbistatin and bafilomycin A1, suggesting that in each
54 ity, while the nonmuscle myosin II inhibitor blebbistatin and the kinesin inhibitor AMP-PNP had no si
55 sforming growth factor-beta, a decrease with blebbistatin, and no change with mechanosensitive channe
56 ulin B (Lat B), inhibition of myosin II with blebbistatin, and treatment with neomycin to sequester p
57 hereas the macropinocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated e
59 , butanedione monoxime, trifluoperazine, and blebbistatin) are modified by twitchin phosphorylation a
60 ric modulators, like the myosin-II inhibitor blebbistatin, are a promising means to achieve specifici
61 tion, as exposure to the myosin-II inhibitor blebbistatin arrested any shortening and also decreased
66 contraction with the myosin ATPase inhibitor blebbistatin attenuated oxidative stress as well as spon
69 lar simulations indicate that the productive blebbistatin-binding site of the myosin head is within t
71 e cytoskeleton inhibitors cytochalasin B and blebbistatin blocked not only PMA-induced apoptosis but
72 trations of the specific myosin II inhibitor blebbistatin blocked PDGF-stimulated matrix contraction
74 2-E1 and myo2-E1-Sup1 on available rigor and blebbistatin-bound myosin II structures suggests that my
75 mall molecules - omecamtiv mecarbil (OM) and blebbistatin (BS) - that bind specifically to myosin and
76 ly Dictyostelium myosin that is inhibited by blebbistatin but also show that blebbistatin-inactivated
80 inhibition of myosin-II ATPase with the drug blebbistatin decreased cell spreading with associated nu
82 r, inhibiting the motor protein myosin II by blebbistatin decreased membrane tension, as well as fusi
83 decreasing contractile level with 10 microM blebbistatin decreased stiffness, whereas increasing con
84 ion by 5% dextran T500 or addition of 25 muM blebbistatin decreased the transition temperature to app
85 n relaxed tarantula fibers in the absence of blebbistatin, demonstrating that the structure of the SR
88 ngly, inhibiting cellular contractility with blebbistatin did not affect the extent of cellular invas
93 actin/myosin machinery with cytochalasin or blebbistatin disrupts polarization of Pk and Stbm, but n
94 in myosin II-null cells, but, unexpectedly, blebbistatin does inhibit macropinocytosis and phagocyto
96 ic inhibitor of non-muscle myosin II (NMII), blebbistatin, enhances the survival of hPS cells under c
97 inhibition of both isoforms in culture with blebbistatin enriches for long-term hematopoietic multil
98 We find that the SRX is stabilized using blebbistatin even in conditions that normally destabiliz
103 ition of strong cross-bridge attachment with blebbistatin had no effect on the length-dependent modul
104 lete inhibition of active force by 25 microM blebbistatin had very little effect on the Ca(2+)-depend
107 ts with inhibitors of cytokinesis, including blebbistatin, hesperadin, and nocodazole, and then assay
108 ination of cell-cell junctions revealed that blebbistatin impaired adherens-junction organization, pa
109 eduction of cytosolic Ca(2+) buffering using blebbistatin in an ex vivo mouse whole heart model incre
110 ich requires myosin II, are not inhibited by blebbistatin in myosin II-null cells, but, unexpectedly,
111 primary porcine TM and CB cells treated with blebbistatin in the presence of serum revealed dose (10-
112 inhibited by blebbistatin but also show that blebbistatin-inactivated myosin II inhibits some myosin
113 he ROCK inhibitor Y27632 or myosin inhibitor blebbistatin increased TER in wild-type cells, whereas Z
114 simplest explanation is that the binding of blebbistatin increases the proportion of myosin in the c
117 ntifies which isoforms are most sensitive to blebbistatin inhibition and that docking against MSMs qu
120 The effects of TNF-alpha were attenuated by blebbistatin inhibition of myosin II-mediated cytoskelet
121 nclusion, based on biochemical studies, that blebbistatin inhibits myosin ATPase and actin interactio
123 ome myosin II-independent processes and that blebbistatin inhibits other activities in the absence of
125 Based on the above data, we surmise that blebbistatin inhibits the ATPase activity of NMIIB S1 pr
134 electron microscopy to study the effects of blebbistatin on the organization of the myosin heads on
135 ues were employed to elucidate the effect of blebbistatin on the various steps of the NMIIB S1 cross-
137 llogenesis was tested by treating cells with blebbistatin or calyculin A to tonically block or augmen
139 thelial carcinoma cells either directly with blebbistatin or indirectly with Y27632 Rho kinase inhibi
140 f nonmuscle myosin II in human NK cells with blebbistatin or ML-9 impaired neither effector-target ce
141 reated with the myosin II-specific inhibitor blebbistatin or myosin II siRNAs exhibited a significant
142 bryos treated with cell movement inhibitors (blebbistatin or RhoK inhibitor), but not cell cycle inhi
143 tor ML-7 or the myosin II-specific inhibitor blebbistatin or selective RNA-mediated repression of myo
145 tion of the excitation-contraction uncoupler blebbistatin or the mechanosensitive channel blocker gad
146 assess whether acute (75 muM ouabain 100 nM blebbistatin) or chronic myocardial Na(i) load (PLM(3SA)
148 Myofilament Ca(2+) desensitization with blebbistatin prevented focal energy deprivation, transve
150 ine eyes for 5 hours with 100 and 200 microM blebbistatin produced a significant increase (P < 0.01,
151 and inhibiting actomyosin contractility with blebbistatin promoted tubulogenesis, whereas inhibition
158 argin via Ca(2+) reduction or treatment with blebbistatin restored uniform migration and eliminated A
159 nhibition of the motor domain of myosin-9 by blebbistatin resulted in a more diffuse PAD4 location, i
160 Inhibition of contractility with 10 mum blebbistatin resulted in an approximately 3-fold increas
161 he M466I mutation sensitized the protein for blebbistatin, resulting in a half-maximal inhibitory con
162 ion of myosin II activity through the use of blebbistatin results in microtubules that are still dyna
165 lind prediction for an isoform (Myh7b) whose blebbistatin sensitivity was unknown, we find good agree
167 l present when active force was blocked with blebbistatin, showing that C1mC2 directly activates the
169 rization, but not if done in the presence of blebbistatin, suggesting an active role for myosin in co
170 ess of stress fibers, which are sensitive to blebbistatin, suggesting contractility is increased.
171 The NM myosin cross-bridge cycling inhibitor blebbistatin suppressed adhesome complex assembly and SM
173 a specific inhibitor of nonmuscle myosin II, blebbistatin, that inhibited contraction of the cleavage
174 azidoblebbistatin, which is a derivative of blebbistatin, the most widely used myosin inhibitor.
176 retraction process, as treating thrombi with blebbistatin to inhibit myosin IIa-mediated platelet con
177 it actin retrograde flow in the LP/dSMAC and blebbistatin to selectively inhibit actomyosin II arc co
178 nd focal adhesions, because of either adding blebbistatin to the cells or use of soft coverslips, als
180 ent followed advancing lamellipodia, whereas blebbistatin-treated cells extended protrusions without
181 s during late cytokinesis, they persisted in blebbistatin-treated cells over an extended period of ti
184 ore, suppression of actomyosin tension using blebbistatin triggered a similar vinculin delocalization
185 orff-perfused rabbit hearts immobilized with blebbistatin using either a confocal microscope or an op
186 rapidly inactivates the inhibitory action of blebbistatin using the in vitro motility of myosin as an
188 inhibitor of phosphatase 250) were applied; blebbistatin was used to disrupt actin-myosin interactio
191 raction in the presence of 20 muM para-nitro-blebbistatin, which abolishes the activity of myosin mot
193 eduction in cortactin content was blocked by blebbistatin, while basal levels were reduced by nocodaz
194 se effects are likely mediated by binding of blebbistatin within the myosin cleft that progressively