ライフサイエンスコーパス: myosin II

1 l ring rich in actin filaments and nonmuscle myosin II.

2 ity to phosphorylate and activate non-muscle myosin II.

3 nd cortical signaling pathways that regulate myosin II.

4 in these Deltaaip1 cells accumulate 30% less myosin II.

5 tical actomyosin activity through non-muscle myosin II.

6 required for the folding of striated muscle myosin II.

7 ns; and with zipper, which encodes nonmuscle myosin II.

8 y a unique form of cycling F-actin driven by myosin II.

9 keletal components: microtubules, actin, and myosin II.

10 intercalation within the cochlea all require myosin II.

11 pressure generation by delocalizing cortical myosin II.

12 phenotypes are surprisingly both mediated by myosin II.

13 rrow of dividing cells--always together with myosin-II.

14 d molecular motors nor pressure generated by myosin-II.

15 nts, the Rho effectors diaphanous formin and myosin-II.

16 folds, formin, and the tail of the essential myosin-II.

17 Anillin interacts with Rho, F-actin, and myosin II [3, 8, 9], all of which regulate cell-cell jun

18 ssess the role of F-actin polymerization and myosin II, a molecular motor that drives memory-promotin

19 irment of endocytosis occurred when blocking myosin II, a motor protein that can be phosphorylated up

20 ulates the mono-ubiquitination of non-muscle Myosin II, a protein associated with hearing loss in hum

21 To investigate the contribution of nonmuscle myosin II-A (NM II-A) to early cardiac development we cr

22 Active myosin II accumulates in puncta on mitochondria in an ac

23 Myosin II accumulates specifically around constricting c

24 Micropipette aspiration of cells shows myosin-II accumulates at stressed sites, but its inhibit

25 In Dictyostelium, this system tunes myosin II accumulation by feedback through the actin net

26 lanar polarity leads to asymmetric pulsatile Myosin II accumulation in the basal, proximal cortex of

27 ions, whereas overall junctional F-actin and myosin II accumulation is reduced when Anillin is deplet

28 Overall, myosin II accumulation is the result of multiple paralle

29 In Shroom mutants, Rho-kinase and myosin II achieve reduced levels of planar polarity, res

30 DCs, which controls cofilin inactivation and myosin II activation and, therefore may control, in part

31 Rho1 is necessary for myosin II activation, leading to its association with ac

32 ion of recycling endosomes through localized myosin II activation.

33 coordinating junctional actin assembly with Myosin II activation.

34 e exchange factor ECT-2, is upstream of both myosin-II activation and diaphanous formin-mediated fila

35 independent of its established function as a myosin II activator, but requires a microtubule-dependen

36 Our results show that myosin II activity and actin polymerization increase cor

37 e stresses (3.4 nN mum(-2)) are dependent on myosin II activity and are more than twofold larger than

38 generation in 3D collagen without affecting myosin II activity and promoted 3D collagen fiber alignm

39 trains revealed that different thresholds of myosin II activity are required for daughter cell symmet

40 gnaling pathway and subsequent inhibition of Myosin II activity at the leading edge are required for

41 Our findings suggest that myosin II activity contributes to increased whole-cell c

42 Similarly, higher Myosin II activity enhances the integrin multilayering p

43 Moreover, loss of myosin II activity has opposing effects on protrusive ac

44 Once NAs have formed, myosin II activity promotes talin association with the i

45 Interestingly, myosin II activity stiffens the cortex and branched acti

46 dent, but not MLCK-dependent, stimulation of myosin II activity yet independent of its effects upon a

47 This strictly depended on myosin II activity, suggesting local network reorganizat

48 that interfere with microtubule dynamics and myosin II activity.

49 f the basement membrane require protease and myosin II activity.

50 elated reorganization, which is dependent on myosin II activity.

51 nly after NAs have formed and in response to myosin II activity.

52 ed by down-regulation of RHOA expression and myosin II activity.

53 nase (ROCK) controlled excessive contractile myosin-II activity and not to elevated F-actin polymeriz

54 RhoA-mediated regulation of myosin-II activity in the actin cortex controls the abil

55 Although actin polymerization or myosin-II activity individually enhances fluctuations, t

56 ucleus across many matrices, timescales, and myosin-II activity levels indicates a constant ratio of

57 latelets, suggesting that fluid stresses and myosin-II activity somehow couple in platelet biogenesis

58 ll analyses that matrix stiffness couples to myosin-II activity to promote lamin-A,C dephosphorylatio

59 NM myosin II actomyosin cross-bridge cycling regulates the

60 Here, we show that non-muscle myosin II, alpha-actinin, and filamin accumulate to mech

61 Here, we show that myosin II also plays a role in fission.

62 Inhibition of non-muscle myosin II also resulted in a disruption of METH-associat

63 Loss of myosin II also selectively inhibits myofibroblast differ

64 le in cell division among protists that lack myosin II and additionally implicate the broad use of me

65 All three phenomena depend on myosin II and are temporally correlated with the pulses

66 ctin via direct interaction with F-actin and myosin II and by activating RhoA signaling via direct in

67 ing in activation of RhoA-ROCK signalling to myosin II and cell contraction.

68 We show that forces are shared between myosin II and different actin crosslinkers, with myosin

69 hat their constriction was sensitive to both myosin II and dynamin inhibition.

70 ased by RNA interference (RNAi) depletion of myosin II and focal adhesion kinase, suggesting that thi

71 ia controlled activation and deactivation of myosin II and HDAC6.

72 Both myosin II and phosphoinositide 3-kinase (PI3K) were foun

73 br3 mutants phenocopy pathogenic variants of Myosin II and that Ubr3 interacts genetically and physic

74 Genetically, blebbing requires myosin-II and increases when actin polymerization or cor

75 uclear stiffness resulting from increases in myosin-II and lamin-A,C.

76 formation of podosomes by inhibition of RhoA/myosin-II and promotion of actin core assembly.

77 tic entry drives Rho-dependent activation of Myosin-II and, in parallel, induces a switch from Arp2/3

78 hesion proteins (alpha-actinin, F-actin, and myosin II) and subcellular organelles (mitochondria, nuc

79 shworks of nuclear lamin A, minifilaments of myosin II, and extracellular matrix collagen fibers-all

80 align the Fn matrix by increasing nonmuscle myosin II- and platelet-derived growth factor receptor a

81 In muscle cells, actin filaments and myosin II appear in a polarized structure called a sarco

82 INTS: Non-muscle (NM) and smooth muscle (SM) myosin II are both expressed in smooth muscle tissues, h

83 increase in diameter when actin filaments or myosin II are disrupted.

84 -guanosine triphosphate [GTP]), F-actin, and myosin II are misregulated at junctions.

85 This work defines novel roles for myosin II as a key regulatory effector molecule of the p

86 Our results establish the importance of myosin II as an active component in modulating suspended

87 Particularly, we identified non-muscle myosin II as an important factor in Kv2.1 trafficking.

88 Myosin II assembly is regulated by myosin heavy chain ki

89 Dictyostelium cells (corA(-)), which impacts myosin II assembly.

90 found no change in the levels of f-actin or myosin-II at the division plane when CYK-4 GAP activity

91 cocytes, which also show that maximal active myosin-II at the synapse can dominate self-signaling by

92 l tension is more sensitive to inhibition of myosin II ATPase activity than to inhibition of ROCK act

93 ei, and for well-spread cells, inhibition of myosin-II ATPase with the drug blebbistatin decreased ce

94 Overall, 4-HAP modifies nonmuscle myosin II-based cell mechanics across phylogeny and dise

95 , and these are likely to underlie how other myosin II-based contractile systems are assembled.

96 ne point contacts is to restrain or "clutch" myosin-II-based filamentous actin (F-actin) retrograde f

97 A myosin-II-based mechanosensory system controls cellular

98 In motile non-neuronal cells, myosin-II binds and exerts force upon actin filaments at

99 We show that initial Myosin II bipolar cell polarization gives way to unipola

100 These MTs suppress Rho activation, nonmuscle myosin II bipolar filament assembly, and actin retrograd

101 oscopy, or TIRF-SIM, to visualize individual myosin II bipolar filaments inside cells.

102 ends on the correct regulation of non-muscle Myosin II, but how this motor protein is spatiotemporall

103 ed in culture by pharmacologic inhibition of myosin-II, but nonmuscle myosin-IIA (MIIA) mutations par

104 Moreover, inhibiting the motor protein myosin II by blebbistatin decreased membrane tension, as

105 cterization showed that RMD1 is required for myosin II cleavage furrow accumulation, acting in parall

106 r a ring of cross-linked actin filaments and myosin-II clusters, we derive the force balance equation

107 the myosin light chain 9 (MYL9) component of myosin II complex and overexpression of CD11b integrin.

108 ation ability, also spontaneously generating myosin II concentration gradients in the solution phase

109 rc line tension is due to the combination of myosin II contractility and a passive elastic component,

110 ue of Science, Shyer et al. (2017) show that myosin II contractility drives the smooth dermal mesench

111 spatial organization of protrusion relies on myosin II contractility, and feedback between adhesion a

112 y together with integrin/ECM association and myosin II contractility.

113 ts, junctional N-cadherin bonds downregulate Myosin-II contractility.

114 , beta-cardiac myosin (CMIIB), Dictyostelium myosin II (DdMII), and nonmuscle myosin IIA, as well as

115 The myosin II defect of corA(-) mutant is alleviated by domi

116 In vivo, thorough depletion of nonmuscle myosin II delayed furrow initiation, slowed F-actin alig

117 ivate TGF-beta through a mechanism involving myosin II dependent contractility.

118 on compliant 3D ECMs, and these effects are myosin-II dependent.

119 , diffusion-based accumulation and a slower, myosin II-dependent cortical flow phase that acts on pro

120 including the regulation of Rac1 GTPase- and myosin II-dependent pathways.

121 ntal data and analytical modelling show that myosin-II-dependent force anisotropy within the lateral

122 a local protrusion and a second involving a myosin-II-dependent mechanical instability of the cell c

123 d regulation of MT growth dynamics through a myosin-II-dependent signaling pathway.

124 Importantly, this myosin II-derived force inhibits vectorial actin polymer

125 We observed that inhibiting myosin II directly or through photo-release of the caged

126 eased overlap of actin filaments produced by myosin II-driven contraction.

127 We suggest that a myosin II-driven, filopodia-based probing mechanism ahea

128 ds to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue.

129 tingly, blocking activity of NMII (nonmuscle myosin II) either before, or after, lumen morphogenesis

130 of actin structures in spines, showing that myosin II exerts tension on the actin network.

131 bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and pulling

132 gest that the CR may be derived from foci of myosin II filaments in a manner similar to what has been

133 In contrast, myosin II filaments in earlier stages of cytokinesis wer

134 nized like muscle sarcomeres, with repeating myosin II filaments separated by the actin bundling prot

135 copy indicated that within the CR, actin and myosin II filaments were organized into tightly packed l

136 mage Velocimetry, we identify posteriorwards Myosin II flows towards the presumptive posterior endode

137 How myosin II force production is shaped by isoform-specific

138 unction disruption, redistribution of active myosin II from junctions to stress fibers, reduced tensi

139 Myosin II function is thought to provide the ingression

140 ing daughter cells, requires coordination of myosin II function, membrane trafficking, and central sp

141 ation of Rab35 compartments does not require Myosin II function.

142 ise with states of nuclear rounding in which myosin-II generates little to no tension.

143 myosin II tails to the plasma membrane, with myosin II heads extending into the cytoplasm.

144 sequence comparison between the schistosome myosin II heavy chain and known striated muscle myosins.

145 n affects the upper 50 kDa sub-domain of the myosin II heavy chain, and cells carrying this lethal mu

146 of the alpha-kinase domain of Dictyostelium myosin-II heavy chain kinase-A (termed A-CAT).

147 severely disabled mutation of the essential myosin-II heavy-chain gene (myo2-E1) and deletion mutati

148 Although, the non-muscle myosin II holoenzyme (myosin) is a molecular motor that

149 Myosin 1b regulates the redistribution of myosin II in actomyosin fibers and the formation of filo

150 We propose that the requirement for myosin II in both cell migration and specific cell funct

151 ine the structural organization of actin and myosin II in isolated cortical cytoskeletons prepared fr

152 The dependence of myosin II in leading-edge advancement helps explain the

153 ular function of non-muscle (NM) isoforms of myosin II in smooth muscle (SM) tissues and their possib

154 corA(-) cells show increased accumulation of myosin II in the cortex of growth-phase cells.

155 om but were dependent on ATP and cytoplasmic myosin-II in the cell cortex.

156 To shift cell mechanics, 4-HAP requires myosin II, including its full power stroke, specifically

157 e cortical localization of the mechanoenzyme myosin II, independent of myosin heavy-chain phosphoryla

158 s, and the lamellipodium buckles upward in a myosin II-independent manner.

159 ctinin-4 and beta-catenin and interacts with myosin II, indicating that it can physically link adhesi

160 thermore, the pharmacological stimulation of myosin II induced the rearward motion of actin structure

161 In addition, myosin II inhibition decreases Drp1 association with mit

162 ROCK and myosin II inhibition reduced long-term contractility.

163 and they respond independently to actin and myosin II inhibition, serum deprivation and microtubule

164 in response to matrix elasticity, knockdown, myosin-II inhibition, and even constricted migration tha

165 and contractions, but this can be blocked by myosin-II inhibition.

166 results were mimicked by treatment with the myosin II inhibitor blebbistatin.

167 microcirculation and after treatment with a myosin-II inhibitor.

168 We have reported previously that nonmuscle myosin II-interacting guanine nucleotide exchange factor

169 previously reported that phosphorylation of myosin II-interacting guanine nucleotide exchange factor

170 Myosin II is a key component of the actomyosin ring, alt

171 We show that myosin II is activated sequentially from posterior to an

172 Myosin II is concentrated in arc-like regions of the lea

173 rized structure called a sarcomere, in which myosin II is localized in the center.

174 Surprisingly, myosin II is organized into an extensive network of fila

175 clude that the assembly and activation of NM myosin II is regulated during contractile stimulation of

176 The RhoA downstream effector myosin II is required for fusion as the expression of mu

177 The role of myosin II is supported by the observation of an increase

178 y cell types, adhesion-induced activation of myosin-II is maximized by adhesion to a rigid rather tha

179 Specifically, myosin-II is required throughout cytokinesis until contr

180 ells depend on the late cytokinetic S. pombe myosin II isoform, Myp2p, a non-essential protein that i

181 immature megakaryocytes express 2 nonmuscle myosin II isoforms (MYH9 [NMIIA] and MYH10 [NMIIB]), onl

182 Myosin II isoforms with varying mechanochemistry and fil

183 tinct myosin population containing nonmuscle myosin II isoforms, which is regulated by phosphorylatio

184 Cell Stem Cell, Shin et al. (2014) show that myosin-II isoforms sense matrix stiffness in hematopoiet

185 the N-cadherin-p120 catenin complex, whereas myosin II light chain and actin filament polarization de

186 ay greater activity at the free end, whereas myosin II light chain and actin filaments are enriched n

187 crease in cellular content of phosphorylated myosin II light chain.

188 sphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.

189 rminal domain of the heavy chains determines myosin II localization to the MK contractile ring and is

190 mbly via the formin FMNL2 and Arp2/3, active myosin-II localization, and integrin-based adhesion dyna

191 How myosin II localizes to the cleavage furrow in Dictyostel

192 migration, such as actin polymerization and myosin II-mediated contractility, are inhibited.

193 al inhibitors of lamellipodium formation and myosin II-mediated contractility.

194 ere attenuated by blebbistatin inhibition of myosin II-mediated cytoskeletal contraction.

195 In sarcomeres, myosin II-mediated sliding of antiparallel F-actin is ti

196 ted regulation of MT growth persistence from myosin-II-mediated regulation of growth persistence spec

197 branching and shape change largely through a myosin-II-mediated reorganization of the actin and micro

198 h two distinct mechanisms: destabilizing the myosin II (MII) hexameric complex and inhibiting MII con

199 ize to anisotropic features under non-muscle myosin II (MII) inhibition, despite MII ordinarily being

200 Nonmuscle myosin II (MII) is a critical mediator of contractility

201 dorsal root ganglion neurons, we found that myosin II (MII) is required for NGF to stimulate faster

202 other cell types are modulated by nonmuscle myosin-II (MII) forces and matrix mechanics.

203 Our simulations also show how myosin II mini-filaments, in tandem with cross-linkers,

204 eshold value, inducing contraction driven by myosin II mini-filaments.

205 and the expression of myosin light chain of myosin II (MLC2), which was identified as another target

206 The organization of filamentous actin and myosin II molecular motor contractility is known to modi

207 We labeled a Cys-lite Dictyostelium myosin II motor domain with donor and acceptor probes at

208 nking vimentin function in cell migration to myosin II motor proteins.

209 e-sensitive cytoskeletal proteins, including myosin II motors and actin cross-linkers such as alpha-a

210 Actin cytoskeletal elements, including myosin II motors and actin crosslinkers, structurally re

211 stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.

212 Myosin II motors embedded within the actin cortex genera

213 Cells with inhibited myosin II motors increased traction force (from 41 nN to

214 ng shear stress and inhibition of non-muscle myosin II motors, respectively.

215 Nonmuscle myosin II (Myo-II) activity at the cluster periphery bec

216 Activation of nonmuscle myosin II (Myo-II) by kinases such as Rho-associated kin

217 isoforms have distinct roles: "Conventional myosin-II Myo2 is crucial to ring assembly, unconvention

218 fission yeast cells depends on conventional myosin-II (Myo2) to assemble and constrict a contractile

219 g of IQGAP-related Rng2p, formin-Cdc12p, and myosin II (Myo2p) restores medial division in mid1 mutan

220 odelling requires the activity of non-muscle myosin II (MyoII) in the interphasic cells neighbouring

221 er these changes are generated by non-muscle myosin II (MyoII) motor proteins pulling filamentous act

222 re, we show that the receiving cell mounts a Myosin II (MyoII)-mediated mechanosensory response to it

223 works are thought to contract when nonmuscle myosin II (myosin) is activated throughout a mixed-polar

224 is crucial to ring assembly, unconventional myosin-II Myp2 is most important for ring constriction,

225 own about the functions of an unconventional myosin-II (Myp2) and a myosin-V (Myo51) that are also pr

226 hat triggers rapid and reversible non-muscle myosin II (NM II) dependent contraction of the actomyosi

227 Nonmuscle myosin II (NM II) powers myriad developmental and cellul

228 formation has been correlated with nonmuscle myosin II (NM-II) activity.

229 Nonmuscle myosin II (NM-II) is an important motor protein involved

230 However, the mechanisms by which nonmuscle myosin II (NM-II) is recruited to those structures and a

231 Nonmuscle myosin IIs (NM IIs) are a group of molecular motors invo

232 ns of polymerized unphosphorylated nonmuscle myosin IIs (NM2s), and this is reversed by phosphorylati

233 pithelium is tightly regulated by non-muscle myosin II (NMII) activity, we tested the role of NMIIA a

234 Inhibition of non-muscle myosin II (NMII) enhances central but impairs peripheral

235 es the critical role of ezrin and non-muscle myosin II (NMII) in the progressive implementation of li

236 Non-muscle myosin II (NMII) is a conserved force-producing cytoskel

237 Non-muscle myosin II (NMII) is reported to play multiple roles duri

238 Nonmuscle myosin II (NMII) is uniquely responsible for cell contra

239 ll shape changes are controlled by nonmuscle myosin II (NMII) motor proteins, which are tightly regul

240 Nonmuscle myosin II (NMII) plays central roles during cell adhesio

241 is study, we show that the role of nonmuscle myosin II (NMII)-B in front-back migratory cell polarity

242 generated by the molecular motor, non-muscle myosin II (NMII).

243 of INM by inhibition of actin or non-muscle myosin-II (NMII) reduced INM measures.

244 We show that two isoforms of nonmuscle myosin II, NMIIA and NMIIB, control distinct steps of th

245 s revealed the distinct roles of 2 nonmuscle myosin IIs (NMIIs) on MK endomitosis: only NMII-B (MYH10

246 ion of both canonical anillin and non-muscle myosin II (NMM-II) to intercellular bridges.

247 n interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining ce

248 s promotes the accumulation of the nonmuscle myosin II NMY-2 and the midbody component CYK-7 at the b

249 tile forces generated within it by nonmuscle myosin II (NMY-2) drive cellular morphogenetic processes

250 we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions.

251 hree of the five eukaryotic supergroups lack myosin II of the actomyosin contractile ring.

252 Blocking myosin-II or adding molecules of ICAM1 on the substrate

253 Note that unlike conventional myosin-II or other processive molecular motors, Ncd requ

254 Multiple myosin II paralogues accumulate at mammalian epithelial

255 in-based signaling pathways recruit distinct myosin II paralogues to generate the contractile apparat

256 easing and reducing the activity of the Rho1-Myosin II pathway enhances and decreases multilayering o

257 ulated by cytoskeletal tension through a Rok-myosin II pathway.

258 changes are accompanied by reorganization of Myosin II, PIP3, adhesion and active Cdc42.

259 equires active cell rearrangements driven by Myosin II planar polarisation.

260 se-binding protein, amplifies Rho-kinase and myosin II planar polarity and junctional localization do

261 NM myosin II plays a critical role in airway SM contraction

262 e an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based

263 downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions.

264 lts indicate that the two spatially distinct myosin II populations coordinately regulate ovulatory co

265 The mono-ubiquitination of Myosin II promotes its physical interaction with Myosin

266 roteins including cortexillin I, IQGAP2, and myosin II recovered much more slowly than actin and pola

267 INF2-mediated actin polymerization leads to myosin II recruitment and constriction at the fission si

268 tic impact of platelets, including nonmuscle myosin II, red blood cells (RBCs), fibrin(ogen), factor

269 Myosin-II regulation thus controls platelet size and num

270 Phosphorylation of the myosin II regulatory light chain (RLC) promotes the asse

271 around the wound, and constitutively active myosin II regulatory light chain suppresses the effects

272 fluorescent 70 kDa dextran, we detected acto-myosin II rings surrounding dextran-positive budding end

273 The acto-myosin II rings therefore play a key role in constrictin

274 3xAsp myosin II's localization to the cleavage furrow was resc

275 ll-atom molecular dynamics simulation of the myosin II S1 domain in the rigor state interacting with

276 ities are associated with altered Rho-kinase/myosin II signaling and loss of apically distributed act

277 over, we identified a role for the RhoA-ROCK-myosin II signaling axis in this MeV internalization pro

278 vigation, was modestly dependent on Rho-ROCK-myosin II signaling on a 2D substrate or in a loose coll

279 ro1A functions associated with both Rac1 and myosin II signaling.

280 p1 on available rigor and blebbistatin-bound myosin II structures suggests that myo2-E1-Sup1 may repr

281 he base of the node that anchors the ends of myosin II tails to the plasma membrane, with myosin II h

282 are periodic pulses of junctional and medial myosin II that result in progressively stronger cortical

283 ted with centrally located, circumferential, myosin-II thick filaments on the membrane-distal side.

284 fector kinase, RhoA kinase (ROCK), activates myosin II to form actomyosin filament bundles and large

285 tion using cDNA library suppression of 3xAsp myosin II to identify factors involved in myosin cleavag

286 osin through the Rho-mediated recruitment of myosin II to the apical cortex.

287 s generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhe

288 midzone MTs), whereas F-actin and non-muscle myosin II, together with other factors, organize into th

289 in an adhesive process that often activates myosin-II, unless the macrophage also engages "marker of

290 of elongate, antiparallel filaments, whereas myosin II was organized into laterally associated, head-

291 Myosin II was required for not only the generation of pr

292 L) bound stereospecifically to Dictyostelium myosin II, we determined with high resolution the orient

293 strains with fluorescently labeled actin and myosin II), which have been carried out in live and fixe

294 al accumulation of Rho kinase and non-muscle myosin II, which coordinate apical constriction.

295 ions produce force-dependent accumulation of myosin II, which is thought to be responsible for their

296 Da regulatory light chain subunits (LC20) of myosin II, which permits cross-bridge cycling and force

297 dherin induces an asymmetric accumulation of Myosin-II, which leads to a highly contractile cell inte

298 y of a phagocytosed cell also hyperactivates myosin-II, which locally overwhelms self-signaling at a

299 Finally, an engineered myosin II with a longer lever arm (2xELC), producing a h

300 CR), the precise ultrastructure of actin and myosin II within the animal cell CR remains an unanswere