ライフサイエンスコーパス: nonmuscle

1 a preference for actin isoforms, nucleating nonmuscle actin but not muscle actin, which has not been

2 wild-type and mutant POF1B proteins to bind nonmuscle actin filaments in vitro.

3 t the capacity of the mutant protein to bind nonmuscle actin filaments was diminished fourfold compar

4 ogenesis of POF by altering POF1B binding to nonmuscle actin filaments.

5 t prolyl hydroxylase 3 (PHD3) interacts with nonmuscle actin in human cells and catalyzes hydroxylati

6 ver, it was only 40 years ago that the first nonmuscle actin-binding protein, filamin, was identified

7 Subsequently many other nonmuscle actin-binding proteins were identified and cha

8 beta- and gamma-nonmuscle actins differ by 4 amino acids at or near the

9 ty through posttranslational modification of nonmuscle actins.

10 filament disassembly but not with UNC-60A, a nonmuscle ADF/cofilin.

11 us CHC22 and CHC17 function independently in nonmuscle and muscle cells.

12 ted from the original MYLK gene that encodes nonmuscle and smooth muscle myosin light chain kinase (s

13 me courses of human cofilin binding to human nonmuscle (beta-, gamma-) actin filaments.

14 tial actin organization and induction of the nonmuscle, beta actin isoform.

15 Here we show that nonmuscle CaD is highly expressed in both premigratory a

16 his similarity explains the fact that single nonmuscle cell and whole-muscle contraction both follow

17 ation and derepression of genes expressed in nonmuscle cell lineages.

18 actin phosphorylation has been implicated in nonmuscle cell migration.

19 that could be responsible for the variety of nonmuscle cell movements, including the "saltatory cytop

20 critical for numerous aspects of muscle and nonmuscle cell physiology.

21 rangements that bring about contractility in nonmuscle cells are currently debated.

22 tures in striated muscle, smooth muscle, and nonmuscle cells contain the actin filament-cross-linking

23 Studies in nonmuscle cells have demonstrated that Ca(2+)/calmodulin

24 in humans and may reduce oxidative stress in nonmuscle cells in vitro.

25 thermore, we show that induction of Myod1 in nonmuscle cells is sufficient to redirect Smad3 to Myod1

26 One wondered whether nonmuscle cells might have a myosin-like molecule, well

27 udy indicated that myomaker could be used in nonmuscle cells to induce fusion with muscle in vivo, th

28 udy indicated that myomaker could be used in nonmuscle cells to induce fusion with muscle in vivo, th

29 -powered force generation and contraction in nonmuscle cells underlies many cell biological processes

30 n kinase family associated with apoptosis in nonmuscle cells where it phosphorylates myosin regulator

31 in II in all species (including myosin II in nonmuscle cells), with the possible exception of insect

32 in filaments can assemble and disassemble in nonmuscle cells, and in some smooth muscle cells, but wh

33 Previous work, in nonmuscle cells, has shown that Hsp27 inhibits TNF-alpha

34 In nonmuscle cells, oscillations in contractility are induc

35 In eukaryotic nonmuscle cells, regulation of the homodimeric actin cro

36 In mammalian nonmuscle cells, the mechanisms controlling the localize

37 dered actomyosin bundles found in muscle and nonmuscle cells.

38 hesion, morphogenesis, and mechanosensing in nonmuscle cells.

39 e actomyosin assemblies in smooth muscle and nonmuscle cells.

40 and cellular and intracellular movements in nonmuscle cells.

41 stability of actin in eukaryotic muscle and nonmuscle cells.

42 yosin contraction found in smooth muscle and nonmuscle cells.

43 oblasts differentiating into myotubes and in nonmuscle cells.

44 mical energy into force/motion in muscle and nonmuscle cells.

45 molecular weight (HMW), found in muscle and nonmuscle cells.

46 mposed of a highly diverse set of muscle and nonmuscle cells.

47 II-based motile activity in both muscle and nonmuscle cells.

48 ching off myosin II-based motile activity in nonmuscle cells.

49 liferation, or cell death, when expressed in nonmuscle cells.

50 olymerization in smooth muscle as well as in nonmuscle cells.

51 ports a vast number of cellular processes in nonmuscle cells.

52 he structure and motility of both muscle and nonmuscle cells.

53 to generate contractile forces in muscle and nonmuscle cells.

54 ovement observed in actomyosin assemblies in nonmuscle cells.

55 s actin isoforms function in both muscle and nonmuscle contractile processes.

56 Nonmuscle cortical actomyosin networks are thought to co

57 many actin isoforms are restricted to either nonmuscle (cytoplasmic) functions, or to myofibril force

58 ishing bladder cancer from controls and also nonmuscle from muscle-invasive bladder cancer.

59 quires proper assembly and regulation of the nonmuscle gamma isoactin-rich cytoskeleton, and six poin

60 Currently, ten point mutations in nonmuscle gamma-actin have been identified as causing pr

61 ngle- and double-headed myosin fragments and nonmuscle IIB thick filaments.

62 as follows: LGN = low grade (grade 1 or 2), nonmuscle invading (stage Ta or T1); HGN = high grade (g

63 = high grade (grade 3 or carcinoma in situ), nonmuscle invading (stage Ta, T1, or TIS); and INV = any

64 ve higher mortality rates than patients with nonmuscle invasive ('superficial') bladder cancer.

65 is challenging, especially in the setting of nonmuscle invasive (NMI) disease.

66 High-risk, nonmuscle invasive bladder cancer (HR-NMIBC) represents

67 Once diagnosed, patients with nonmuscle invasive bladder cancer (NMIBC) are committed

68 PURPOSE OF REVIEW: As high-risk nonmuscle invasive bladder cancer (NMIBC) has a high pro

69 The management of nonmuscle invasive bladder cancer (NMIBC) recurrent afte

70 ravesical bacillus Calmette-Guerin (BCG) for nonmuscle invasive bladder cancer (NMIBC).

71 roversies in the diagnosis and management of nonmuscle invasive bladder cancer (NMIBC).

72 DINGS: The mainstay definitions of high-risk nonmuscle invasive bladder cancer are based on grade and

73 PURPOSE OF REVIEW: Nonmuscle invasive bladder cancer represents a large maj

74 The management of nonmuscle invasive bladder cancer with variant histology

75 ts should change management of patients with nonmuscle invasive bladder cancer.

76 of microRNAs to help evaluate patients with nonmuscle invasive bladder cancer.

77 In patients with recurrent high-grade nonmuscle invasive cancer and patients undergoing radica

78 Management of high-risk patients with nonmuscle invasive cancer continues to be controversial,

79 In patients with nonmuscle invasive cancer, there is a need for enhanced

80 r, with a focus upon their role in high-risk nonmuscle invasive tumors.

81 thelial carcinomas, both muscle invasive and nonmuscle invasive.

82 tiveness and harms of interventions for both nonmuscle-invasive and muscle-invasive disease will enha

83 and controversies in the management of both nonmuscle-invasive and muscle-invasive urothelial carcin

84 treatment for muscle-invasive and high-risk nonmuscle-invasive bladder cancer (BCa), but is associat

85 Trials in nonmuscle-invasive bladder cancer are evaluating the rol

86 improvements in diagnosis and management of nonmuscle-invasive bladder tumors, the risk of both recu

87 Management of high-risk patients with nonmuscle-invasive cancer remains a challenge, with cont

88 tion to risk stratification of patients with nonmuscle-invasive tumors permits appropriate timing of

89 sin genes imply the existence of additional, nonmuscle isoforms.

90 Both ERK1/2 activity and nonmuscle l-caldesmon phosphorylation are blocked by h3/

91 y PRC1/Bmi1 concentrates at genes specifying nonmuscle lineages, helping to retain H3K27me3 in the fa

92 n-cell-autonomously, acting through adjacent nonmuscle mesenchyme.

93 e more abundant and persistently unpolarized nonmuscle MIIA (myosin-IIA).

94 We show that nonmuscle MIIB (myosin-IIB) is unpolarized in cells on s

95 The 3 isoforms of nonmuscle myosin (NM) II (NMII-A, NMII-B, and NMII-C) pl

96 Ablation of nonmuscle myosin (NM) II-A or NM II-B results in mouse e

97 Ablation of nonmuscle myosin (NM) II-B in mice during embryonic deve

98 alization of two motor complexes, dynein and nonmuscle myosin (NM)II.

99 e the behavior of the cortical motor protein nonmuscle myosin (NMY-2) to complement recent efforts th

100 ene that encodes the molecular motor protein nonmuscle myosin 2a (MYH9) with ESRD in African American

101 We discovered that nonmuscle myosin 2A (NM2A) directly bound the BAR-PH tan

102 Inhibitors of nonmuscle myosin activity repressed the assembly of myof

103 gulator of this process as it activates both nonmuscle myosin and a nucleator of actin filaments [1].

104 mask-plating, or inhibition of Rho kinase or nonmuscle myosin attenuated stress fiber accumulation an

105 Nonmuscle myosin copurifies with polysomes, and there is

106 Here we show that intact nonmuscle myosin filaments are required for the synthesi

107 cate that association of collagen mRNAs with nonmuscle myosin filaments is necessary to coordinately

108 Dissociation of nonmuscle myosin filaments results in secretion of colla

109 in vitro by studying mice and cells in which nonmuscle myosin heavy chain (NMHC) II-A is genetically

110 e studied 2 transgenic mouse models in which nonmuscle myosin heavy chain (NMHC) II-A was genetically

111 , we used homologous recombination to ablate nonmuscle myosin heavy chain (NMHC) II-B by inserting cD

112 ternative splicing of a cassette exon N30 of nonmuscle myosin heavy chain (NMHC) II-B in the mouse ce

113 ium (LD) detected strong association between nonmuscle myosin heavy chain 9 gene (MYH9) variants on c

114 ss spectrometry as nuclear alphaII-spectrin, nonmuscle myosin heavy chain alpha, Lmo7 (a predicted tr

115 monoclonal antibody (m21G6) directed against nonmuscle myosin heavy chain II may inhibit IgM binding

116 A highly conserved self-antigen, nonmuscle myosin heavy chain II, has been identified as

117 Here, we show that nonmuscle myosin heavy chain IIA (MyH9) is recruited to

118 Subset 6 CLL mAbs recognize nonmuscle myosin heavy chain IIA (MYHIIA).

119 that was identified by mass spectrometry as nonmuscle myosin heavy chain IIA (MYHIIA).

120 c variants of the MYH9 gene that encodes the nonmuscle myosin heavy chain IIA are associated with dia

121 otein S100A4 and the C-terminal fragments of nonmuscle myosin heavy chain IIA has been studied by equ

122 we have also identified a new Rab3 effector, nonmuscle myosin heavy chain IIA, as part of the complex

123 we reported that RUNX1-mediated silencing of nonmuscle myosin heavy chain IIB (MYH10) was required fo

124 Proteomic screening identified nonmuscle myosin heavy chain IIB (NMHCIIB), a subunit of

125 , localization of the actin-bundling protein nonmuscle myosin heavy chain IIB, and junction remodelin

126 desmoplakin, fibrillarin, nuclear lamin B1, nonmuscle myosin heavy chain IIB, paxillin, Sec61 beta,

127 anging from 0.2 to 0.6) in the gene encoding nonmuscle myosin heavy chain type II isoform A (MYH9) we

128 en the Wingless (Wg) signaling pathway and a nonmuscle myosin heavy chain, encoded by the crinkled (c

129 A similar structure was observed in nonmuscle myosin II (also phosphorylation-regulated).

130 Nonmuscle myosin II (MII) is a critical mediator of cont

131 Nonmuscle myosin II (Myo-II) activity at the cluster per

132 Activation of nonmuscle myosin II (Myo-II) by kinases such as Rho-asso

133 myosin networks are thought to contract when nonmuscle myosin II (myosin) is activated throughout a m

134 Here, we demonstrate that nonmuscle myosin II (NM II) is required for the internal

135 Nonmuscle myosin II (NM II) powers myriad developmental

136 t contractile ring constriction is driven by nonmuscle myosin II (NM II) translocation of antiparalle

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

138 better understand the mechanism controlling nonmuscle myosin II (NM-II) assembly in mammalian cells,

139 Nonmuscle myosin II (NM-II) is an important motor protei

140 However, the mechanisms by which nonmuscle myosin II (NM-II) is recruited to those struct

141 Nonmuscle myosin II (NMII) is thought to be the master i

142 Nonmuscle myosin II (NMII) is uniquely responsible for c

143 cological inhibition or genetic silencing of nonmuscle myosin II (NMII) markedly accelerates axon gro

144 These cell shape changes are controlled by nonmuscle myosin II (NMII) motor proteins, which are tig

145 The motor protein nonmuscle myosin II (NMII) must undergo dynamic oligomer

146 Nonmuscle myosin II (NMII) plays central roles during ce

147 ber and increased fibripositor length; thus, nonmuscle myosin II (NMII) powers the transport of these

148 In this study, we show that the role of nonmuscle myosin II (NMII)-B in front-back migratory cel

149 ifferentially interacts with the isoforms of nonmuscle myosin II (NMIIA, K(d) = 0.5 muM; IIB, K(d) =

150 nd contractile forces generated within it by nonmuscle myosin II (NMY-2) drive cellular morphogenetic

151 cts of TNF-alpha signaling, including apical nonmuscle myosin II accumulation and myosin light chain

152 Finally, we show that nonmuscle myosin II activation contributes to the cytosk

153 Inhibition of nonmuscle myosin II activation may provide a novel appro

154 We demonstrate that nonmuscle myosin II activity guides adhesion phenotype i

155 ; however, there was no detectable change in nonmuscle myosin II activity in nesprin-1 deficient cell

156 A activity and associated Rho kinase-induced nonmuscle myosin II activity.

157 end genetic interaction studies to show that nonmuscle myosin II and an unconventional myosin, encode

158 The roles of nonmuscle myosin II and cortical actin filaments in chro

159 Subsequently, bridge bundles recruit nonmuscle myosin II and mature into stress fibers.

160 Additional requirements for nonmuscle myosin II are in the correct formation of othe

161 associated with an accumulation of actin and nonmuscle myosin II around the wound, forming a purse st

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

163 Inhibition of nonmuscle myosin II blocks all elasticity-directed linea

164 In vivo, thorough depletion of nonmuscle myosin II delayed furrow initiation, slowed F-

165 Inhibition of nonmuscle myosin II dissipates this traction polarizatio

166 the elucidation of post-embryonic roles for nonmuscle myosin II during targeted stages of fly develo

167 onstrate that truncation alleles can perturb nonmuscle myosin II function via two distinct mechanisms

168 tional perturbation, in a graded fashion, of nonmuscle myosin II function.

169 t reversine functions as a dual inhibitor of nonmuscle myosin II heavy chain and MEK1, and that both

170 Mice carrying floxed alleles of the nonmuscle myosin II heavy chain gene (NMHC IIA(flox/flox

171 Inhibition of MEK1 and nonmuscle myosin II heavy chain results in altered cell

172 Despite functional significance of nonmuscle myosin II in cell migration and invasion, its

173 Inhibition of nonmuscle myosin II in human NK cells with blebbistatin

174 ly reduced translocation velocity, while the nonmuscle myosin II inhibitor blebbistatin and the kines

175 he mammalian homologue of Lgl (Lgl1) and the nonmuscle myosin II isoform A (NMII-A).

176 Although immature megakaryocytes express 2 nonmuscle myosin II isoforms (MYH9 [NMIIA] and MYH10 [NM

177 Nonmuscle myosin II isoforms A and B (hereafter, IIA and

178 in II rather than the ubiquitously expressed nonmuscle myosin II isoforms, suggesting that a rich fun

179 has a distinct myosin population containing nonmuscle myosin II isoforms, which is regulated by phos

180 blocked by inhibiting RLC phosphorylation or nonmuscle myosin II motor activity.

181 wild-type centration depends equally on the nonmuscle myosin II NMY-2 and the Galpha proteins GOA-1/

182 ch in turns promotes the accumulation of the nonmuscle myosin II NMY-2 and the midbody component CYK-

183 The nonmuscle myosin II NMY-2 is required for cytokinesis as

184 s provided by the recruitment of F-actin and nonmuscle myosin II on the granule membranes that is tri

185 Nonmuscle myosin II plays essential roles in embryonic d

186 Microtubule-directed nonmuscle myosin II polarization is aberrant in embryos

187 Nonmuscle myosin II produces contractile forces involved

188 l activation, we observed phosphorylation of nonmuscle myosin II regulatory light chain (RLC), which

189 rrow regression, but also mislocalization of nonmuscle myosin II with a phosphorylated myosin regulat

190 Interestingly, blocking activity of NMII (nonmuscle myosin II) either before, or after, lumen morp

191 gs were caused by Rac-mediated inhibition of nonmuscle myosin II, a cell polarity determinant.

192 development they demonstrate novel roles for nonmuscle myosin II, including in adhesion between the d

193 le apparatus [5-7], given that inhibition of nonmuscle myosin II, myosin light chain kinase, and Rho

194 We show that two isoforms of nonmuscle myosin II, NMIIA and NMIIB, control distinct s

195 d mechanistic impact of platelets, including nonmuscle myosin II, red blood cells (RBCs), fibrin(ogen

196 studies was to learn whether one isoform of nonmuscle myosin II, specifically nonmuscle myosin II-A,

197 CAFs align the Fn matrix by increasing nonmuscle myosin II- and platelet-derived growth factor

198 To investigate the contribution of nonmuscle myosin II-A (NM II-A) to early cardiac develop

199 lines, each with a different mutation in the nonmuscle myosin II-A gene, Myh9 (R702C, D1424N, and E18

200 isoform of nonmuscle myosin II, specifically nonmuscle myosin II-A, could functionally replace a seco

201 -A, could functionally replace a second one, nonmuscle myosin II-B, in mice.

202 Overall, 4-HAP modifies nonmuscle myosin II-based cell mechanics across phylogen

203 Pharmacologic inhibition of nonmuscle myosin II-based contractility blunts this rigi

204 The functional role of the C2 insert of nonmuscle myosin II-C (NM II-C) is poorly understood.

205 We have reported previously that nonmuscle myosin II-interacting guanine nucleotide excha

206 he other, driven by oscillations of cortical nonmuscle myosin II.

207 signaling pathway, including Rho GTPase and nonmuscle myosin II.

208 a cortical ring rich in actin filaments and nonmuscle myosin II.

209 zing formins; and with zipper, which encodes nonmuscle myosin II.

210 Inhibition of nonmuscle myosin IIA (NM-MHC-IIA) motor activity prevent

211 In studies initially focused on roles of nonmuscle myosin IIA (NMIIA) in the developing mouse epi

212 It binds to the nonmuscle myosin IIA (NMIIA) tail near the assembly comp

213 In addition, MyoGEF co-localizes with nonmuscle myosin IIA (NMIIA) to the front of migrating c

214 -interacting protein, cofilin, Munc13-4, and nonmuscle myosin IIA (NMIIA).

215 (2+)]i, and the association of gelsolin with nonmuscle myosin IIA (NMMIIA) at collagen adhesions are

216 recipitates showed that FliI associated with nonmuscle myosin IIA (NMMIIA), which was confirmed by im

217 l stem cells-as a prototypical adherent cell-nonmuscle myosin IIA and vimentin are just two of the cy

218 reviously that NK-cell cytotoxicity requires nonmuscle myosin IIA function and that granule-associate

219 The nonmuscle myosin IIA heavy chain (Myh9) is strongly asso

220 trongly suggest that base-line expression of nonmuscle myosin IIA inhibits osteoclast precursor fusio

221 We also found that nonmuscle myosin IIA is a major determinant of ROCK1 cor

222 tal muscle myosin, nonmuscle myosin IIB, and nonmuscle myosin IIA revealed three distinct regimes of

223 on epithelial cadherin (E-cadherin), NMMIIA (nonmuscle myosin IIA), and p120-catenin.

224 CMIIB), Dictyostelium myosin II (DdMII), and nonmuscle myosin IIA, as well as myosin V.

225 by Mg(2+) in myosin V, smooth muscle myosin, nonmuscle myosin IIA, CMIIB, and DdMII, although the ADP

226 f our top hits-including Myh9, which encodes nonmuscle myosin IIa-have not been linked to tumor devel

227 icity of tractions depend on the activity of nonmuscle myosin IIA.

228 Nonmuscle myosin IIB (NMIIB) is a cytoplasmic myosin, wh

229 he discovery of a viable therapeutic target, nonmuscle myosin IIB (NMIIB), a molecular motor that sup

230 osin heavy chain IIB (NMHCIIB), a subunit of nonmuscle myosin IIB (NMIIB), as an ER stress-dependent

231 Suppressing nonmuscle myosin IIB disrupts directional cell rearrange

232 al. report that a short serine-rich motif in nonmuscle myosin IIB is required to establish the cell's

233 s and show that the individual nonprocessive nonmuscle myosin IIB molecules form a highly processive

234 rs representative of skeletal muscle myosin, nonmuscle myosin IIB, and nonmuscle myosin IIA revealed

235 This zone is also enriched for nonmuscle myosin IIB.

236 leus, enriched in tropomodulin 1 (Tmod1) and nonmuscle myosin IIB.

237 ngly to a homologous heavy chain fragment of nonmuscle myosin IIC as to NMIIA.

238 Nonmuscle myosin IIs (NM IIs) are a group of molecular m

239 of solutions of polymerized unphosphorylated nonmuscle myosin IIs (NM2s), and this is reversed by pho

240 studies has revealed the distinct roles of 2 nonmuscle myosin IIs (NMIIs) on MK endomitosis: only NMI

241 Nonmuscle myosin IIs play an essential role during cytok

242 Two nonmuscle myosin isoforms (II-B and Va), were identified

243 Concurrent, but not individual, knockdown of nonmuscle myosin isoforms IIA and IIB also decreases con

244 The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa sm

245 ry mediated by TRPC6, in turn, activates the nonmuscle myosin light chain kinase (MYLK), which not on

246 Nonmuscle myosin light chain kinase (nmMLCK), a multi-fu

247 Nonmuscle myosin light-chain kinase (MYLK) mediates incr

248 Nonmuscle myosin light-chain kinase (nmMLCK), the predom

249 Boyden chambers, we demonstrated the role of nonmuscle myosin light-chain kinase (nmMYLK) in Tat(1)(-

250 Nonmuscle myosin light-chain kinase contributes to ather

251 We found that polarized distributions of the nonmuscle myosin NMY-2 at the cell cortex are independen

252 MLC-4, a nonmuscle myosin regulatory light chain, localizes to sm

253 LARP6 interacts with nonmuscle myosin through its C-terminal domain and assoc

254 Here, we show that nonmuscle myosin type IIA (NM-IIA) interacts with MG53 t

255 response mediated by natural IgM directed to nonmuscle myosin with complement activation that results

256 ates activity of RhoA and phosphorylation of nonmuscle myosin, both implicated in actomyosin contract

257 ynaptic strength was distinct from that of a nonmuscle myosin, myosin IIb.

258 on of green fluorescent protein (GFP)-tagged nonmuscle myosin, we have found that the astral pathway

259 onsensus amino acid Met466 in the Drosophila nonmuscle myosin-2 active-site loop switch-2 acts as ble

260 the overall enzymatic signatures across the nonmuscle myosin-2 complement from model organisms indic

261 Together, these data show that Drosophila nonmuscle myosin-2 is a bona fide molecular motor and es

262 Nonmuscle myosin-2 is the primary enzyme complex powerin

263 Drosophila nonmuscle myosin-2 is uniquely insensitive toward blebbi

264 e kinetic characterization of the Drosophila nonmuscle myosin-2 motor domain.

265 x, the relay helix, and the lever, abolishes nonmuscle myosin-2 specific kinetic signatures.

266 complexes containing filamentous beta-actin, nonmuscle myosin-2B (NM-2B) constructs, and either tropo

267 tate (ADPVO4) crystal structure of the human nonmuscle myosin-2C motor domain, one of the slowest myo

268 icates that the Drosophila protein resembles nonmuscle myosin-2s from metazoa rather than protozoa, t

269 es that in other cell types are modulated by nonmuscle myosin-II (MII) forces and matrix mechanics.

270 odel for collective cell migration, requires nonmuscle myosin-II (Myo-II).

271 Surprisingly, unlike with smooth muscle and nonmuscle myosin-II, RLC phosphorylation does not influe

272 y pharmacologic inhibition of myosin-II, but nonmuscle myosin-IIA (MIIA) mutations paradoxically caus

273 ons with specific protein targets, including nonmuscle myosin-IIA (MIIA).

274 illin, F-actin, and the major motor isoform, nonmuscle myosin-IIA.

275 olymerization and is negatively regulated by nonmuscle myosin.

276 ation and is negatively regulated by Rho and nonmuscle myosin.

277 ins and extend our previous EPR studies to a nonmuscle myosin.

278 Mammalian cells express three Class II nonmuscle myosins (NM): NM2A, NM2B, and NM2C.

279 most closely related to conventional class-2 nonmuscle myosins (NM2).

280 Nonmuscle myosins (NMs) II-A and II-B are essential for

281 n 2 heads bound to actin, we find that human nonmuscle myosins 2A and 2B show marked load-dependent c

282 raction of the actin cytoskeleton, driven by nonmuscle myosins and regulated by the Rho family GTPase

283 In contrast to nonmuscle myosins from animal cells that require phospho

284 ases, the activity of motor proteins such as nonmuscle myosins is required for appropriate constricti

285 ultured human cholangiocytes express several nonmuscle myosins, including myosins IIA and IIB.

286 (ACD), conserved among skeletal, smooth and nonmuscle myosins, prevents multimerization, inhibition

287 not identical energetics in both muscle and nonmuscle myosins.

288 nal in vivo and whether the newly introduced nonmuscle nuclei undergoes nuclear reprogramming has not

289 on of sarcomeric cardiac RLC and cytoplasmic nonmuscle RLC increased markedly in hearts from TG mice

290 lue 2-fold greater than the value for smooth/nonmuscle RLC; cardiac RLC is a favorable biochemical su

291 cytokine action on muscle promotes atrophy, nonmuscle sites of action for inflammatory mediators are

292 y mixtures of F-actin and thick filaments of nonmuscle, smooth, and skeletal muscle myosin isoforms w

293 tem cells that reside in skeletal muscle and nonmuscle stem cell populations.

294 ature of cardiac, skeletal muscle, and other nonmuscle systems requires further analysis to take into

295 re important for its interaction with TM5 (a nonmuscle TM isoform).

296 The actin-binding protein nonmuscle tropomyosin (Tm) provides spatially specific r

297 Only one nonmuscle tropomyosin (Tm1A) has previously been describ

298 rminal model peptide complexed with a smooth/nonmuscle tropomyosin C-terminal peptide.

299 ntifies and characterizes previously unknown nonmuscle tropomyosins in Drosophila, 2) reveals a funct

300 , indicating that dysferlin is important for nonmuscle vesicular trafficking.