ライフサイエンスコーパス: myosin IIA

1 and persistently unpolarized nonmuscle MIIA (myosin-IIA).

2 rsal interpodosomal filaments crosslinked by myosin IIA.

3 or the phosphorylation of granule-associated myosin IIA.

4 ractions depend on the activity of nonmuscle myosin IIA.

5 n uropod formation, and in the regulation of myosin IIa.

6 nt on actin and the involvement of nonmuscle myosin IIA.

7 foci interspersed with linear filaments and myosin IIa.

8 l synapses are active processes dependent on myosin IIA.

9 K cells, were constitutively associated with myosin IIA.

10 xin A2, the tumor-suppressor protein p53 and myosin IIA.

11 f the regulatory light chain associated with myosin IIA.

12 ered in a screen for inhibitors of nonmuscle myosin IIA.

13 ication of myosin (Myo) XVIIIA and nonmuscle myosin IIA.

14 eric interactions of SERT, specifically with myosin IIA.

15 sin- (HMM-) like fragment of human nonmuscle myosin IIA.

16 This dynamics was dependent on myosin IIA.

17 ylation of cytoskeleton-regulating nonmuscle myosin IIa.

18 Ks and preplatelet fragments, which requires myosin IIA.

19 ulture, including tumor suppressor nonmuscle myosin IIA.

20 ivation of a pathway involving Vav, Rac, and myosin IIA.

21 anism for mediating the binding of S100A4 to myosin-IIA.

22 arcinoma cell motility via interactions with myosin-IIA.

23 ctin, and the major motor isoform, nonmuscle myosin-IIA.

24 ion compared with cells expressing wild-type myosin-IIA.

25 ional motility via a direct interaction with myosin-IIA.

26 ffecting the assembly of myosin-IIB, but not myosin-IIA.

27 e, appears to be similar to rabbit nonmuscle myosin-IIA.

28 MYH9 encodes the heavy chain of non-muscle myosin IIA, a cellular motor involved in motility.

29 ite and is recycled by binding to non-muscle myosin IIA, a motor protein, via the cytoplasmic tail (C

30 elated macrothrombocytopenias, MYH9, encodes myosin-IIA, a protein that enables morphogenesis in dive

31 Pharmacological inhibition or knockdown of myosin IIA abolishes the filopodia adhesion to the beads

32 It was suppressed by inhibitors of nonmuscle myosin IIA, actin polymerization, and integrin alphaIIbb

33 Drugs inhibiting actin polymerization or myosin IIA activation prevented nanotube formation and v

34 ing asymmetric self-renewal and constitutive myosin-IIA activation promoting cytokine-triggered diffe

35 Both uropod formation and myosin IIa activity are compromised in flotillin 1 knock

36 on both their filamentous actin content and myosin IIA activity, although the relative contribution

37 tin polymerization, down-regulates nonmuscle myosin IIA activity, and destabilizes kidney podocyte ad

38 In contrast, elevation of myosin-IIA activity, by exogenous expression or by mimic

39 ast to clot retraction, requires anisotropic myosin IIa-activity at the platelet rear which is preced

40 corresponding region of GFP-tagged nonmuscle myosin IIA also abolished this localization.

41 However, while targeting just myosin IIA also impairs tumor invasion, it surprisingly

42 EphA2 associates with c-Cbl-myosin IIA and augmented KSHV-induced Src and PI3-K sign

43 vivo, disruption of microtubules or loss of myosin IIA and B resulted in loss of tight junction-medi

44 onent of the Sec61 translocon, and nonmuscle myosin IIA and beta-actin.

45 tes the dynamic redistribution of non-muscle myosin IIA and beta2-integrin, which facilitate neutroph

46 ables, which were also determined to contain myosin IIA and exhibit additional characteristics of pur

47 ociated actin regulatory proteins, including myosin IIA and ezrin, and that these effects are depende

48 primordium and observed interactions between myosin IIA and F-actin in cells encapsulated in collagen

49 Myosin IIA and IIB are the most prevalent isoforms of my

50 Myosin IIA and IIB demonstrate differential expression d

51 The positioning and dynamics of myosin IIA and IIB depend on the self-assembly regions i

52 Nonmuscle myosin IIA and IIB distribute preferentially toward oppo

53 L are, in part, related to a deregulation of myosin IIA and IIB expression leading to both a defect i

54 Studies of myosin IIA and IIB in cultured cells and null mice sugge

55 Our data suggest that the myosin IIA and IIB isoforms are regulated by different s

56 e performed using monospecific antibodies to myosin IIA and IIB isotypes.

57 Expression of nonmuscle myosin IIA and IIB was confirmed in both human TM and CB

58 d and what role they play in cell migration, myosin IIA and IIB were examined during wound healing by

59 COS7 and B16 melanoma cells lack myosin IIA and IIB, respectively; and show isoform-speci

60 Arp2/3 disruption depleted junctions of both myosin IIA and IIB, suggesting that dynamic actin assemb

61 s the interaction of C2GnT-M with non-muscle myosin IIA and its transportation to the endoplasmic ret

62 : the scattered meiotic chromosomes initiate myosin IIA and microfilament assemble in the vicinity of

63 icking BM stiffness contributes, through the myosin IIA and MKL1 pathways, to a more favorable in vit

64 Myosin IIA and MLC phosphorylation are important in plat

65 orylation that correlates the recruitment of myosin IIA and myosin IIB into this spreading margin.

66 orms of non-muscle myosin II, referred to as myosin IIA and myosin IIB.

67 xistence of a compensatory mechanism between myosin IIA and myosin IIB.

68 e structures (SLSs) with periodically spaced myosin IIA and synaptopodin appear in injured podocytes

69 ls-as a prototypical adherent cell-nonmuscle myosin IIA and vimentin are just two of the cytoskeletal

70 This effect occurs only in the presence of myosin-IIA and implies that myosin-IIA influences thromb

71 that S100A4 specifically binds to nonmuscle myosin-IIA and promotes the unassembled state.

72 express several nonmuscle myosins, including myosins IIA and IIB.

73 ial cadherin (E-cadherin), NMMIIA (nonmuscle myosin IIA), and p120-catenin.

74 lin microdomains specifically associate with myosin IIa, and spectrins.

75 BMMs form unstable protrusions, overassemble myosin-IIA, and exhibit altered colony-stimulating facto

76 ulted in opposing migration phenotypes, with myosin IIA- and IIB-depleted cells exhibiting higher and

77 o show that the mechanism requires localized myosin-IIA- and alpha5beta1 integrin/fibronectin-mediate

78 unctional experiments, the microinjection of myosin IIA antibody disrupts meiotic maturation to metap

79 The interactions between Myosin VIIa and Myosin IIa are conserved in the mammalian cochlea and in

80 We examined the role of myosin IIA as a candidate for facilitating this prefinal

81 ctyostelium myosin II (DdMII), and nonmuscle myosin IIA, as well as myosin V.

82 rvations are consistent with mts1 regulating myosin IIA assembly by monomer sequestration and suggest

83 A heavy chain that has comparable effects on myosin-IIA assembly as S100A4.

84 sions in the rod, cause defects in nonmuscle myosin-IIA assembly.

85 ell center through the dynamic shortening of myosin IIA-associated actin stress fibers to drive rapid

86 When isolated using density gradients, myosin IIA-associated NK cell lytic granules directly bo

87 Phosphorylation of myosin IIA at residue serine 1943 (S1943) in the tailpie

88 agonism results from transient enrichment of myosin IIA at the cell front, which disrupts the back-to

89 ator of myosin II assembly, colocalizes with myosin IIA at the leading edge of cancer cells, suggesti

90 selective aggregation of myosin IIB but not myosin IIA at the region of parasite attachment, as asse

91 t to inhibit S100A4 function with respect to myosin-IIA binding and depolymerization.

92 l mechanism for myosin II function, in which myosin IIA can act as a single-molecule actin motor, cla

93 ion-dependent stabilization of lamin-A,C and myosin-IIA can suitably couple nuclear and cell morpholo

94 s contained Plectin 1, Filamin A, non-muscle myosin IIA, clathrin, alpha-actinin, vimentin, actin, ca

95 in myosin V, smooth muscle myosin, nonmuscle myosin IIA, CMIIB, and DdMII, although the ADP affinity

96 Defective myosin-IIA complexes are presumed to perturb megakaryocy

97 tent of polymerization depend on the initial myosin-IIA concentration; however, mts1 had only a small

98 le integrity and is part of a GOLGIN45 (G45)-myosin IIA-containing protein complex that activates sec

99 Localization of actin and myosin IIA contraction dictates the extrusion direction:

100 sruption of F-actin retrograde flow, but not myosin IIA contraction, arrested MC centralization and i

101 The forces generated by myosin IIa contractions ruptured most individual BCR-ant

102 s was dependent on the level and activity of myosin IIA, DAAM1, and FlnA.

103 Here we show that in vivo, myosin IIA-deficient T cells had a triad of defects, inc

104 specific inhibition of its activity prevents myosin IIA degradation.

105 s due to a temporary increase in the rate of myosin IIA degradation.

106 On soft surfaces myosin IIA deletion enhances ERK1/2 activity, while on s

107 chanical signals from integrin adhesions and myosin IIA-dependent actin dynamics.

108 This motility occurred via a myosin IIA-dependent rapid 'walking' mode with multiple

109 nsported to the plasma membrane by nonmuscle myosin IIA-dependent trafficking in human lung cancer ce

110 In addition, myosin IIA-depleted cells demonstrated impaired thrombin

111 ed tension of neighboring cells and sort out myosin IIA-depleted cells.

112 Thus, NK cell lytic granule-associated myosin IIA enables their interaction with actin and fina

113 ore, we show that inhibition or silencing of myosin IIa enhances aggregation, suggesting that cytoske

114 Further, knockdown of myosin IIA enhances cell spreading and lessens motility.

115 We further highlight that myosin IIA enrichment at the cell front requires the MHC

116 Time-lapse cinemicrography showed myosin IIA entering lamellipodia shortly after their for

117 nhanced fibronectin deposition and nonmuscle myosin-IIA expression, which altogether optimize conditi

118 n tracheal SM tissues, which can regulate NM myosin IIA filament assembly in vitro.

119 eases the critical monomer concentration for myosin-IIA filament assembly by approximately 11-fold.

120 ly impaired the ability of S100A4 to promote myosin-IIA filament disassembly.

121 he effects of heavy chain phosphorylation on myosin-IIA filament formation and also examined mts1 bin

122 Thus, centripetal force generated by myosin IIA filaments at the base of filopodium and trans

123 a positively correlates with the presence of myosin IIA filaments at the filopodia bases.

124 he cell, which is composed of actin arcs and myosin IIA filaments.

125 Mts1 destabilized PKC-phosphorylated myosin-IIA filaments and inhibited the assembly of myosi

126 only weakly disassembled CK2-phosphorylated myosin-IIA filaments and weakly inhibited the assembly o

127 TFP to block S100A4-mediated disassembly of myosin-IIA filaments demonstrate that significant inhibi

128 in RhoA-GTP levels and triggered assembly of myosin-IIA filaments in THP1 cells, whereas the suppress

129 to filaments and promotes the disassembly of myosin-IIA filaments into monomers; however, mts1 has li

130 e that mts1 has a 9-fold higher affinity for myosin-IIA filaments than for myosin-IIB filaments.

131 inhibits S100A4-mediated depolymerization of myosin-IIA filaments.

132 Myosin IIA forms de novo filaments away from the myosin

133 G55-dependent secretion by relieving G55 and myosin IIA from miR-34a-dependent silencing.

134 ished F-actin flow in the lamella, displaced myosin IIA from the cell edge, and decreased FA turnover

135 Collapse is associated with movement of myosin IIA from the growth cone to the neurite.

136 that NK-cell cytotoxicity requires nonmuscle myosin IIA function and that granule-associated myosin I

137 ls showed that the degree of confinement and myosin IIA function, rather than integrin adhesion (as p

138 Regulation of Myosin-IIA function in T cells is thus a key mechanism t

139 utations in the rod region disrupt nonmuscle myosin-IIA function, we examined the in vitro behavior o

140 ct link between S100A4 and the regulation of myosin-IIA function, we prepared an antibody to the S100

141 MYH9-RD) results from defects in nonmuscular myosin-IIA function.

142 shape and motility through the modulation of myosin-IIA function.

143 hrombin, Ca(2+), the integrin alphaIIbbeta3, myosin IIa, FXIIIa cross-linking, and platelet count all

144 hits-including Myh9, which encodes nonmuscle myosin IIa-have not been linked to tumor development, ye

145 The nonmuscle myosin IIA heavy chain (Myh9) is strongly associated wit

146 ntation or chemical inhibition of non-muscle myosin IIA heavy chain activity.

147 Using Jurkat T cells expressing fluorescent myosin IIA heavy chain and F-tractin-a novel reporter fo

148 Specific knockdown of the myosin IIA heavy chain by RNA interference impaired cyto

149 s PP1cbeta, myosin light chain 2 (MLC2), and myosin IIA heavy chain coimmunoprecipitated from EC lysa

150 Mutations in the human nonmuscle myosin IIA heavy chain gene (MYH9) have been linked to t

151 demonstrate that during osteoclastogenesis, myosin IIA heavy chain levels are temporarily suppressed

152 Ongoing suppression of the myosin IIA heavy chain via RNA interference results in f

153 result from mutations in the human nonmuscle myosin-IIA heavy chain gene.

154 ned the EGF-dependent phosphorylation of the myosin-IIA heavy chain in human breast cancer cells.

155 In EGF-stimulated cells, the myosin-IIA heavy chain is phosphorylated on the casein k

156 demonstrate that CK2 phosphorylation of the myosin-IIA heavy chain protects against mts1-induced fil

157 n antibody to the S100A4 binding site on the myosin-IIA heavy chain that has comparable effects on my

158 that mts1 binds to residues 1909-1924 of the myosin-IIA heavy chain, which is near the C-terminal tip

159 both the assembly and phosphorylation of the myosin-IIA heavy chains.

160 These observations support a direct role for myosin-IIA heavy-chain phosphorylation in mediating moti

161 Cells expressing green fluorescent protein-myosin-IIA heavy-chain S1943E and S1943D mutants display

162 ith the immunologic synapse-related proteins myosin IIA, high mobility group box 1, and the TCR Vbeta

163 Whereas myosin IIA, IIB, and phosphorylated myosin light chain d

164 By using antibodies specific for myosins IIA, IIB, IIIA, IIIB, VI, VIIA, and IXB, we exam

165 1 cells expressing green fluorescent protein-myosin IIA, immobilised on fibronectin micropatterns to

166 proposed convergence measure correlates with myosin IIa immuno-localization and is capable to resolve

167 afness and suggests a molecular function for Myosin IIa in auditory organs.

168 genesis, and they establish a novel role for Myosin IIA in signal transduction events modulating VEGF

169 the presence of myosin-IIA and implies that myosin-IIA influences thrombopoiesis negatively.

170 ggest that base-line expression of nonmuscle myosin IIA inhibits osteoclast precursor fusion and that

171 58) or Leu(293) residues are involved in the myosin IIA interaction, leading to ceramidosome formatio

172 ied as an inhibitor that disrupts the S100A4/myosin-IIA interaction and inhibits S100A4-mediated depo

173 n in which phenothiazines disrupt the S100A4/myosin-IIA interaction by sequestering S100A4 via small

174 ied as an inhibitor that disrupts the S100A4/myosin-IIA interaction.

175 additional level of regulation for the mts1-myosin-IIA interaction.

176 sein kinase 2 (CK2) inhibits the assembly of myosin-IIA into filaments.

177 We also found that nonmuscle myosin IIA is a major determinant of ROCK1 cortical stab

178 Myosin IIA is also required for this mitochondrial calci

179 Myosin IIa is diminished in human SCCs with poor surviva

180 erform distinct cellular activities and that myosin IIA is preferentially required for Rho-mediated c

181 Thus, myosin IIA is required for a critical step between NKIS

182 ependent on maternal MATER and document that myosin IIA is required for biphasic trafficking to the p

183 Myosin IIA is required for normal granule motility and p

184 Myosin IIA is required for strain polarization, generati

185 Adhesion discrimination provided by myosin IIA is thus necessary for the optimization of mot

186 Myosin-IIA is necessary for fast amoeboid motility, and

187 e kinetic characterization of the non-muscle myosin IIA isoform.

188 temporary, cathepsin B-mediated decrease in myosin IIA levels triggers precursor fusion during osteo

189 Thus, by controlling myosin IIA localization, Ii imposes on dendritic cells a

190 Actin and myosin IIA localize to the IS, and depletion of F-actin

191 In Caco2 cells, myosin IIA localized to the basal cortex and apical brus

192 es of force transmission requires non-muscle myosin IIA-mediated contractility and ankyrin G.

193 polymerization of actin filaments as well as myosin IIA-mediated contraction.

194 owed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invag

195 reating thrombi with blebbistatin to inhibit myosin IIa-mediated platelet contractility prevented shr

196 t cadherin contractions enable cells to test myosin IIA-mediated tension of neighboring cells and sor

197 sin IIA function and that granule-associated myosin IIA mediates the interaction of granules with F-a

198 arity emerges from the cooperative effect of myosin IIA (MIIA) and IIB (MIIB) on adhesive signaling.

199 Cell dissociation is triggered by myosin IIA (MIIA) dismantling of E-cadherin cell-cell ju

200 logic inhibition of myosin-II, but nonmuscle myosin-IIA (MIIA) mutations paradoxically cause MYH9-rel

201 pecific protein targets, including nonmuscle myosin-IIA (MIIA).

202 tinin cross-linking proteins, and non-muscle myosin IIA mini-filaments.

203 tory light chains of the contractile protein myosin IIa (MLC).

204 imaging techniques demonstrated that single myosin IIA molecules associate with NK-cell lytic granul

205 metric levels, mts1 inhibits the assembly of myosin-IIA monomers into filaments and promotes the disa

206 -IIA filaments and inhibited the assembly of myosin-IIA monomers with maximal inhibition of assembly

207 inhibited the assembly of CK2-phosphorylated myosin-IIA monomers.

208 in the context of naturally occurring human myosin IIA mutation.

209 main in chicken gizzard myosin and nonmuscle myosin IIA (MYH-9) but exhibit little binding to skeleta

210 to mechanical stress, specifically nonmuscle myosin IIA (MYH9) and IIC (MYH14), alpha-actinin 4, and

211 and human myosin IIC (MYH14), but not human myosin IIA (MYH9).

212 eins include fodrin (nonerythroid spectrin), myosin-IIA, myosin-IG, alpha-actinin 1, alpha-actinin 4,

213 from patients with a truncation mutation in myosin IIA, NK cell cytotoxicity, lytic granule penetrat

214 l alternatively spliced isoform of nonmuscle myosin IIA (NM IIA), called NM IIA2, which is generated

215 ain (MYH9) of the molecular motor non-muscle myosin IIA (NM-IIA), to ultimately suppress phagocytosis

216 Inhibition of nonmuscle myosin IIA (NM-MHC-IIA) motor activity prevents formatio

217 e identify the heavy chain of the non-muscle myosin IIA (NMHC-IIA) as being phosphorylated in a speci

218 ia and filopodia protrusions are balanced by myosin IIA (NMIIA) and actin-related protein 2/3 (Arp2/3

219 revealed that EphA3 ICD binds to non-muscle myosin IIA (NMIIA) and increases its phosphorylation (Se

220 Nonmuscle myosin IIA (NMIIA) heavy chain gene (MYH9) mutations cau

221 s in the S1943 phosphorylation of non-muscle Myosin IIA (NMIIA) heavy chain, thus facilitating NMIIA

222 show that conditional deletion of nonmuscle myosin IIA (NMIIA) impairs invagination, resulting in ab

223 dies initially focused on roles of nonmuscle myosin IIA (NMIIA) in the developing mouse epidermis, we

224 nds on the contractile activity of nonmuscle myosin IIA (NMIIA) motor proteins.

225 It binds to the nonmuscle myosin IIA (NMIIA) tail near the assembly competence dom

226 talin2 binds to the N-terminus of non-muscle myosin IIA (NMIIA) through its F3 subdomain.

227 addition, MyoGEF co-localizes with nonmuscle myosin IIA (NMIIA) to the front of migrating cells, and

228 ng protein, cofilin, Munc13-4, and nonmuscle myosin IIA (NMIIA).

229 culminating in the activation of non-muscle myosin IIA (NMIIA).

230 ell proliferation and identified nonmuscular myosin IIA (NMM-IIA) as a receptor required for binding

231 Nonmuscle myosin IIA (NMM-IIA) is involved in the formation of foc

232 d the association of gelsolin with nonmuscle myosin IIA (NMMIIA) at collagen adhesions are regulated

233 s showed that FliI associated with nonmuscle myosin IIA (NMMIIA), which was confirmed by immunoprecip

234 Collapse is inhibited by overexpression of myosin IIA or growth on high substrate-bound laminin-1.

235 n mediating co-assembly with existing furrow myosin IIA or IIB filaments.

236 the mechanosensation of myosin IIB, but not myosin IIA or IIC.

237 In the absence of myosin IIA or its ATPase activity, T cell signaling was

238 erfering RNA (siRNA)-mediated suppression of myosin IIA or myosin IIB causes an increase in mitochond

239 Inhibiting actin polymerization, myosin IIA, or the formin INF2 reduces both un-stimulate

240 a disruption of podosome rosettes caused by myosin-IIA overassembly, and a myosin-independent increa

241 that interference with the putative Rho-ROCK-myosin-IIA pathway selectively decreases the number of c

242 bly and predominately affected the extent of myosin IIA polymerization.

243 Myosin IIA promoted internalization of MHCI and myosin I

244 ary driver of actin retrograde flow, whereas myosin IIA promotes long-term integrity of the IS.

245 ably through depletion of spindle-associated myosin IIA protein and antibody binding to chromosome su

246 Here, we show that a recombinant myosin IIA protein that assembles constitutively and is

247 ar myosin phosphatase complexes that include myosin IIA, protein phosphatase 1delta, and myosin phosp

248 ts in THP1 cells, whereas the suppression of myosin-IIA rescued podosome formation regardless of ARF1

249 Supervillin, myosin-IG, and myosin-IIA resist extraction with 0.1 m sodium carbonate

250 Earlier, we found that myosin IIA responds to Rho-ROCK signaling to support jun

251 Rac2 and Myosin 9 (Myh9), the heavy chain of Myosin IIA, resulting in augmented vascular endothelial

252 numbers of nuclei, whereas overexpression of myosin IIA results in less osteoclast fusion.

253 myosin, nonmuscle myosin IIB, and nonmuscle myosin IIA revealed three distinct regimes of behavior,

254 ation decreased the affinity of mts1 for the myosin-IIA rod by approximately 6.5-fold.

255 rring at a molar ratio of one mts1 dimer per myosin-IIA rod.

256 In human and mouse keratinocytes, myosin IIa's function is manifested not only in conventi

257 n flow, and depletion of myosin IIB, but not myosin IIA, showed similar nondirectional nuclear moveme

258 Similar to non-muscle myosin IIB, non-muscle myosin IIA shows high ADP affinity and little enhancemen

259 ter Inhibition of ceramidosome formation via myosin IIA silencing limited germ line stem cell signali

260 Immunofluorescence showed that myosin IIA skewed toward the front of migrating cells, c

261 This implies that non-muscle myosin IIA spends only a small fraction of its ATPase cy

262 en nucleotide and actin binding to nonmuscle myosin IIA subfragment-1.

263 We conclude myosin IIA suppresses tumorigenesis in at least two ways

264 Increased multinucleation caused by myosin IIA suppression does not require RANKL.

265 -Aldrich syndrome protein (WASp), actin, and myosin IIA that formed during NK cell activation was ide

266 Instead, we find that local inactivation of Myosin IIA, through a noncanonical Ser1/2 phosphorylatio

267 Levels of myosin-IIA thus parallel levels of lamin-A,C, with phosp

268 ibitory signal, the recruitment of actin and myosin IIA to a constitutive WIP-WASp complex was greatl

269 A response that involves loss of growth cone myosin IIA to facilitate actin meshwork instability and

270 This requires myosin IIA to generate polarized periodic anterior contr

271 hat monitors the Ca(2+)-dependent binding of myosin-IIA to S100A4, NSC 95397 was identified as an inh

272 Depletion of myosin IIA via small interfering RNA impaired migration

273 n of endogenous HeLa cell BIG1 and BIG2 with myosin IIA was demonstrably independent of Arf guanine n

274 Myosin IIA was expressed in T84 cells and colocalized wi

275 Here we show that myosin IIA was necessary for complete assembly and movem

276 myosin IIB, but not anterior distribution of myosin IIA, was inhibited by dominant-negative rhoA and

277 ing NK cells from patients with mutations in myosin IIA, we found that the nonhelical tailpiece is re

278 The F-actin and myosin IIA were identified as coprecipitates with PRRSV

279 Both actin and myosin IIA were recruited to WIP in the absence of WASp.

280 On fibronectin, NGF caused inactivation of myosin IIA, which negatively regulated actin bundling.

281 yosin-like recombinant fragment of nonmuscle myosin IIA, which was expressed in baculovirus along wit

282 we evaluate the nature of the association of myosin IIA with lytic granules.

283 microM inhibited anterior redistribution of myosin IIA, with 100 microM blebbistatin causing posteri