ライフサイエンスコーパス: myosin IIA

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

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

3 l synapses are active processes dependent on myosin IIA.

4 K cells, were constitutively associated with myosin IIA.

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

6 f the regulatory light chain associated with myosin IIA.

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

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

9 eric interactions of SERT, specifically with myosin IIA.

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

11 Ks and preplatelet fragments, which requires myosin IIA.

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

13 or the phosphorylation of granule-associated myosin IIA.

14 ractions depend on the activity of nonmuscle myosin IIA.

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

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

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

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

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

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

21 arcinoma cell motility via interactions with myosin-IIA.

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

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

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

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

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

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

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

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

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

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

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

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

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

35 Myosin IIA and IIB demonstrate differential expression d

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

37 Nonmuscle myosin IIA and IIB distribute preferentially toward oppo

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

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

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

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

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

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

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

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

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

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

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

49 Myosin IIA and MLC phosphorylation are important in plat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 Defective myosin-IIA complexes are presumed to perturb megakaryocy

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

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

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

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

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

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

86 specific inhibition of its activity prevents myosin IIA degradation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 Myosin IIA forms de novo filaments away from the myosin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 1 cells expressing green fluorescent protein-myosin IIA, immobilised on fibronectin micropatterns to

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

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

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

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

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

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

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

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

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

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

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

151 Myosin IIA is also required for this mitochondrial calci

152 Myosin IIa is diminished in human SCCs with poor surviva

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

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

155 Myosin IIA is required for normal granule motility and p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Depletion of myosin IIA via small interfering RNA impaired migration

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

228 Myosin IIA was expressed in T84 cells and colocalized wi

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

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

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

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

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

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

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

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

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