ライフサイエンスコーパス: lamellipodium

1 ng to describe the growth of a reconstituted lamellipodium.

2 prevents Abi-1 from reaching the tip of the lamellipodium.

3 of the protrusion and retraction shapes the lamellipodium.

4 required for translocation of Wave-1 to the lamellipodium.

5 AC, but not pAC, localized to the lamellipodium.

6 from a perinuclear region to the base of the lamellipodium.

7 low, and the speed of retrograde flow in the lamellipodium.

8 nts and bundles near the leading edge of the lamellipodium.

9 motion of filopodia and actin bundles of the lamellipodium.

10 ium an actin bundle forms and grows into the lamellipodium.

11 omers into actin filaments at the tip of the lamellipodium.

12 of 4-8 microm from the leading edge into the lamellipodium.

13 nd composition of actin bundles in the whole lamellipodium.

14 of the cytoskeleton at opposite ends of the lamellipodium.

15 with MSP depolymerization at the base of the lamellipodium.

16 sport of the actin cytoskeleton in the whole lamellipodium.

17 e concentrated in the lateral extrema of the lamellipodium.

18 nd heterodimeric capping protein (CP) in the lamellipodium.

19 mentalized macromolecule distribution in the lamellipodium.

20 d in actin-rich lamella, situated behind the lamellipodium.

21 confined regions or microdomains within the lamellipodium.

22 egrin complexes help nucleate NAs within the lamellipodium.

23 on of Rac1, the nucleus moved toward the new lamellipodium.

24 ecting capping or severing activities to the lamellipodium.

25 and along microspikes radiating through the lamellipodium.

26 tagonizing effect of INF2 in maintaining the lamellipodium.

27 te distribution and kinetics of actin in the lamellipodium.

28 assembly, extension, and stabilization of a lamellipodium.

29 d, and on the mechanics and structure of the lamellipodium.

30 usion coefficient of capping proteins in the lamellipodium.

31 elles are transported on microtubules to the lamellipodium.

32 pathway controls cofilin activity within the lamellipodium.

33 etrograde flow, resulting in widening of the lamellipodium.

34 bule lattice in the leading edge lamella and lamellipodium.

35 correlated with the enhanced motility of the lamellipodium.

36 In motile cells, protrusion of the lamellipodium (a type of cell margin) requires assembly

37 onal antibody 281.2 initially extend a broad lamellipodium, a response accompanied by membrane ruffli

38 moting heart fibroblasts, as expected in the lamellipodium, actin filaments flow rearward with respec

39 rted locally from the tip to the base of the lamellipodium, activating the next contraction/extension

40 Subsequently, the lamellipodium adapts to the stalled state.

41 e that microvillar actin is mobilized at the lamellipodium, allowing optimal migration.

42 nd Cdc42 and is recruited to the rear of the lamellipodium and along microspikes radiating through th

43 d on the dorsal membrane at the front of the lamellipodium and at the approximate boundary between th

44 cytoskeletal disassembly at the base of the lamellipodium and cell body retraction continued.

45 l impairs both the assembly of the polarized lamellipodium and directional migration along a diffusib

46 eurites as phosphorylated forms, entered the lamellipodium and filopodia of growth cones, and concent

47 s place most efficiently in the F-actin-rich lamellipodium and is F-actin dependent in stages of form

48 c stimulation to facilitate expansion of the lamellipodium and its anchorage to the extracellular mat

49 and at the approximate boundary between the lamellipodium and lamella and continued to grow as they

50 However, its function in modulating lamellipodium and lamella dynamics, and the implications

51 by modulating the spatial interaction of the lamellipodium and lamella in response to upstream signal

52 ompanied by increased spatial overlap of the lamellipodium and lamella networks and reduced cell-edge

53 The actin network segregates into lamellipodium and lamellum, whereas the adhesion complex

54 the actin network exhibits segregation into lamellipodium and lamellum, whereas the cell edge either

55 ntial for establishment of a stable, leading lamellipodium and persistent keratinocyte migration.

56 d the leading edge and grew beneath both the lamellipodium and the cell body.

57 ruptly became lateral at the boundary of the lamellipodium and the cell body.

58 f two actin filament (F-actin) networks, the lamellipodium and the lamella.

59 2) were present at the interface between the lamellipodium and the substrate.

60 nal changes involved dissolution of both the lamellipodium and uropod and reformation of these struct

61 how forces are generated in a motile cell, a lamellipodium, and a comet tail is the subject of this n

62 vinculin at focal adhesions, actin within a lamellipodium, and the distribution of the retroviral pr

63 nism of cell motility: (1) low forces in the lamellipodium are applied in the direction of cortical f

64 ells become permanently stationary, extend a lamellipodium around the soma, and emit several thin pro

65 rom the leading edge and receded through the lamellipodium as its disassembly at the cell body contin

66 om nascent focal contacts along the circular lamellipodium, as revealed by integrin beta1 and FAK sta

67 th the WASP and p38 MAPK pathways to promote lamellipodium assembly and chemotaxis.

68 bly, p38 MAPK inhibition results in impaired lamellipodium assembly and loss of directional migration

69 ils to specifically deliver substrate to the lamellipodium at high concentrations, thus facilitating

70 imes and slow decays, which nucleated in the lamellipodium at the hyperpolarized side of the cells an

71 integrins required for stabilization of the lamellipodium at the keratinocyte leading edge.

72 membrane (PM) proteins from the leading edge lamellipodium backward, which when coupled to substrate

73 Unlike the well-elucidated mechanisms of lamellipodium-based mesenchymal migration, the dynamics

74 cell process that can be regarded as a giant lamellipodium because it is an actively growing structur

75 subunits typically diffuse across the entire lamellipodium before reassembling into the network.

76 ting fibroblast results in marked changes in lamellipodium behaviour and actin network organization a

77 e tension increases, velocity slows, and the lamellipodium buckles upward in a myosin II-independent

78 Protrusion of a lamellipodium by the very filaments supporting the membr

79 rces, of up to 1.4 kPa, at each flank of the lamellipodium, ColXVII knockdown keratinocytes fail to d

80 n periodically builds a mechanical link, the lamellipodium, connecting myosin motors with the initiat

81 The lamellipodium consists of a treadmilling F-actin array w

82 distal sites of channel insertion inside the lamellipodium does, therefore, not require intact actin

83 f FGF controlling Rac activity, switching to lamellipodium-driven migration.

84 directional motion, although some vestigial lamellipodium-driven motility remained.

85 sassembly is necessary for protrusion of the lamellipodium during fibroblast migration.

86 ation in stimulus-induced actin assembly and lamellipodium extension during cell migration, we develo

87 Lamellipodium extension in response to growth factors is

88 Lamellipodium extension, incorporating actin filament dy

89 FAK, promoting Rac1 activation and polarized lamellipodium extension.

90 e short branched filaments that characterize lamellipodium formation and are required for cell migrat

91 of Rac, a key signaling event that controls lamellipodium formation and cell spreading.

92 Ca(2+) influx did not significantly inhibit lamellipodium formation and chemotaxis, suggesting that

93 r tyrosine kinase c-Src/14-3-3zeta-dependent lamellipodium formation and functions independent of sol

94 ed in response to cytoskeletal inhibitors of lamellipodium formation and myosin II-mediated contracti

95 defective cell motility in response to PDGF, lamellipodium formation and Rac-mediated actin polymeriz

96 which has been shown in other cells to drive lamellipodium formation by enhancing actin nucleation vi

97 y unrecognized actions of NIK: regulation of lamellipodium formation by growth factors and phosphoryl

98 omplex is the main catalyst of pseudopod and lamellipodium formation during cell migration.

99 s the organization of actin cytoskeleton and lamellipodium formation during PDGF stimulation.

100 Third, like Rac, Mas induced lamellipodium formation in porcine aortic endothelial ce

101 the first time direct evidence that platelet lamellipodium formation is not required for stable throm

102 going cell curve conversion, indicating that lamellipodium formation is not the primary driver of ear

103 However, lamellipodium formation of mutant platelets was complete

104 Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism.

105 ficient for stimulation of Rac activation or lamellipodium formation, although it was sufficient for

106 pensable for Rac1-induced transformation and lamellipodium formation, as well as activation of JNK, p

107 e important for MCP-1 binding and consequent lamellipodium formation, chemotaxis, and signal transduc

108 e role of another second messenger, cGMP, in lamellipodium formation, our data indicate that cAMP and

109 ecifically, it prevented axon retraction and lamellipodium formation, reduced neurite growth, and pro

110 kedly stimulated Rac activation and enhanced lamellipodium formation.

111 involved in regulation of actin dynamics and lamellipodium formation.

112 P and cGMP play opposite roles in modulating lamellipodium formation.

113 factor-induced fibroblast cell migration and lamellipodium formation.

114 alization show that this inhibits functional lamellipodium formation.

115 ctron microscopy shows that the regenerating lamellipodium forms a cohesive, separable layer of actin

116 A zone of high shear separates the lamellipodium from the cell body, suggesting that they a

117 ine the polarity of the extracted keratocyte lamellipodium from the cell periphery to the cell nucleu

118 the disposition of the actin bundles in the lamellipodium frozen at any time point preserves and por

119 ntrols both the rate and the steering during lamellipodium growth.

120 ther chlamydiae were translocated across the lamellipodium in a highly directed manner toward the mic

121 hat nucleates actin filament assembly in the lamellipodium in adherent cells crawling on planar 2-dim

122 in polymerization at the leading edge of the lamellipodium in carcinoma cells, occurs as two transien

123 show that VLA-4 activation localizes to the lamellipodium in living cells.

124 een the local viscoelastic properties of the lamellipodium (including the transitional region to the

125 This hastens the commitment to a single lamellipodium initiated in response to multiple, complex

126 temporally coordinates the formation of both lamellipodium/invadopodia and nascent cell-matrix adhesi

127 properties of the cell membrane, explain why lamellipodium is a flat organelle.

128 The lamellipodium is an important structure for cell migrati

129 g edge of migrating cells, protrusion of the lamellipodium is driven by Arp2/3-mediated polymerizatio

130 e active, nonphosphorylated state within the lamellipodium is necessary to maintain polarized protrus

131 d F-actin flow in maturing FA to establish a lamellipodium-lamellum border and generate high extracel

132 lastic properties of filaments, close to the lamellipodium leading edge, and retrograde flow shape th

133 by periodically compressing and relaxing the lamellipodium, leading to the positioning of adhesions a

134 on of lamellipodium protrusion, during which lamellipodium length increased linearly with no increase

135 xplained by the dense dendritic structure of lamellipodium-like networks.

136 which Arp2/3 initiates disc formation in a "lamellipodium-like" mechanism.

137 The lamellipodium-localized LRAP25-MRCK complex is essential

138 Filopodia that protrude forward from the lamellipodium, located at the leading edge of a neuronal

139 ensity of growing actin filament ends at the lamellipodium margin (241 +/- 100/microm) and the maximu

140 In large gaps, closure is dominated by lamellipodium-mediated cell migration.

141 Even pN opposing forces slow down lamellipodium motion by three orders of magnitude.

142 A lamellipodium network assembled at the leading edge but

143 The fact that the lamellipodium of a cell is very thin (<1000 nm) imparts

144 he actin-binding protein Ena/Vasp within the lamellipodium of a migrating fibroblast results in marke

145 osins and a model F-actin cortex, namely the lamellipodium of a migrating fish epidermal keratocyte.

146 t the Tpm isoforms 1.8/9 are enriched in the lamellipodium of fibroblasts as detected with a novel is

147 When NAD(P)H waves reach the lamellipodium of morphologically polarized neutrophils,

148 appearance of EGFP-actin speckles within the lamellipodium of motile cells that indicate actin monome

149 havior of cytoskeletal fine structure in the lamellipodium of nerve growth cones using a new type of

150 HPK1 was enriched at the lamellipodium of polarized dHL-60 cells, where it coloca

151 These observations demonstrate that the lamellipodium of the fibroblast is able to generate inte

152 As expected, actin filaments in the lamellipodium of these cells have uniform polarity with

153 scoelasticity of the leading edge, i.e., the lamellipodium, of a cell is the key property for a deepe

154 ociate to the F-actin network throughout the lamellipodium or break up into monomers after a characte

155 n the cell body and lamellum, but not in the lamellipodium or convergence zone.

156 polarity and continuously protrude a single lamellipodium, polarized in the direction of migration.

157 tivating many actin-regulating proteins as a lamellipodium-producing core.

158 n-filament disassembly is tightly coupled to lamellipodium protrusion in migrating chick fibroblasts

159 n cells, we assessed their role in polarized lamellipodium protrusion in migrating fibroblasts.

160 generates branched actin networks that power lamellipodium protrusion of migrating cells.

161 In migrating chick fibroblasts, lamellipodium protrusion was blocked within 1-5 minutes

162 ults show that in spite of an abrupt halt of lamellipodium protrusion, CB affects various actin filam

163 nset of jasplakinolide-induced inhibition of lamellipodium protrusion, during which lamellipodium len

164 , and therefore do not translate into faster lamellipodium protrusion.

165 migration of cells through the activation of lamellipodium protrusion.

166 For normal cells, the lamellipodium provides almost all the forces for forward

167 anti-uPAR F(ab')2s traffic to the uropod and lamellipodium, respectively, during polarization of unca

168 AM-containing adhesions are primarily in the lamellipodium; RIAM is subsequently reduced in mature fo

169 Consequently, Lpd controls lamellipodium size, cell migration speed, and persistenc

170 namic behavior: rapid retrograde flow in the lamellipodium, slow retrograde flow in the lamellum, ant

171 l, suggesting that microspikes contribute to lamellipodium stability.

172 Furthermore, in turning cells, both lamellipodium structure and intracellular diffusion dyna

173 rsible intracellular diffusion variation and lamellipodium structure deformation.

174 the intracellular diffusion dynamics and the lamellipodium structure in regulating their migrations.

175 cellular diffusion and the three-dimensional lamellipodium structures of fish keratocyte cells, we ob

176 traction forces within front portions of the lamellipodium, suggesting that a retrograde flow of acti

177 retrograde flow of actin within the leading lamellipodium that is inversely proportional to both pro

178 odial protrusions and focal complexes in the lamellipodium; the Rho family of small GTPases may thus

179 zation was promoted within one micron of the lamellipodium tip.

180 tion and increased molecular crowding in the lamellipodium to explain how cells spatiotemporally coor

181 nanonewtons at submicrometer spots under the lamellipodium to several hundred nanonewtons under the c

182 s of these findings for the arc formation in lamellipodium-to-lamellum architectural remodeling.

183 cells surrounded by a flattened, actin-rich lamellipodium transform to produce thin, microtubule-fil

184 howed that during spreading and crawling the lamellipodium undergoes periodic contractions that are s

185 zed, rapidly migrating interphase cells, the lamellipodium was dramatically enriched for MHC-B sugges

186 In such cells, the single polarized lamellipodium was replaced by multiple nonpolarized lame

187 When a new lamellipodium was triggered with photoactivation of Rac1

188 Most of the actin filaments in the lamellipodium were generated by polymerization away from

189 nin 1B, which acts by directing SSH1L to the lamellipodium where it activates the actin-severing prot

190 are positioned in rows, and the base of the lamellipodium, where a vinculin-dependent clutch couples

191 y recruits Arp2/3 to the leading edge of the lamellipodium, where it may couple the actin polymerizat

192 Occasionally "pioneering" MTs grow into the lamellipodium, where microtubule bending and reorientati

193 The buckling occurs between the front of the lamellipodium, where nascent adhesions are positioned in

194 eading edge until they reach the base of the lamellipodium, where they oscillate between short phases

195 uted on microvilli tips along the top of the lamellipodium, whereas the interleukin 8 receptors CXCR1

196 lish a novel regulatory mechanism within the lamellipodium whereby Tpm collaborates with Arp2/3 to pr

197 ed propagating waves toward the front of the lamellipodium, which are characteristic for dynamic reor

198 in the newly-found slow mode have a deformed lamellipodium with swollen-up front and thinned-down rea

199 disassembles and reassembles throughout the lamellipodium within seconds, so the lamellipodial netwo