ライフサイエンスコーパス: lamellipodium

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

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

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

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

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

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

7 motion of filopodia and actin bundles of the lamellipodium.

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

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

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

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

12 nd composition of actin bundles in the whole lamellipodium.

13 of the cytoskeleton at opposite ends of the lamellipodium.

14 with MSP depolymerization at the base of the lamellipodium.

15 sport of the actin cytoskeleton in the whole lamellipodium.

16 e concentrated in the lateral extrema of the lamellipodium.

17 egrin complexes help nucleate NAs within the lamellipodium.

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

19 ecting capping or severing activities to the lamellipodium.

20 and along microspikes radiating through the lamellipodium.

21 tagonizing effect of INF2 in maintaining the lamellipodium.

22 te distribution and kinetics of actin in the lamellipodium.

23 assembly, extension, and stabilization of a lamellipodium.

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

25 ng to describe the growth of a reconstituted lamellipodium.

26 of the protrusion and retraction shapes the lamellipodium.

27 usion coefficient of capping proteins in the lamellipodium.

28 elles are transported on microtubules to the lamellipodium.

29 pathway controls cofilin activity within the lamellipodium.

30 etrograde flow, resulting in widening of the lamellipodium.

31 bule lattice in the leading edge lamella and lamellipodium.

32 correlated with the enhanced motility of the lamellipodium.

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

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

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

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

37 Subsequently, the lamellipodium adapts to the stalled state.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Lamellipodium extension in response to growth factors is

81 Lamellipodium extension, incorporating actin filament dy

82 FAK, promoting Rac1 activation and polarized lamellipodium extension.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 involved in regulation of actin dynamics and lamellipodium formation.

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

99 factor-induced fibroblast cell migration and lamellipodium formation.

100 alization show that this inhibits functional lamellipodium formation.

101 kedly stimulated Rac activation and enhanced lamellipodium formation.

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

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

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

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

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

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

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

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

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

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

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

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

114 The lamellipodium is an important structure for cell migrati

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

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

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

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

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

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

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

122 The lamellipodium-localized LRAP25-MRCK complex is essential

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

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

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

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

127 A lamellipodium network assembled at the leading edge but

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 migration of cells through the activation of lamellipodium protrusion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 When a new lamellipodium was triggered with photoactivation of Rac1

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

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

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

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

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

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

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

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

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

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

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