ライフサイエンスコーパス: pseudopod

1 ergoes wholesale reorganization to produce a pseudopod.

2 sufficient for long-range inhibition by the pseudopod.

3 2)beta is recruited to the membrane-enriched pseudopod.

4 ich is also restricted to the transmigrating pseudopod.

5 recovery of the cytoskeleton network with no pseudopod.

6 active, causing frequent small, disorganized pseudopods.

7 ux, directing movement with blebs instead of pseudopods.

8 rane-like particles that mimic Lm-containing pseudopods.

9 classes of protrusion: short stubs and long pseudopods.

10 n, and excessive F-actin localization within pseudopods.

11 th diminished actin polymerization and small pseudopods.

12 leading to the formation of multiple lateral pseudopods.

13 ated amoeboid cell that extends and develops pseudopods.

14 s in gradient direction by extending lateral pseudopods.

15 ization and the formation of 'pedestal-like' pseudopods.

16 ads to robust proliferation and extension of pseudopods.

17 y move, forming highly dynamic, actin-filled pseudopods.

18 leading edges rather than by initiating new pseudopods.

19 of branched actin assembly-make actin-filled pseudopods.

20 ow crawl at >30 microm/min with actin-filled pseudopods.

21 ding edge to generate morphologically normal pseudopods.

22 ciently in the epidermis, with nearly static pseudopods.

23 ECM, led by advancing protruding actin-rich pseudopods.

24 shedding) specifically within transmigrating pseudopods.

25 r the production and retention of upgradient pseudopods.

26 grate slower, and generate fewer and thinner pseudopods.

27 ned shift to movement with blebs rather than pseudopods.

28 and lysosomal membranes to form plasmalemmal pseudopods.

29 assembly and stability of F-actin underneath pseudopods.

30 tting single pseudopod, 8% emitting multiple pseudopods, 17% with vacuoles, 28% eosinophils releasing

31 ocal complexes localized at leading edges of pseudopods; 2) activation of intracellular signaling mol

32 ation: >/=14% of eosinophils emitting single pseudopod, 8% emitting multiple pseudopods, 17% with vac

33 We conclude that WASP and SCAR can regulate pseudopod actin using similar mechanisms.

34 lls, implying that phosphorylation modulates pseudopods after they have been formed, rather than cont

35 ity, maintaining F-actin levels but blocking pseudopod and bleb formation and migration.

36 naling cues tame actin dynamics to produce a pseudopod and guide cellular motility is a critical open

37 ar/WAVE complex is the principal catalyst of pseudopod and lamellipod formation.

38 le to generate and sustain a single-dominant pseudopod and migrate with increased speed and reduced d

39 Together, the pseudopod and round gonocyte populations will provide po

40 Two gonocyte subpopulations, designated pseudopod and round, were identified and isolated from n

41 tion of neutrophil polarity has been how the pseudopod and the uropod are coordinated.

42 c42 to maintain a proper balance between the pseudopod and the uropod.

43 ture spermatozoa, SPE-38 is localized to the pseudopod and TRP-3/SPE-41 is localized to the whole pla

44 inished stress fiber formation, and enhanced pseudopod and uropod formation.

45 aracterized by the formation of leading-edge pseudopods and a highly contractile cell rear known as t

46 weak, transient traction scatter among small pseudopods and appear to act against one another.

47 el; under load, these cells persist in using pseudopods and chemotax poorly.

48 We have shown that leukocytes retract their pseudopods and detach from substrates after exposure to

49 neutrophils, which showed fewer and smaller pseudopods and fewer membrane irregularities.

50 a plausible mechanism for the zig-zagging of pseudopods and for the ability of cells both to swim in

51 nting backness from reducing the strength of pseudopods and from impairing directional migration.

52 actin-rich degradative protrusions (invasive pseudopods and invadopodia), which allows their efficien

53 The formation of pseudopods and lamellae after ligation of chemoattractan

54 n mutants, altering the dynamics and size of pseudopods and lamellipods and thus changing migration s

55 s association with the surfaces of extending pseudopods and maturing phagosomes, whereas inactivating

56 PIKI-1 is recruited to extending pseudopods and nascent phagosomes prior to the appearanc

57 However, pseudopods and patches of phosphorylation-deficient Scar

58 horylation-deficient Scar, with longer-lived pseudopods and patches of Scar recruitment.

59 the recruitment of intracellular vesicles to pseudopods and phagosomes.

60 to fluid shear stresses, they often retract pseudopods and reduce their attachment.

61 er show that cAMP is excluded from extending pseudopods and remains restricted to the cell body of mi

62 ized to and tethered at the tips of invasive pseudopods and to allow RCP-dependent alpha5beta1 recycl

63 milar dynamics to normal SCAR, forming split pseudopods and traveling waves.

64 dhesion to the endothelium, the formation of pseudopods, and migration into tissues.

65 dhesion to the endothelium, the formation of pseudopods, and migration into tissues.

66 colocalized with G proteins in lamellae and pseudopods, and precipitated Gbetagamma in pull downs.

67 ecruitment to IQGAP1 at the tips of invasive pseudopods, and RacGAP1 then locally suppresses the acti

68 nd segregating the localization of competing pseudopod- and uropod-inducing signaling pathways during

69 the exploration and prevent the formation of pseudopods; and (3) Slime mold placed in an adverse envi

70 Blebs and F-actin-driven pseudopods are alternative ways of extending the leading

71 Although we find that Arp2/3-dependent pseudopods are dispensable for three-dimensional locomot

72 also (ii) impairs fMLP-dependent frontness: pseudopods are flatter, contain less F-actin, and show d

73 Pseudopods are replaced in double SCAR/WASP mutants by a

74 y to initiate blebs and thus migrate, though pseudopods are still lost.

75 axis requires the formation of one prominent pseudopod at the cell front characterized by actin polym

76 and cytoskeletal elements in the protruding pseudopod at the front of cells and the retracting uropo

77 zed morphology, with F-actin in a protruding pseudopod at the leading edge and contractile actin-myos

78 The extension of a pseudopod at the leading edge of a migratory cell and th

79 the direction and regulates the formation of pseudopods at the anterior.

80 ient motility requires polarized cells, with pseudopods at the front and a retracting rear.

81 an neutrophils, concentrates with F-actin in pseudopods at the front of motile, chemotaxing cells, bu

82 on, and polarized actin formation and single pseudopods at the leading edge of cells.

83 ls can move with both blebs and actin-driven pseudopods at the same time, and blebs, like pseudopods,

84 ty LFA-1 provided orientation along a uropod-pseudopod axis that required calcium flux through Orai1.

85 o gain insight into the machinery needed for pseudopod-based amoeboid motility and how it evolved.

86 TIP, CLASP1, is also needed to form invasive pseudopods because it prevents catastrophes specifically

87 and a single back not only by strengthening pseudopods but also, at longer range, by promoting RhoA-

88 to a micropipette, the active extension of a pseudopod by a neutrophil exposed to a local stimulus, a

89 contractility balances the extension of long pseudopods by effecting retraction and allowing force ge

90 They also continually extend new pseudopods by widening and splitting existing leading ed

91 Blebs and pseudopods can both power cell migration, with blebs oft

92 pseudopods at the same time, and blebs, like pseudopods, can be orientated by chemotactic gradients.

93 olarization is maintained by restricting the pseudopod catalyst, active Rac, to the front.

94 tion bias mediated by secreted chemicals and pseudopod collapse following collisions.

95 Pseudopods colocalized with active Rac, whether driven b

96 , where directed MSP disassembly facilitates pseudopod contraction.

97 te mutants cannot replace SCAR's role in the pseudopod cycle, though they rescue cell size and growth

98 ssays show lack of GSP-3/4 causes defects in pseudopod development and the rate of pseudopodial tread

99 litates engagement of FcgammaR at the tip of pseudopods, directing the progression of phagocytosis.

100 This phenomenon is observed both for the pseudopod-dominated migration of the amoeboid Dictyostel

101 ld still spread, migrate, and chemotax using pseudopods driven by the Arp2/3 complex.

102 The pseudopod driver suppressor of cAR mutations (SCAR)/WASP

103 concentration at the leading edge of single pseudopods during their growth.

104 decreases the frequency of cell turning, and pseudopod dynamics increase when cells change direction,

105 lation of Dictyostelium SCAR controls normal pseudopod dynamics.

106 g of alpha5beta1 within the tips of invasive pseudopods elicits signals that promote the reorganizati

107 es microtubule resistance to compression and pseudopod elongation.

108 We conclude that pseudopod engagement with substratum is more important t

109 r spread involves cell fusion, as opposed to pseudopod engulfment and bacterial escape from double-me

110 CED-1 signaling is necessary for the pseudopod enrichment of EPN-1 and CHC-1.

111 In the first phase, pseudopods extended rapidly, with actin polymerization p

112 to phagocytic cups and phagosomes to support pseudopod extension and apoptotic cell degradation.

113 ing the chemoattractant, leading to directed pseudopod extension and chemotaxis.

114 toward chemoattractants, leading to lateral pseudopod extension and impaired chemotaxis.

115 ma membrane-based cellular processes such as pseudopod extension and macropinocytosis.

116 beta-, overexpressing cells exhibited marked pseudopod extension and migrated successfully through th

117 1 signals via Scar/WAVE and Arp2/3 to effect pseudopod extension and migration of melanoblasts in ski

118 llular signaling for directional sensing and pseudopod extension at the leading edge of migrating cel

119 orms of PI 3 kinase are required for maximal pseudopod extension but not phagocytosis per se.

120 ther GM-CSF or insulin increased the rate of pseudopod extension by 50% when the cells were stimulate

121 gonist, and a diverse set of signals mediate pseudopod extension by different receptors.

122 a mechanism by which a single GPCR mediates pseudopod extension during cell migration and bacterial

123 amin lies downstream from Roco2 and controls pseudopod extension during chemotaxis and random cell mo

124 gulating cortical F-actin polymerization and pseudopod extension in a pathway that requires Rab1A.

125 The pseudopod extension induced using micropipets was oscill

126 dependent, in contrast to 55% of the rate of pseudopod extension induced with interleukin-8.

127 ortmannin showed that 72%-80% of the rate of pseudopod extension induced with N-formyl-methionyl-leuc

128 actin polymerization to the measured rate of pseudopod extension is limited by a slowest (bottleneck)

129 where rearrangements of the cytoskeleton and pseudopod extension occur.

130 We observed that pseudopod extension occurred in two phases.

131 The dependence of the rate of pseudopod extension on the concentration of individual c

132 The dependence of the rate of pseudopod extension on the concentration of these chemoa

133 easing bead size, and hence the magnitude of pseudopod extension required for particle engulfment, re

134 activity with wortmannin showed that rate of pseudopod extension stimulated with N-formyl-Met-Leu-Phe

135 Membrane ruffling and pseudopod extension via the BLTR was also completely inh

136 This oscillatory pseudopod extension was controlled by activated RhoA and

137 In these conditions, the rate of pseudopod extension was dependent on the concentration o

138 the rate of interleukin-8 (IL-8)-stimulated pseudopod extension was less dependent on PI3K.

139 The rate of pseudopod extension was measured in the presence of inhi

140 nd the temperature dependence of the rate of pseudopod extension was measured in the presence of phar

141 Here, pseudopod extension was stimulated with chemoattractant

142 ection of cell movement, suppressing lateral pseudopod extension, and proper retraction of the poster

143 ab1A and controls the actin cytoskeleton and pseudopod extension, and thereby, cell polarity and moti

144 s pathway to provide membranes necessary for pseudopod extension, leading to clearance of senescent a

145 not polymerize during Fc gamma RIA-mediated pseudopod extension, nor were tyrosine kinases activated

146 However, both compounds prevented maximal pseudopod extension, suggesting that PI 3-kinase inhibit

147 Phagocytosis requires actin assembly and pseudopod extension, two cellular events that coincide s

148 peak of RacB activation, which is linked to pseudopod extension, whereas a PTEN hypomorph exhibits e

149 Arp2/3 complex drive actin assembly for long pseudopod extension, which also depends on microtubule d

150 hagocytic cup formation, actin assembly, and pseudopod extension.

151 ncing F-actin polymerization at the sites of pseudopod extension.

152 ent F-actin polymerization during neutrophil pseudopod extension.

153 re to the substratum and to suppress lateral pseudopod extension.

154 regulated activation of F-actin assembly and pseudopod extension.

155 in polarization of the cell and movement via pseudopod extension.

156 coordinating exocytic membrane insertion and pseudopod extension.

157 oduced a limitation in membrane required for pseudopod extension.

158 arget particles efficiently, but did mediate pseudopod extension.

159 N-1 and CHC-1 regulate actin assembly during pseudopod extension.

160 antigen are important in triggering dramatic pseudopod extensions and uptake by spacious pseudopod lo

161 inhibition of total PKA activity, inhibited pseudopod formation and chemotactic cell migration.

162 ired for cellular cortical functions such as pseudopod formation and macropinocytosis, as demonstrate

163 in 2 at the leading edge occurs during early pseudopod formation and that its localization is sensiti

164 alization via a mechanism involving membrane pseudopod formation and then escaped into the cytoplasm

165 e/Akt/PKB to induce actin polymerization and pseudopod formation at the front of a cell, and PTEN to

166 ormation rate, but rather appears to inhibit pseudopod formation at the side of cells closest to the

167 nteractions, the latter being dominated by a pseudopod formation bias mediated by secreted chemicals

168 sential for specifically suppressing lateral pseudopod formation during the response to an increasing

169 sis of adherent Th1-type cells by augmenting pseudopod formation in conjunction with actin rearrangem

170 myosin Is play a critical role in regulating pseudopod formation in Dictyostelium, and their activity

171 tic activity of calpain is required to limit pseudopod formation in the direction of chemoattractant

172 induce actin polymerization or increase the pseudopod formation rate, but rather appears to inhibit

173 that in addition to enhanced vascular tone, pseudopod formation with lack of normal fluid shear resp

174 involved in explosive actin polymerization, pseudopod formation, and cell migration.

175 source that leads to F-actin polymerization, pseudopod formation, and directional movement up the gra

176 an elevated rate of phagocytosis, increased pseudopod formation, and excessive F-actin localization

177 ir redistribution to the leading edge guides pseudopod formation, migration, and extravasation.

178 lateral sides of cells and PI3K can initiate pseudopod formation, providing evidence for a direct ins

179 eukaryotes, we identify a genetic marker of pseudopod formation, the morphological feature of alpha-

180 Although SCAR has been shown to drive pseudopod formation, WASP's role in this process is cont

181 R's regulatory complex are not essential for pseudopod formation.

182 as a fluid shear stress sensor that controls pseudopod formation.

183 fy a new pathway that is required for proper pseudopod formation.

184 the ability of cells to restrict the site of pseudopod formation.

185 ting uropod function and suppressing ectopic pseudopod formation.

186 ey have lost the ability to suppress lateral pseudopod formation.

187 re increase in normal rats, which depends on pseudopod formation.

188 etabolism, localize these lipids, and direct pseudopod formation.

189 in polymerization at the leading edge during pseudopod formation.

190 ape changes indicative of activation such as pseudopod formation.

191 tep in the cytoskeletal changes resulting in pseudopod formation.

192 migration, consistent with its known role in pseudopod formation.

193 tion of cytoskeletal components required for pseudopod formation.

194 uced disassembly of microtubules and limited pseudopod formation.

195 of alpha-motility because both are used for pseudopod formation.

196 hat distinguish cortical actin from dynamic, pseudopod-forming actin networks, and (ii) adapted molec

197 stes, were present almost exclusively in the pseudopod gonocyte subpopulation.

198 to demonstrate that chemoattractant-induced pseudopod growth and mechanically stimulated cytoskeleto

199 SCAR/WAVE is a principal regulator of pseudopod growth in crawling cells.

200 Chemoattractant-stimulated pseudopod growth in human neutrophils was used as a mode

201 Pseudopod growth was stimulated using N-formylated pepti

202 d lipids and supporting positive feedback of pseudopod growth.

203 pool is a key step in SCAR activation during pseudopod growth.

204 emoattractant stimulation on the dynamics of pseudopod growth.

205 fundamental processes by which cells move - pseudopods have been found to be generated in many diffe

206 Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capil

207 t step in this process is the extension of a pseudopod in the direction of the agonist, and a diverse

208 -1 transiently accumulates to the surface of pseudopods in a manner dependent on ced-1, ced-6, and ce

209 eart for the ordered-stochastic extension of pseudopods in buffer and for efficient directional exten

210 able to become polarized or correctly orient pseudopods in chemotactic gradients.

211 r and for efficient directional extension of pseudopods in chemotactic gradients.

212 mammals and major sperm protein (MSP)-based pseudopods in nematodes.

213 Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces p

214 We find that macropinosomes, but not pseudopods, in growing cells are dependent on PIP(3).

215 hat SCAR is specifically dephosphorylated in pseudopods, increasing activation by Rac and lipids and

216 Actin pseudopods induced by SCAR/WAVE drive normal migration a

217 N-WASP is crucial for extension of invasive pseudopods into which MT1-MMP traffics and for providing

218 We find that the leading pseudopod is bent under centrifugal force in all stalled

219 in all stalled amoebae, suggesting that this pseudopod is very dense indeed.

220 Blebs expand faster than pseudopods leaving behind F-actin scars, but are less pe

221 ed cell speed and directionality and shorter pseudopod lifetime when Arp2 phosphorylation mutant cell

222 rriers had outer retinal tubulations forming pseudopod-like extensions from islands of preserved elli

223 ld-type bacteria with regard to formation of pseudopod-like extensions, here termed listeriopods, and

224 albicans interactions with human BMEC, e.g., pseudopod-like structures on human BMEC membrane and int

225 ss of engulfment within asymmetric, spacious pseudopod loops, a process that differs ultrastructurall

226 larensis LVS is internalized within spacious pseudopod loops, mutant LVS is internalized within tight

227 mutant LVSs are internalized within spacious pseudopod loops.

228 pseudopod extensions and uptake by spacious pseudopod loops.

229 bition of depolymerization is sufficient for pseudopod maintenance but not remodeling.

230 high-affinity LFA-1 aligned along the uropod-pseudopod major axis, which was essential for efficient

231 Once extended, these pseudopods may take on one of two newly described morpho

232 nd membrane material must be inserted in the pseudopod membrane as it extends over the phagocytic tar

233 ve forces requires a turgid forward-pointing pseudopod, most likely sustained by cortical actomyosin

234 rong correlation between the velocity of the pseudopod moving up the cAMPS gradient to the total velo

235 cAMPS gradient to the total velocity of the pseudopods moving up and down the gradient over a large

236 ated SCAR is acting at the edges of existing pseudopods, not elsewhere in the cell.

237 ents, SPE-38 was found to concentrate on the pseudopod of mature sperm, consistent with it playing a

238 emporal resolution required to track complex pseudopods of cells moving in three dimensions.

239 es the growth of dendritic actin networks in pseudopods of eukaryotic cells during chemotaxis.

240 nts and dynamic microtubules in filopodia of pseudopods of invading cells under a chemotactic gradien

241 ods, rather than by simple generation of new pseudopods on demand.

242 ly produce first microspikes, then blebs and pseudopods only later.

243 ivation of the neutrophil with protrusion of pseudopods or a uniform recovery of the cytoskeleton net

244 by cells to propel themselves, including by pseudopods or blebbing.

245 generated on the flanks of either extending pseudopods or blebs themselves.

246 72 [53.7%]), globules and dots (68 [50.7%]), pseudopods or streaks (47 [35.1%]), and blue-black sign

247 anomas were the presence of blue-white veil, pseudopods or streaks, and pigment network.

248 nce of the blue-black sign, pigment network, pseudopods or streaks, and/or blue-white veil, despite t

249 or cyclic AMP and moving with both blebs and pseudopods or with blebs only.

250 both SCAR and WASP are unable to grow, make pseudopods or, unexpectedly, migrate using blebs.

251 rectional bias, and overall only PIP(3)-free pseudopods orient up-gradient.

252 romotes macropinocytosis and interferes with pseudopod orientation during chemotaxis of growing cells

253 To extend pseudopods over the surface of targeted particles during

254 e direction, highlighting the important role pseudopods play in pathfinding.

255 ical changes (emission of single or multiple pseudopods, presence of cytoplasmic vacuoles, releasing

256 hological changes were emissions of multiple pseudopods, presence of cytoplasmic vacuoles, spreading,

257 Pseudopod projection after exposure to a step fluid shea

258 es respond to fluid shear stress with active pseudopod projection and cell spreading.

259 The number of leukocytes responding with pseudopod projection and the extent of cell spreading in

260 In inflammation, however, pseudopod projection during spreading and firm adhesion

261 in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wi

262 suppressing inappropriate activation of the pseudopod-promoting Gi/PI3-kinase signaling pathway.

263 WIPa localizes to sites of new pseudopod protrusion and colocalizes with WASP at the le

264 esults suggest that WIPa is required for new pseudopod protrusion and prompt reorientation of cells t

265 timulated P2X4 receptors, Ca(2+) influx, and pseudopod protrusion at the front.

266 mediated by multiple checks on the number of pseudopods, rather than by simple generation of new pseu

267 verall rate of F-actin polymerization in the pseudopod region by measuring the rate of extension of s

268 olymerization of cytoskeletal F-actin in the pseudopod region induced by G-protein coupled chemoattra

269 ling pathways of actin polymerization in the pseudopod region: a phosphoinositide 3-kinase gamma (PI3

270 igh incidence of circulating leukocytes with pseudopods results in slower cell passage through capill

271 rming resulted in restoration of disc shape, pseudopod retraction, disassembly of new actin filaments

272 sponses in circulating leukocytes, including pseudopod retraction.

273 by measuring the rate of extension of single pseudopods stimulated by f-Met-Leu-Phe.

274 t nucleated cells crawl about by extending a pseudopod that is driven by the polymerization of actin

275 ve recruitment to the front results in large pseudopods that fail to bifurcate because they continual

276 of F-actin polymerization and suppression of pseudopods that point in other directions.

277 n mode characterized by dynamic actin-filled pseudopods that we call "alpha-motility." Mining genomic

278 rane tension in spatially coupling blebs and pseudopods, thus contributing to clustering protrusions

279 activity and that phosphorylation acts as a pseudopod timer by promoting Scar/WAVE turnover.

280 ods, while GFP-alpha-actinin concentrated in pseudopod tips and cortex.

281 domain was not capable of being tethered at pseudopod tips.

282 telium cells switch from using predominantly pseudopods to blebs when migrating under agarose overlay

283 -MMP; MMP14), which functions in actin-based pseudopods to drive invasion by extracellular matrix deg

284 ve different effects on the cytoskeleton and pseudopods to induce neutrophil chemoattraction or chemo

285 CHC-1 is enriched on extending pseudopods together with EPN-1, in an EPN-1-dependent ma

286 ttractant source due to delayed extension of pseudopod toward the new gradient.

287 Surprisingly, three-dimensional pseudopods turn out to be composed of thin (<0.75 microm

288 p55(-/-) neutrophils form multiple transient pseudopods upon chemotactic stimulation, and do not migr

289 To analyze three-dimensional pseudopods we: (i) developed fluorescent probe combinati

290 se SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukoc

291 tivity to the front, and cannot generate new pseudopods when SCAR/WAVE is absent.

292 bodies that sequester MSP at the base of the pseudopod, where directed MSP disassembly facilitates ps

293 r SCAR/WAVE controls actin polymerization in pseudopods, whereas Wiskott-Aldrich syndrome protein (WA

294 attractants neutrophils extend an actin-rich pseudopod, which imparts morphological polarity and is r

295 ced fMLP-dependent Rac activity and unstable pseudopods, which is consistent with the established rol

296 egulates the frequency of initiation of long pseudopods, which promote migration speed and directiona

297 st showed shrinkage, then displayed multiple pseudopods, which rapidly extended and retracted, giving

298 ery was observed to function entirely within pseudopods, while GFP-alpha-actinin concentrated in pseu

299 ts were elongated and displayed large, bulky pseudopods with dynamic actin bursts.

300 the shedding was localized to transmigrating pseudopods within the subendothelial space.