ライフサイエンスコーパス: pseudopod

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

2 re amoeboid cells that crawl via an extended pseudopod.

3 ich is also restricted to the transmigrating pseudopod.

4 recovery of the cytoskeleton network with no pseudopod.

5 ergoes wholesale reorganization to produce a pseudopod.

6 sufficient for long-range inhibition by the pseudopod.

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

8 active, causing frequent small, disorganized pseudopods.

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

10 classes of protrusion: short stubs and long pseudopods.

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

12 th diminished actin polymerization and small pseudopods.

13 leading to the formation of multiple lateral pseudopods.

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

15 s in gradient direction by extending lateral pseudopods.

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

17 ding edge to generate morphologically normal pseudopods.

18 ads to robust proliferation and extension of pseudopods.

19 leading edges rather than by initiating new pseudopods.

20 delling and results in the hyperformation of pseudopods.

21 ciently in the epidermis, with nearly static pseudopods.

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

23 shedding) specifically within transmigrating pseudopods.

24 r the production and retention of upgradient pseudopods.

25 grate slower, and generate fewer and thinner pseudopods.

26 and lysosomal membranes to form plasmalemmal pseudopods.

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

28 assembly and stability of F-actin underneath pseudopods.

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

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

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

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

33 During the formation of pseudopods, an increase in fluorescence intensity coinci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 gocytosis requires extension of F-actin-rich pseudopods and is accompanied by membrane fusion events.

51 The formation of pseudopods and lamellae after ligation of chemoattractan

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

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

54 the recruitment of intracellular vesicles to pseudopods and phagosomes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Pseudopods colocalized with active Rac, whether driven b

86 Unlike those in other crawling cells, this pseudopod contains little or no actin; instead, it utili

87 , where directed MSP disassembly facilitates pseudopod contraction.

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

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

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

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

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

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

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

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

96 lation of Dictyostelium SCAR controls normal pseudopod dynamics.

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

98 es microtubule resistance to compression and pseudopod elongation.

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

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

101 The morphology that these pseudopods exhibit suggest that they may play both senso

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

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

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

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

106 Our data suggest that pseudopod extension and internalization are functionally

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

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

109 1 signals via Scar/WAVE and Arp2/3 to effect pseudopod extension and migration of melanoblasts in ski

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

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

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

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

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

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

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

117 The pseudopod extension induced using micropipets was oscill

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

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

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

121 where rearrangements of the cytoskeleton and pseudopod extension occur.

122 We observed that pseudopod extension occurred in two phases.

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

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

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

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

127 This is consistent with the models of pseudopod extension that predict an increase in the loca

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

129 This oscillatory pseudopod extension was controlled by activated RhoA and

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

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

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

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

134 Here, pseudopod extension was stimulated with chemoattractant

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

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

137 icant defects in cortical activities such as pseudopod extension, cell migration, and macropinocytosi

138 Chilling caused loss of disc shape, pseudopod extension, disassembly of microtubule coils, a

139 o four major steps: receptor-ligand binding, pseudopod extension, internalization, and lysosomal fusi

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

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

142 d been deleted was also capable of mediating pseudopod extension, showing that neither the gamma chai

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

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

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

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

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

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

149 ent F-actin polymerization during neutrophil pseudopod extension.

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

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

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

153 coordinating exocytic membrane insertion and pseudopod extension.

154 oduced a limitation in membrane required for pseudopod extension.

155 arget particles efficiently, but did mediate pseudopod extension.

156 ization by all Fc gamma R, but did not block pseudopod extension.

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

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

159 ol across marrow endothelium requires active pseudopod formation and adhesion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 cocapping of both molecules with subsequent pseudopod formation, while CytoD pretreatment blocked th

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

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

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

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

182 ting uropod function and suppressing ectopic pseudopod formation.

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

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

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

186 in polymerization at the leading edge during pseudopod formation.

187 ape changes indicative of activation such as pseudopod formation.

188 tep in the cytoskeletal changes resulting in pseudopod formation.

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

190 tion of cytoskeletal components required for pseudopod formation.

191 uced disassembly of microtubules and limited pseudopod formation.

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

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

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

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

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

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

198 Pseudopod growth was stimulated using N-formylated pepti

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

200 emoattractant stimulation on the dynamics of pseudopod growth.

201 d lipids and supporting positive feedback of pseudopod growth.

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

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

204 d in the presence of CMF in that they extend pseudopods, have an activated PLC, have a low cAMP-stimu

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

206 -1 transiently accumulates to the surface of pseudopods in a manner dependent on ced-1, ced-6, and ce

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

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

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

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

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

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

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

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

215 chemotactic source involves the extension of pseudopods initiated by the focal nucleation and polymer

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

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

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

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

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

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

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

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

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

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

226 mutant LVSs are internalized within spacious pseudopod loops.

227 pseudopod extensions and uptake by spacious pseudopod loops.

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

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

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

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

232 The protein also becomes highly enriched in pseudopods, microvilli, axons, denticles, the border cel

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

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

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

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

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

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

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

240 Rewarming caused retraction of pseudopods on taxol-treated, discoid cells.

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

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

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

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

245 72 [53.7%]), globules and dots (68 [50.7%]), pseudopods or streaks (47 [35.1%]), and blue-black sign

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

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

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

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

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

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

252 To extend pseudopods over the surface of targeted particles during

253 y of MSP fibers near the leading edge of the pseudopod plasma membrane.

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 r stress in the circulation serves to reduce pseudopod projection and adhesion of circulating leukocy

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

260 id shear stress in turn led to the return of pseudopod projection and cell spreading.

261 ice versa reduction of shear stress leads to pseudopod projection and spreading of leukocytes on the

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

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

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

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

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

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

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

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

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

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

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

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

274 sponses in circulating leukocytes, including pseudopod retraction.

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

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

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

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

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

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

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

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

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

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

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 oid platelets to rounded cells that extended pseudopods when chilled and retracted them when rewarmed

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.