ライフサイエンスコーパス: amoeboid

1 that are classified as either mesenchymal or amoeboid.

2 l for the migration of both mesenchymals and amoeboids.

3 enchymal cells create paths that are used by amoeboids.

4 -catalytic mechanism, MMP-9 promotes rounded-amoeboid 3D migration through regulation of actomyosin c

5 ithelial/mesenchymal (E/M), mesenchymal (M), amoeboid (A) and hybrid amoeboid/mesenchymal (A/M) pheno

6 e reduced, and microglia reverted from their amoeboid, active form to a ramified, resting configurati

7 while fs164 and fs120 cells adopted rounded/amoeboid and a mix of rounded and elongated morphologies

8 Here we compare MMP levels in rounded-amoeboid and elongated-mesenchymal melanoma cells.

9 ions to maintain the precise balance between amoeboid and mesenchymal cell behaviors required for cel

10 found that melanoma cells can switch between amoeboid and mesenchymal forms via two different routes

11 ed in order to facilitate conversion between amoeboid and mesenchymal forms, as cells are either sear

12 TPases are required for the morphogenesis of amoeboid and mesenchymal forms, others are required for

13 g DOCK10 and Rac1 expression suppresses both amoeboid and mesenchymal migration and results in decrea

14 igated in the context of transitions between amoeboid and mesenchymal migration modes, which involve

15 elucidate novel roles of Cdc42 signaling in amoeboid and mesenchymal movement and tumor cell invasio

16 s can adopt two functionally distinct forms, amoeboid and mesenchymal, which facilitates their abilit

17 ferent phenotypes of motility and invasion - amoeboid and mesenchymal.

18 ctive pressures imposed by such organisms as amoeboid and nematode predators.

19 Amoeboid and spherical shapes represent perhaps the simp

20 lia are initially mitotic, rounded in shape (amoeboid), and phagocytically active.

21 F-beta, SMAD2 and its adaptor CITED1 control amoeboid behavior by regulating the expression of key ge

22 ransition and therefore suppresses efficient amoeboid bleb-based invasion.

23 It has been suggested that rounded-amoeboid cancer cells do not require matrix metalloprote

24 Rounded-amoeboid cancer cells use actomyosin contractility drive

25 l retina is characterized by the presence of amoeboid, carbonic anhydrase-positive microglial cells e

26 l cells undergo a series of conversions from amoeboid cell behaviors to more mesenchymal and finally

27 panin CD9 and facilitates the maintenance of amoeboid cell invasion.

28 as exhibited by fibroblasts is distinct from amoeboid cell migration and is characterized by dynamic

29 ports a key role for lateral contractions in amoeboid cell motility, whereas the differences in their

30 ch to probe the basic molecular mechanism of amoeboid cell motility.

31 ay for evaluating the molecular mechanism of amoeboid cell motility.

32 Rho-dependent amoeboid cell movement is a crucial mechanism in both tu

33 cal process involved in both cytokinesis and amoeboid cell movement.

34 EMT-like and EMT-independent amoeboid cell subsets showed stable amoeboid movement ov

35 MDA-MB-435S cells, with typical features of amoeboid cells (poor collagenolytic activity, rounded ce

36 Some responses perceived by 7TM receptors in amoeboid cells and possibly in human cells can initiate

37 Leukocytes and other amoeboid cells change shape as they move, forming highly

38 Amoeboid cells have high levels of actomyosin contractil

39 hat, in the crawling of neutrophils or other amoeboid cells inside a micropipette, measurement of vel

40 rs can lead to profound transformations from amoeboid cells into cells mimicking keratocytes, neurons

41 Cell motility of amoeboid cells is mediated by localized F-actin polymeri

42 gical limitations, but finding such modes in amoeboid cells is more difficult as they lack these cons

43 As amoeboid cells migrate, signaling events such as Ras and

44 emonstrated that eukaryotic cells, including amoeboid cells of Dictyostelium discoideum and neutrophi

45 Migration of highly motile, amoeboid cells such as neutrophils has significant physi

46 In nematodes, sperm are amoeboid cells that crawl via an extended pseudopod.

47 D. discoideum lives as haploid, free-living, amoeboid cells that divide asexually.

48 o motility system from Ascaris sperm, unique amoeboid cells that use filament arrays composed of majo

49 Therefore, rounded-amoeboid cells use both catalytic and non-catalytic acti

50 Analogous to the chemotaxis of amoeboid cells, we found that a gradient of chemoattract

51 yield signal amplification and adaptation in amoeboid cells.

52 ownstream effectors in metazoan, fungal, and amoeboid cells.

53 logous to that formed by actin in many other amoeboid cells.

54 ts analogous to that formed by actin in many amoeboid cells.

55 s of migration may be conserved in mammalian amoeboid cells.

56 singly, we found that pathways implicated in amoeboid chemotaxis, such as PI3K and mammalian target o

57 MMP-9 is upregulated in a panel of rounded-amoeboid compared with elongated-mesenchymal melanoma ce

58 Hypoxia-induced amoeboid detachment was driven by hypoxia-inducible fact

59 for the pseudopod-dominated migration of the amoeboid Dictyostelium discoideum and for the lamellipod

60 l cells migrating over a substratum crawl in amoeboid fashion; how the force against the substratum i

61 we find that in melanoma, TGF-beta promotes amoeboid features such as cell rounding, membrane blebbi

62 onapoptotic membrane blebs, a feature of the amoeboid form of cell motility.

63 dynamics of the chemotactic migration of the amoeboid form of Dictyostelium discoideum.

64 to 1 microg ml(-1) LPS, most cells showed an amoeboid ('fried egg'-shaped) morphology with a 62% incr

65 how that distinct from mesenchymal invasion, amoeboid invasion is independent of intracellular calpai

66 ells demonstrates that Net1A is required for amoeboid invasion, and loss of Net1A expression causes c

67 ion, and impair actomyosin contractility and amoeboid invasion.

68 2-mediated integrin adhesion turnover during amoeboid invasion.

69 hment of CSMD1 in the nerve growth cone, the amoeboid-leading edge of the growing neuron.

70 ind that RhoC expression induces a primitive amoeboid-like cell invasion characterized by the formati

71 at the membrane-cortex traveling wave led to amoeboid-like cell migration.

72 They also lack the customary amoeboid-like cell movements and active membrane project

73 /ROCK signalling, which specifically impairs amoeboid-like invasion, restores cell surface expression

74 than their parental counterparts and assumed amoeboid-like invasive abilities upon glycolysis inhibit

75 Here we demonstrate that in amoeboid-like invasive tumour cell lines, the v-SNARE, V

76 on of LECs across a membrane (which involves amoeboid-like transmigration), it did not increase LEC c

77 cally reduces cell invasion, impairing both "amoeboid-like" and mesenchymal-like modes of invasion in

78 es are motile in two distinct modes: a fast "amoeboid-like" mode, which uses sequential discontinuous

79 dicating that Vannella represents a separate amoeboid lineage and the subclass Gymnamoebia is polyphy

80 lar processes, we show that many features of amoeboid locomotion emerge from a simple mechanochemical

81 The amoeboid locomotion of nematode sperm is mediated by the

82 In vitro, pre-PCs displayed processive amoeboid locomotion on surfaces coated with integrin lig

83 generate both of these central components of amoeboid locomotion.

84 nics in determining the emergent features of amoeboid locomotion.

85 crawling force generated by cells undergoing amoeboid locomotion.

86 s from a typical resting configuration to an amoeboid, macrophage-like morphology, increased expressi

87 ng genome-wide transcriptomics, we find that amoeboid melanoma cells are enriched in a TGF-beta-drive

88 As a result, rounded-amoeboid melanoma cells degrade collagen I more efficien

89 Surprisingly, we find that rounded-amoeboid melanoma cells secrete higher levels of several

90 e the circuit's three possible states to the amoeboid, mesenchymal and amoeboid/mesenchymal hybrid ph

91 M), mesenchymal (M), amoeboid (A) and hybrid amoeboid/mesenchymal (A/M) phenotypes.

92 ible states to the amoeboid, mesenchymal and amoeboid/mesenchymal hybrid phenotype.

93 on in MTLn3 cells (an apolar randomly moving amoeboid metastatic tumor cell) caused them to extend pr

94 t, there is an increase in ferritin-positive amoeboid microglia and a decrease in immunohistochemical

95 d differentiation, is expressed in forebrain amoeboid microglia during the first two postnatal weeks.

96 nd white matter areas of the brain, but only amoeboid microglia in discrete foci in the subcortical w

97 ssociated with accumulation of ERK-activated amoeboid microglia in mice, and is also observed in huma

98 Runx1 inhibits mouse amoeboid microglia proliferation and promotes progressio

99 At the cellular level, fewer amoeboid microglia/macrophages appeared adjacent to the

100 t is densely populated with intermediate and amoeboid microglia; the latter is indicative of an activ

101 le is known about the mechanisms controlling amoeboid microglial cell proliferation, activation, and

102 , collective, and single-cell mesenchymal or amoeboid migration [2-4].

103 ccur in many physiological contexts, such as amoeboid migration and cytokinesis.

104 chyme transition that involves activation of amoeboid migration and loss of cell-cell adhesion.

105 dhering to it, and which may be relevant for amoeboid migration in complex three-dimensional environm

106 How amoeboid migration is regulated by extracellular signals

107 nsional migration and the 3-dimensional (3D) amoeboid migration mode of HIV-1-infected human monocyte

108 last spreading through either mesenchymal or amoeboid migration modes.

109 ykinin during glioma invasion by stimulating amoeboid migration of glioma cells.

110 cortex contractility plays a crucial role in amoeboid migration of metastatic cells [6] and during di

111 mal cells can spontaneously switch to a fast amoeboid migration phenotype.

112 Fast amoeboid migration requires cells to apply mechanical fo

113 f reduced integrin-dependent migration, i.e. amoeboid migration, is a known phenotype.

114 anges, but in contrast to other instances of amoeboid migration, trailing edge retraction involves ep

115 s distinct from conventional mesenchymal and amoeboid migration, whereby long-lived episodes of slow,

116 or mesenchymal migration but dispensable for amoeboid migration.

117 SCAR/WAVE complex plays in the mechanics of amoeboid migration.

118 ve and quantify wave-like characteristics of amoeboid migration.

119 fied DOCK10, a Cdc42 GEF, as a key player in amoeboid migration; accordingly, we find that expression

120 tic dissemination of cancer cells, and fast "amoeboid" migration in the invasive fronts of tumors is

121 y use the protease- and podosome-independent amoeboid mode in more porous matrices.

122 D) environment in either mesenchymal-type or amoeboid modes.

123 This occurs through a mesenchymal-amoeboid morphological switch that signals through the R

124 surveillant microglia undergo a ramified-to-amoeboid morphological transformation and become phagocy

125 omoted microglial activation, as assessed by amoeboid morphology and increased expression of MHC clas

126 ted microglia to assume their characteristic amoeboid morphology during brain inflammation.

127 on leads to increased microglial numbers and amoeboid morphology in the DG.

128 ed by WNV infection, as exemplified by their amoeboid morphology, the development of filopodia and la

129 CCL2hi tg+ mice were defective in expressing amoeboid morphology.

130 ntexts, protrusions adopt lamellipodia or an amoeboid morphology.

131 assays, with cells expressing TNCEGFL having amoeboid morphology.

132 est the hypothesis that AQP-1 is involved in amoeboid motility and angiogenic invasion during cirrhos

133 nto the machinery needed for pseudopod-based amoeboid motility and how it evolved.

134 sperm protein (MSP) of Ascaris suum mediates amoeboid motility by forming an extensive intermeshed sy

135 sperm protein (MSP) of Ascaris suum mediates amoeboid motility by forming an extensive intermeshed sy

136 K activation during planar cell movement and amoeboid motility during extracellular matrix (ECM) inva

137 Cells employing amoeboid motility exhibit repetitive cycles of rapid exp

138 n bone marrow (BM) was strictly dependent on amoeboid motility mediated by CXCR4 and CXCL12 and by al

139 The major sperm protein (MSP)-based amoeboid motility of Ascaris suum sperm requires coordin

140 in, a cytoskeletal molecule required for the amoeboid motility of sperm in Caenorhabditis elegans, al

141 Amoeboid motility requires spatiotemporal coordination o

142 Myosin-IIA is necessary for fast amoeboid motility, and our data suggests that this occur

143 ependently in eukaryotes that evolved active amoeboid motility.

144 f Arp2/3-nucleated actin networks that drive amoeboid motility.

145 cytoskeletal element's role during effective amoeboid motility.

146 ver, we construct a comprehensive catalog of amoeboid-motility genes.

147 ge microscopic technique and showed they had amoeboid movement and phagocytic abilities.

148 s that control the activation of GTPases for amoeboid movement are poorly understood, we sought to id

149 sociated neurons use somal translocation and amoeboid movement as they migrate to their final positio

150 erstood, we sought to identify regulators of amoeboid movement by screening an siRNA library targetin

151 Amoeboid movement is characterized by relatively non-pol

152 Induced by metabolic challenge, amoeboid movement may thus constitute a common endpoint

153 How is the amoeboid movement of lymphocytes in secondary lymphoid o

154 ependent amoeboid cell subsets showed stable amoeboid movement over hours as well as leukocyte-like t

155 to direct mesenchymal movement and suppress amoeboid movement through decreasing actomyosin contract

156 Transition from mesenchymal to amoeboid movement was associated with decreased levels o

157 In amoeboid movement, cells have a rounded morphology, are

158 Conversely, in amoeboid movement, Rho-kinase signaling activates a Rac

159 of protoplasm of conical form, endowed with amoeboid movements.

160 sition (CAT), promoting the dissemination of amoeboid-moving single cells from collective invasion st

161 In the postnatal brain, immature amoeboid myeloid precursors only induce SPARC expression

162 These results suggest that the amoeboid myosin I consensus phosphorylation site and SH3

163 ension, and those that mildly overexpress an amoeboid myosin I exhibit increased cortical tension.

164 The amoeboid myosin I's are required for cellular cortical f

165 Given that the amoeboid myosin I's possess both actin- and membrane-bin

166 elium cells either lacking or overexpressing amoeboid myosin Is have significant defects in cortical

167 Amoeboid myosin Is play a critical role in regulating ps

168 m-rich inclusion (CAI) accretionary rims and amoeboid olivine aggregates (AOAs), are oxygen-16 (16O)

169 itions via the apolar or polar route and not amoeboid or mesenchymal morphogenesis per se.

170 extracellular proteases; however, cells with amoeboid or rounded morphologies are able to invade even

171 n correlated with a reduced number of Cox-2+ amoeboid phagocytes adjacent to the injury.

172 icroglia reduced microglial activation to an amoeboid phenotype and decreased the phagocytosis of inj

173 eformable environments, tumor cells adopt an amoeboid phenotype and release microvesicles.

174 CITED1 is coupled to a contractile-rounded, amoeboid phenotype in a panel of 16 melanoma cell lines,

175 n elongated/mesenchymal phenotype to a round/amoeboid phenotype in the absence of similar effects on

176 ocytoma cells resulted in a transition to an amoeboid phenotype that was abolished with the ROCK inhi

177 olon cancer cells are able to transfer their amoeboid phenotype to isogenic primary cancer cells thro

178 rphology, whereas Hic-5 knockdown induced an amoeboid phenotype with both cell populations exhibiting

179 required for the maintenance of the rounded-amoeboid phenotype.

180 RASAL2 knockdown leads to a conversion to an amoeboid phenotype.

181 population of mesenchymals kept in a mostly-amoeboid population.

182 d of host-microbe interactions that includes amoeboid predation and endosymbiotic existence.

183 acquired microbes, biotic pressures, such as amoeboid predators, may select for the capacity for viru

184 ating the RhoA/ROCK pathway, known to induce amoeboid properties and destabilization of endothelial j

185 algae, a green alga and a relatively derived amoeboid protist.

186 icroscopy showed that Ptpro(-/-) mice had an amoeboid rather than the typical octopoid structure seen

187 he defined target, for different mesenchymal/amoeboid ratios.

188 We show that the incredible variety in amoeboid shape across a population can be reduced to a f

189 Endoderm cells move by amoeboid shape changes, but in contrast to other instanc

190 Amoeboid sperm crawl around fertilized eggs to the sperm

191 Leading edge protrusion in the amoeboid sperm of Ascaris suum is driven by the localize

192 pment and motility of Caenorhabditis elegans amoeboid sperm.

193 unpolarized round spermatids into polarized amoeboid spermatozoa capable of both motility and fertil

194 he developmental cycle and when cells in the amoeboid stage are subjected to stress but the phosphory

195 mors [9], as an inducer of the collective-to-amoeboid transition (CAT), promoting the dissemination o

196 n phenotypes, specifically the Collective-to-Amoeboid Transition (CAT).

197 enchymal Transition (EMT) and Mesenchymal-to-Amoeboid Transition (MAT) - have been carefully investig

198 The mesenchymal-amoeboid transition (MAT) was proposed as a mechanism fo

199 ion of activated Cdc42 induces a mesenchymal-amoeboid transition and increases cell invasion.

200 tomyosin levels and favours an epithelial to amoeboid transition contributing to tumour aggressivenes

201 However, direct epithelial to amoeboid transition has not been characterized to date.

202 al that ECT2 has a novel role in mesenchymal-amoeboid transition in human astrocytoma cells.

203 hly metastatic cancer, undergo epithelial to amoeboid transition in physiological environments, such

204 some tumour cells undergo a 'mesenchymal to amoeboid' transition that allows invasion in the absence

205 ontexts including mitosis and mesenchymal-to-amoeboid transitions.

206 Hence, the loss of cofilin caused an amoeboid tumor cell to assume a mesenchymal-type mode of

207 Herein, we show that amoeboid tumor cells export large (1- to 10-mum diameter

208 Amoeboid tumor cells generate sufficient actomyosin forc

209 Emerging research implicates amoeboid-type motility and membrane blebbing as features

210 g apparent that some cancer cells move in an amoeboid way similar to leukocytes.