ライフサイエンスコーパス: cell migration

1 that PIKfyve and PtdIns(5)P control Rac and cell migration.

2 ment of traction stresses that permit single-cell migration.

3 ing embryonic development, inflammation, and cell migration.

4 ers and focal adhesions, leading to enhanced cell migration.

5 y and clonogenicity and promoted lung cancer cell migration.

6 utilization during three-dimensional cancer cell migration.

7 I) is an important motor protein involved in cell migration.

8 MII ordinarily being essential for polarized cell migration.

9 the anisotropic mechanical strain of single-cell migration.

10 tors such as RHOJ regulated breast carcinoma cell migration.

11 11 in cancer cells reduced pancreatic cancer cell migration.

12 ropinocytosis, receptor internalization, and cell migration.

13 d actin reinforcement response and increased cell migration.

14 contact dynamics and coordinated collective cell migration.

15 have been well studied within the context of cell migration.

16 the edge of migrating monolayers, regulating cell migration.

17 flammatory response, cell proliferation, and cell migration.

18 cellular environment have a strong effect on cell migration.

19 and sphingomyelin pools in cells and inhibit cell migration.

20 n extracellular fragment that also regulates cell migration.

21 g on spatial distribution of an activator of cell migration.

22 coordinating MTs and actin at FAs to direct cell migration.

23 hus, GCK-dependent glycolysis regulates Treg cell migration.

24 s the expression of key proteins involved in cell migration.

25 nucleates actin assembly to promote directed cell migration.

26 ith important but poorly understood roles in cell migration.

27 -specific effects on ARHGAP29 expression and cell migration.

28 nical responses during single and collective cell migration.

29 ease critical for cranial neural crest (CNC) cell migration.

30 , down-regulation of mitogenic receptors and cell migration.

31 iological processes, such as cytokinesis and cell migration.

32 phatidic acid (LPA), linking it with GPAM to cell migration.

33 via detyrosinated microtubules, and enhance cell migration.

34 thus regulating focal adhesion dynamics and cell migration.

35 ney and mediates calcium influx and promotes cell migration.

36 M-II activity through effects on MRLC during cell migration.

37 -mesenchymal transition (EMT) and epithelial cell migration.

38 degradability modulates the collectivity of cell migration.

39 s distinct spatiotemporal regulation of germ cell migration.

40 macrophages, whereas CXCL6 also induced dNK cell migration.

41 is not required for matrix alignment before cell migration.

42 as a model system to quantify the collective cell migration.

43 tin polymerization, pseudopod formation, and cell migration.

44 thout the confounding effect of differential cell migration.

45 ration and cell density, to directly promote cell migration.

46 (FLNa) to modulate filopodium formation and cell migration.

47 e C, an enzyme regulating neurite growth and cell migration.

48 specification does not rescue mesendodermal cell migration.

49 ctin cytoskeleton, and decreased velocity of cell migration.

50 promote actin polymerization and endothelial cell migration.

51 567E phosphomimetic mutants exhibit enhanced cell migration.

52 increased cytosolic Ca(2+) concentration and cell migration.

53 the inhibitory activity towards endothelial cell migration.

54 on and pathological conditions such as tumor cell migration.

55 nated cellular functions such as directional cell migration.

56 Deltadriven vectorial migration, while CD8 T cell migration across LEC was not.

57 pplied by an atomic force microscope, or via cell migration across uneven microsurfaces - results in

58 t RNA subgroup is functionally important for cell migration.Adenomatous polyposis coli (APC) regulate

59 ; GDE5; GDPD6) has been suggested to promote cell migration, adhesion, and spreading, but its mechani

60 activating Cxcl12 expression and endothelial cell migration against blood flow into developing arteri

61 g affect cytoplasmic energy distribution and cell migration, an energy-expensive process.

62 CCR2 converts J113863 from an antagonist for cell migration and a partial agonist in other assays to

63 sis also identified gene modules involved in cell migration and adhesion, processes that are likely c

64 tion between talin stability and the rate of cell migration and also found that talin destabilization

65 IT D816V-dependent key regulator of vascular cell migration and angiogenesis in SM.

66 In this model, Gsc provides a switch between cell migration and CE, i.e. cell intercalation.

67 Cell migration and cell-cell communication involve the p

68 their ability to promote corneal epithelial cell migration and corneal wound healing, respectively.

69 es showed that 19 can impair CXCL12-mediated cell migration and CXCR4 internalization more efficientl

70 d levels of cell survival, colony formation, cell migration and decreased cellular apoptosis, and thi

71 oding a peptide factor that promotes pigment cell migration and differentiation in other vertebrates.

72 ived peptide C3a regulates neural progenitor cell migration and differentiation in vitro and that C3a

73 However, how plasticity of tumor cell migration and EMT is spatiotemporally controlled an

74 ereby, Lpd supports lamellipodia protrusion, cell migration and endocytosis.

75 phagy and concurrently inhibited endothelial cell migration and evasion from a 3D matrix.

76 to fundamental cellular processes, including cell migration and extracellular matrix (ECM) assembly.

77 deformations on their surroundings underlies cell migration and extracellular matrix (ECM) remodeling

78 , VEGF and SDF-1 abolished VEGFR1(+) myeloid cell migration and fibroblast activation induced by CYP4

79 CYP4A inhibition decreased VEGFR1(+) myeloid cell migration and fibronectin expression, accompanied w

80 ent has been implicated in modulating cancer cell migration and independently predicts progression to

81 S myelin, in general, inhibit rodent Schwann cell migration and induce their death via cleavage of th

82 DU145 and PC3 cells significantly increased cell migration and induced the expression of the mesench

83 lecules, while mesenchymal genes involved in cell migration and invasion are repressed.

84 Cell migration and invasion are very characteristic feat

85 SOCS1 silencing inhibited cell migration and invasion as well as in vitro growth b

86 Overexpression of miR-218 inhibited cell migration and invasion as well as the EMT process.

87 r acidification from pHe7.4 to 6.4 decreases cell migration and invasion but increases single cell de

88 ysis, anchorage-independent cell growth, and cell migration and invasion in HPV-transformed cells.

89 EMT) has been recognized as a key element of cell migration and invasion in lung cancer; however, the

90 ver, coactivation of ER and IKKbeta promoted cell migration and invasion in vitro and drove experimen

91 d TGF-beta signal transduction and inhibited cell migration and invasion via activation of Smad7 tran

92 ition, NLS treatment significantly decreased cell migration and invasion via phenotypic inversion of

93 y in vitro, attenuated TNFalpha-induced TNBC cell migration and invasion, and inhibited the tumor gro

94 unctions of NID1, including enhancing cancer cell migration and invasion, promoting adhesion to the e

95 RO3/growth arrest specific 6-mediated cancer cell migration and invasion.

96 (2+)-binding proteins, is a key regulator of cell migration and invasion.

97 nd activation of TGF-beta signaling promoted cell migration and invasion.

98 chymal-to-epithelial transition, and reduced cell migration and invasion.

99 cells are more efficient in promoting cancer cell migration and invasion.

100 l for exploring the thermodynamics of cancer cell migration and invasion.

101 rmation in achieving polarized secretion for cell migration and invasion.

102 o in nude mice, and suppress cervical cancer cell migration and invasion.

103 correlates with poor prognosis, reduces GBM cell migration and invasiveness by suppressing PCP signa

104 tion from hypoxia, angiogenesis, DNA repair, cell migration and invasiveness, and cell metabolism.

105 Cell migration and its dependence on the cytoskeleton an

106 d PAQR11 was found to be essential for tumor cell migration and metastasis in EMT-driven lung adenoca

107 y regulates genes and pathways implicated in cell migration and metastasis, and demonstrate, using fu

108 a potential regulator in MSI1/TNS3-mediated cell migration and morphological changes.

109 uption of beta-actin gene critically impacts cell migration and mouse embryogenesis, we demonstrate h

110 -PML axis-mediated inhibition of endothelial cell migration and network formation.

111 and lipid metabolism pathways, and inhibited cell migration and phagocytosis.

112 ine system, which is essential for directing cell migration and plays a crucial role in a variety of

113 es (AuNPs) were discovered to inhibit cancer cell migration and prevent metastasis.

114 antibody, 107_A07, inhibited HGF/SF-induced cell migration and proliferation in vitro and inhibited

115 aired microtubule polymerization, as well as cell migration and proliferation properties, of mutant P

116 antially attenuated BI-induced smooth muscle cell migration and proliferation, resulting in reduced n

117 me is required for human retinal endothelial cell migration and proliferation.

118 Our findings link TPC to cancer cell migration and provide a preclinical proof of concep

119 function assay showed gga-miR-219b inhibited cell migration and reduced cell proliferation by promoti

120 ncing GPAM in ovarian cancer cells decreased cell migration and reduced the growth of tumor xenograft

121 Hepatocyte growth factor (HGF) induces cell migration and scattering by mechanisms that are tho

122 The extracellular matrix (ECM) regulates cell migration and sculpts organ shape.

123 a mechanosensitive signaling molecule during cell migration and shear stress.

124 perform crucial cell functions, ranging from cell migration and signaling to membrane trafficking, by

125 ficantly reduces Twist1 and CD44 expression, cell migration and sphere formation.

126 eases of stress fiber formation and impaired cell migration and spreading.

127 nd PI3K inhibitors reduce SOX11-enhanced MCL cell migration and stromal interactions and revert cell

128 aft and human primary MCL tumors overexpress cell migration and stromal stimulation gene signatures c

129 controls central cellular processes such as cell migration and substrate sensing.

130 reduced paracrine stimulation of endothelial cell migration and survival, and wounds of epidermis-spe

131 invasion between two distinct modes: single-cell migration and the multicellular, strand-like invasi

132 and Fgf signaling feedback loop coordinating cell migration and the self-organization of rosette-shap

133 to provide protection to the embryo, directs cell migration and the spreading of embryonic tissue dur

134 ) made defective in tubulin binding returned cell migration and transendothelial migration back to co

135 M increased cell adherence, while inhibiting cell migration and tube formation of HUVECs in vitro.

136 PHF8 plays important roles in breast cancer cell migration and tumor growth.

137 meable glutamate receptor, which can promote cell migration and tumor invasion.

138 ntrast, CCL2 deficient MSCs did not induce T cell migration and VCAM-1 expression, resulting in insuf

139 All cell migration and wound healing assays are based on the

140 nd cost-effective method to study collective cell migration and wound healing.

141 tin protein, and vice versa, does not affect cell migration and/or organism survival.

142 factor, known to be involved in myogenesis, cell migration, and immunoregulation.

143 d that MSI1 alters cell morphology, promotes cell migration, and increases viscoelasticity of GBM cel

144 ections to discrete points within ECM during cell migration, and provides a plausible means by which

145 eratinocytes, SIRT1 knockdown inhibited EMT, cell migration, and TGF-beta signaling.

146 ble expression of VHR suppressed directional cell migration, and VHR deficiency resulted in a higher

147 olarized mechanisms that control directional cell migration are poorly defined.

148 the mechanisms by which CAFs regulate cancer cell migration are poorly understood.

149 mechanism, whereby filopodium formation and cell migration are regulated through the Arl4C-FLNa-medi

150 molecular mechanisms by which MSI1 regulates cell migration are still undetermined.

151 have previously described the acquisition of cell migration as a feature of NK cell terminal maturati

152 We found that FOSL1 is involved in melanoma cell migration as well as cell proliferation and anoikis

153 in increased levels of colony formation and cell migration as well as reduced apoptosis along with i

154 Using a microfluidic 3D cell migration assay, we found that the presence of macr

155 pes was analyzed with vascular smooth muscle cell migration assays and platelet aggregation analyses.

156 al, lymphatic endothelial, and breast cancer cell migration assays.

157 anscriptome analysis of cranial neural crest cell migration at three progressive stages in chick and

158 (PI) staining and growth curves, and blocks cell migration based on transwell assay.

159 impacted three-dimensional MDA-MB-231 tumor cell migration behavior.

160 approach, demonstrating that manipulating T cell migration between the gut and systemic sites alters

161 Propionate suppressed T effector cell migration between the intestine and the spleen in E

162 ral development, have been shown to regulate cell migration beyond the nervous system.

163 ny worm laboratory for real-time analysis of cell migration, BM turnover and cell-membrane dynamics.

164 cing epithelial-myofibroblast transition and cell migration but did not prevent fiber cell differenti

165 ses known to modify ECM proteins and promote cell migration, but demonstrated roles for AdamTS protei

166 d by inflammation or injury, can influence T cell migration, but how T cell migration is affected by

167 by down-regulation of its inhibitory role in cell migration, but not affecting its other regulatory f

168 zed role of cytoplasmic YAP/TAZ in promoting cell migration by activating CDC42 and provide insight i

169 Directed cell migration by contact guidance in aligned collagenou

170 nals required for this distinctive mode of T cell migration by inhibiting key cytoskeletal components

171 further demonstrated that MKL can influence cell migration by modulating Pfn1 expression, indicating

172 ns support the hypothesis that DAN restrains cell migration by regulating cell speed.

173 ses acts in signaling pathways that regulate cell migration, cell adhesion, and proliferation.

174 Mesodermal cell migration defects in toddler mutants result from a

175 (KO) mice have shown that RB plays roles in cell migration, differentiation and apoptosis, in develo

176 Contractile forces are the end effectors of cell migration, division, morphogenesis, wound healing a

177 at Toddler signaling regulates mesendodermal cell migration downstream of Nodal signaling.

178 Cell migration drives cell invasion and metastatic progr

179 xpression on cell surfaces inhibits in vitro cell migration due to excessive adhesion.

180 liferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epith

181 200c as a critical determinant that inhibits cell migration during skin repair after injury and may c

182 he branched actin filament arrays that drive cell migration, endocytosis, and other processes.

183 l tyrosine kinase signaling network controls cell migration, epithelial organization, axon patterning

184 ly reduced the level of colony formation and cell migration facilitating ATO-induced apoptosis.

185 protein kinase that plays critical roles in cell migration, focal adhesion formation, and is an impo

186 Dermal mast cell migration from the skin to the draining lymph nodes

187 es up-regulated in hPGCLCs were enriched for cell migration genes, and their promoters were enriched

188 Rab coupling protein (RCP)-induced tumor cell migration has been implicated in tumor pathophysiol

189 nases) have emerged as central regulators of cell migration; however, the mechanisms mediating RSK-de

190 Chemotaxis is a specialized form of directed cell migration important for normal development, wound h

191 ymmetric alternating current (AC) EF directs cell migration in a frequency-dependent manner.

192 Here, we show T cell migration in a mouse model of acute lung injury wit

193 We combine theoretical modeling of cell migration in a tail-bud-like geometry with experime

194 Cell migration in a three-dimensional matrix requires th

195 ecessary for ovarian cancer tumor growth and cell migration in culture and tumor formation in mice.

196 We find that knockdown of KPNA4 reduces cell migration in multiple PCa cell lines, suggesting a

197 adiation assay that allows us to follow stem cell migration in planarians.

198 inhibited HCEC proliferation and stimulated cell migration in primary human epithelial cells.

199 However the mechanisms driving cell migration in prostate cancer patients are not fully

200 l device is therefore capable of influencing cell migration in real time and offers a convenient appr

201 cell proliferation, and dramatically reduced cell migration in response to TGFbeta.

202 tigating healing progression and endothelial cell migration in the absence and presence of an inflamm

203 cus as a model system, we query interstitial cell migration in the context of migratory barriers usin

204 us-induced gene 2 (EBI2 or GPR183) directs B-cell migration in the lymphoid follicles in response to

205 vations, manipulating CHKA did not influence cell migration in the same set of cell lines.

206 sm explaining how tenascin-C promotes cancer cell migration in the tumor microenvironment.

207 hat inhibition of ICMT significantly reduced cell migration in vitro and cancer invasion and metastas

208 AM depletion, like KDM3A depletion, inhibits cell migration in vitro and experimental metastasis in v

209 ant decrease in oncogenic transformation and cell migration in vitro as well as xenograft tumor growt

210 y altered EGF receptor trafficking, enhanced cell migration in vitro, and increased the metastatic ef

211 how that CRMP2 is required for PDGF-directed cell migration in vitro.

212 nizing signal in blood vessel-directed tumor cell migration in vivo and highlight a promising role fo

213 e the membrane source that allows bleb-based cell migration in vivo.

214 about the mechanisms that regulate mesoderm cell migration in vivo.

215 x (ECM) is a crucial precursor to collective cell migration in wound closure and cancer metastasis, r

216 Inhibition of ROCK, a key regulator of cell migration, in neuroblastoma cells highlighted that

217 scription factor NF-kappaB to promote cancer cell migration independently of MCT1 transporter activit

218 gnature of invasive cancer cell activity and cell-migration-induced ECM and collagen remodeling and r

219 hanisms by which NPM-ALK signaling regulates cell migration, invasion and contributes to the oncogene

220 d gene 1 (TUG1) induces marked inhibition of cell migration, invasion, and glycolysis through suppres

221 ft models, SOX11(+) MCL cells display higher cell migration, invasion, and growth compared with SOX11

222 tabolic activities in tumors promotes cancer cell migration, invasion, and metastasis.

223 dherin promoter, reversed EMT, and decreased cell migration/invasion.

224 Chemokine-induced directional cell migration is a universal cellular mechanism and pla

225 y, can influence T cell migration, but how T cell migration is affected by such topographical structu

226 Nor is it known precisely how villus cell migration is affected when proliferation is perturb

227 lization, focal adhesion tension, and cancer cell migration is CSD dependent.

228 Cell migration is dependent on adhesion dynamics and act

229 Cell migration is dependent on the dynamic formation and

230 Cell migration is essential for morphogenesis, organ for

231 ating that the mechanism of action for NA in cell migration is evolutionarily conserved.

232 more dynamic cell behaviors during directed cell migration is much less understood.

233 Given the importance of orchestrating cell migration, it is vital that chemokine receptor sign

234 e genes, involved in proliferation and tumor cell migration like REPIN1/AP4, ST3GAL6, TRNAU1AP and PF

235 m, that the stiffness optimum of U251 glioma cell migration, morphology and F-actin retrograde flow r

236 ification of surface proteins did not change cell migration motility nor directionality in EFs.

237 G protein-coupled receptors are critical for cell migration, not only in many fundamental biological

238 eas, thus allowing reliable and reproducible cell migration of a wide range of surface sensitive anch

239 lation that also increases CXCL12-mediated B-cell migration of normal B cells.

240 tion results in the synchronized response of cell migration on the villi.

241 al crypts is the principal driving force for cell migration on villi.

242 gulator for many essential processes such as cell migration or division.

243 ayer and in 3D sponges but did not affect MM cell migration, organization, or vasculogenesis.

244 encing prevented HuR-mediated stimulation of cell migration over the wounded area by altering the sub

245 Collective cell migration plays a pivotal role in the formation of

246 Collective cell migration plays an important role in development.

247 unction in Apc mutant cells reduces directed cell migration, potentially explaining the decreased mig

248 d post-SCI (dpi) resulted in extensive donor cell migration, predominantly neuronal and oligodendrocy

249 orepellent, is involved in the regulation of cell migration, proliferation, and angiogenesis.

250 l roles in collective cell behaviors such as cell migration, proliferation, and differentiation.

251 The results also show that cell migration, proliferation, and myogenic differentiat

252 ew branches form by "budding" or "clefting." Cell migration, proliferation, rearrangement, deformatio

253 previously identified the cancer-associated cell migration protein Tetraspanin 1 (TSPAN1) as a clini

254 lycoprotein targets of FUT8 were enriched in cell migration proteins including the adhesion molecule

255 , we aim to understand how proliferation and cell migration rates in the intestinal epithelium are re

256 idence that SIRT1 in the epidermis regulates cell migration, redox response, inflammation, epidermis

257 identify that ROCK-dependent intermittent T cell migration regulates tissue-sampling during acute lu

258 BCR signaling was mildly affected, whereas cell migration remained normal in TC10-deficient B cells

259 urther, live cell imaging and analysis of 3D cell migration reveals that alignment of collagen does n

260 ition did not modulate MCT1-dependent cancer cell migration, silencing or genetic deletion of MCT1 in

261 Here we present a cell migration simulator that predicts a stiffness optim

262 4A1 in TNBC cells plays an essential role in cell migration, SMAD7 degradation, EMT, and induction of

263 Although several methods exist to study cell migration (such as Boyden chamber assay, barrier as

264 ental to the establishment of the body axis, cell migration, synaptic plasticity, and a vast range of

265 which with PAX3-FOXO1A, contributed to tumor cell migration that was blocked by C-DIM/NR4A1 antagonis

266 As a major mediator of follicular B-cell migration, the G protein-coupled receptor Epstein-B

267 enhanced the speed and persistence of cancer cell migration through a 3D extracellular matrix in a ma

268 Tumor cell metastasis to the brain involves cell migration through biochemically and physically comp

269 R), and sortilin decreased cell survival and cell migration through decreased SRC and ERK activation.

270 Chemokines drive cell migration through their interactions with seven-tra

271 tasis or physiological events such as immune cell migration through tissue, the cells must move throu

272 Effector T cell migration through tissues can enable control of inf

273 ng these unique domains for highly efficient cell migration throughout the composite construct.

274 ll growth and an inhibitory effect on cancer cell migration, thus indicating that SOD3 might be a nov

275 shown an essential role for PLCepsilon1 in T-cell migration to inflamed skin, but not for cytokine se

276 e GI mucosal injury, TFF peptides accelerate cell migration to seal the damaged area from luminal con

277 This phenotype is attributed to decreased T-cell migration to secondary lymphoid organs (SLOs), redu

278 uitment to the salivary gland, we compared T cell migration to the salivary gland in mice that were i

279 development, commensals induce regulatory T cell migration to the skin to ensure cutaneous homeostas

280 ensin 3 (TNS3) mRNA, a negative regulator of cell migration, to inhibit its translation.

281 Ibrutinib inhibited ALL cell migration toward CXCL12 and beneath marrow stromal

282 Concordantly, SOX11(+) MCL cells have higher cell migration, transmigration through endothelial cells

283 HHSteC proliferation (AlamarBlue assay) and cell migration (transwell migration assays).

284 significantly decreased IL-6-mediated tumor cell migration, tumorsphere formation and ALDH-positive

285 Collective cell migration underlies many biological processes, incl

286 haracterize WRAMP structures during extended cell migration using live-cell imaging.

287 We found that epithelial cell migration velocities along the villi are coupled to

288 f p38 MAPK to influence actin remodeling and cell migration via a zyxin-independent process.

289 el mechanism by which IL-37 suppressed tumor cell migration via its intracellular mature form (amino

290 results clearly showed that GPAM influenced cell migration via the signaling lipid lysophosphatidic

291 e release by IFC tissue, less monocyte and T cell migration was detected in a chemotaxis system.

292 coordinate its downstream targets in guiding cell migration, we develop an optogenetic tool for Plexi

293 Although best known for its role in cell migration, we recently showed that the ability of C

294 cts in CXCL12-mediated CXCR4 signaling and B-cell migration, whereas B cells from IgM-deficient mice

295 Removal of centrosome impairs directional cell migration, whereas the removal of nucleus alone mak

296 e lymphatics stimulates YAP1 to drive cancer cell migration; whereas intensities of fluid wall shear

297 Cell migration, which is central to many biological proc

298 vents EC proliferation, but does not prevent cell migration, which relies instead on aerobic glycolys

299 ly enriched at the cell front during dynamic cell migration, which requires the Pumilio-related RNA-b

300 wn of Sgpl1 in rat mesangial cells inhibited cell migration, which was partially rescued by VPC23109,