ライフサイエンスコーパス: cell migration

1 iated focal adhesions (FAs) is essential for cell migration.

2 major regulator of collective versus single cell migration.

3 ct of hypoxia on FN matrix reorganization or cell migration.

4 riction, convergent extension and collective cell migration.

5 pressed in fetal cardiomyocytes and promotes cell migration.

6 to animal cells, crawl using actin-mediated cell migration.

7 ntial processes, ranging from cytokinesis to cell migration.

8 ophages altered cell morphology and impaired cell migration.

9 H in AP-1B-positive cells) slowed epithelial-cell migration.

10 inhibition of Akt activity and reduction in cell migration.

11 thelial cells reduced the tube formation and cell migration.

12 alternative splicing and polyadenylation in cell migration.

13 ghly invasive mesenchymal transformation and cell migration.

14 ale grooves to promote neurite outgrowth and cell migration.

15 and Rac1/Cdc42-GTPase signaling critical for cell migration.

16 surrounding the lens was a barrier to immune cell migration.

17 adhesion turnover, and increased epithelial cell migration.

18 ions and stabilizes cell polarization during cell migration.

19 ular signal-regulated kinase 1/2 and promote cell migration.

20 hether PGs regulate Fascin to promote border cell migration.

21 ity, modulated RNA processing, and inhibited cell migration.

22 es the timing of wound repair by controlling cell migration.

23 ctively downregulates IL-6 but also inhibits cell migration.

24 n is a general mechanism for ensuring robust cell migration.

25 R3 from CCA cells impaired proliferation and cell migration.

26 eceptor stimulation and mediating fibroblast cell migration.

27 ore, enhanced nuclear plasticity can promote cell migration.

28 matrix (ECM) organization, angiogenesis and cell migration.

29 er and size of focal adhesions, and impaired cell migration.

30 d, contrary to LAPTM4B-35, failed to promote cell migration.

31 n contribute to the regulation of collective cell migration.

32 t links calcium influx to FA turnover during cell migration.

33 F-actin (MPA) during membrane protrusion and cell migration.

34 d with alternative signaling for directional cell migration.

35 ithelial-mesenchymal transition, and induces cell migration.

36 inhibits Rho activity to enhance directional cell migration.

37 porin-5 (AQP5) plays a role in breast cancer cell migration.

38 l activation of the GTPase and for efficient cell migration.

39 nosine triphosphatase (GTPase) Rac1 mediates cell migration.

40 rs, and stimulated melanoma transendothelial cell migration.

41 ntly, the transfection of each miRNA impeded cell migration.

42 d populate hair follicles through long-range cell migration.

43 NAs to cellular protrusions is a hallmark of cell migration.

44 active VAV3 is involved in ERBB4-stimulated cell migration.

45 ated to the cytoskeleton, cell adhesion, and cell migration.

46 a key regulator of their translation during cell migration.

47 its role in regulating single and collective cell migration.

48 fibers provide topological cues that direct cell migration.

49 ted with CRC progression and promoted HCT116 cell migration.

50 type and evidence for hepatoblast collective cell migration.

51 y in a signaling pathway relevant for cancer cell migration.

52 are fully consistent with their promotion of cell migration.

53 tom computational algorithm for viscoelastic cell migration.

54 atiotemporal mobilization of Ca(2+) to drive cell migration.

55 le for the RAP1/RAC1 signaling axis in HNSCC cell migration.

56 on and as a regulator of mechanically guided cell migration.

57 lly be slowed by disrupting the machinery of cell migration.

58 egrin-linked, ras-like protein that promotes cell migration.

59 s its functional significance on chemotactic cell migration.

60 point factors that play an essential role in cell migration.

61 r directing RAB13 GTPase activity to promote cell migration.

62 mesenchymal spheroids and different modes of cell migration.

63 , and the gradient in turn drives and guides cell migration.

64 otein (MAP) kinases, NF-kappaB signaling, or cell migration.

65 llowed high-content time-resolved imaging of cell migration.

66 ct subcellular compartments to drive forward cell migration.

67 ain development, beginning with neural crest cell migration.

68 der, for reconstructing the routes of cancer cell migrations.

69 of key adhesion molecules involved in immune cell migration across the BBB in vivo.

70 normal cellular processes such as signaling, cell migration, adhesion to the extracellular matrix, an

71 an important developmental gene involved in cell migration, adhesion, and morphogenesis.

72 To address this, we use Drosophila border cell migration, an invasive, collective migration that o

73 The combination with cell migration analysis and traction force microscopy sh

74 as required for TGFbeta-induced increases in cell migration and adhesion dynamics.

75 letion may coordinate vascular smooth muscle cell migration and adhesion to different extracellular m

76 Cell migration and affinity results indicated that the c

77 hat loss of PI4KIIIbeta expression decreases cell migration and alters cell shape in NIH3T3 fibroblas

78 ent for Rho-GAP activity and for suppressing cell migration and anchorage-independent growth.

79 idual GRASP proteins, focusing on GRASP65 in cell migration and apoptosis and GRASP55 in unconvention

80 d by sorting through concentration dependent cell migration and apoptosis, independent of the morphog

81 d previously identified roles in melanocytic cell migration and apoptosis.

82 es cellular adhesions and regulates melanoma cell migration and cell-cell interactions.

83 ugh its effects on TRPM4 that KCTD5 promotes cell migration and contractility.

84 nonselective cationic channel that regulates cell migration and contractility.

85 surfaces provide a unique framework to probe cell migration and cytoskeletal dynamics in a standardiz

86 key regulator of ribosome biogenesis during cell migration and demonstrate a role for this process i

87 p27 also regulates other processes including cell migration and development independent of its cyclin

88 Cell migration and differentiation were also impeded by

89 s of adhesion molecules in collective cancer cell migration and discuss the utility of three-dimensio

90 Loss of Pxt results in both delayed border cell migration and elongated clusters, whereas somatic P

91 in A induced ligand-dependent CRC epithelial cell migration and epithelial to mesenchymal transition

92 evolution to couple phagocytic processing to cell migration and facilitate space exploration by immun

93 is activity is required in vivo for directed cell migration and for maintaining normal levels of F-ac

94 s HT C1, C2, C4 and C6 inhibited endothelial cell migration and formation of tubular-like structures.

95 Cell migration and glucose uptake assays combined with p

96 ses play an important role in the control of cell migration and have been implicated in Ras-mediated

97 ported by additional data indicating reduced cell migration and increased alphavbeta3 and alphavbeta5

98 ss and signaling mechanisms linked to immune cell migration and inflammation.

99 ultured from PDACs from mice and analyzed in cell migration and invasion assays and by immunoblots, r

100 aled that RAB11B-AS1 increased breast cancer cell migration and invasion in vitro and promoted tumor

101 Further, silencing furin reduced tumor cell migration and invasion in vitro and tumor growth an

102 P2 overexpression significantly promotes GBM cell migration and invasion in vitro, and GBP2 silencing

103 measured gene expression, binding activity, cell migration and invasion, and transcriptional activit

104 GLS2 was linked to enhanced in vitro cell migration and invasion, mesenchymal markers (throug

105 olecular mechanism by which ZNF750 regulates cell migration and invasion, suggesting a role in breast

106 otypes, which leads to functional changes in cell migration and invasion.

107 ion, and is necessary and sufficient for RMS cell migration and invasion.

108 lular signaling to increase nAR-negative BCa cell migration and invasion.

109 R (mAR-SLC39A9) to increase nAR-negative BCa cell migration and invasion.

110 s of MMP-9 markedly inhibited MCV sT-induced cell migration and invasion.

111 eta-catenin nuclear translocation to promote cell migration and invasion.

112 lates cytoskeletal dynamics to promote tumor cell migration and invasion.

113 factor beta (TGFbeta)-induced breast cancer cell migration and invasion.

114 1 (AQP1) channels and impairs AQP1-dependent cell migration and invasiveness in cancer cell lines.

115 tegrators of chemotactic cues in directional cell migration and may serve as candidate therapeutic ta

116 at regulate a variety of processes including cell migration and oriented cell divisions.

117 decreased exosome functions to promote tumor cell migration and other activities, which could contrib

118 that an interplay between mechanical forces, cell migration and proliferation allows jellyfish fragme

119 microfluidic assay for the quantification of cell migration and proliferation can categorize patients

120 t supports a Warburg phenotype with enhanced cell migration and proliferation characteristics.

121 lation system can provide insight into CAR T-cell migration and proliferation during clinical trials

122 arkedly inhibited mitochondrial respiration, cell migration and proliferation of various cancer cells

123 Cell migration and proliferation were also significantly

124 mediator by increasing intestinal epithelial cell migration and proliferation, and highlight potentia

125 egulation of organogenesis, differentiation, cell migration and proliferation.

126 r (EGFR) signaling cascade is known to drive cell migration and proliferation.

127 BALB/3T3 and NHDF cultures, inhibited cancer cell migration and reduced ROS formation.

128 ncer cell adhesiveness, impairs HGF-mediated cell migration and reduces 3D invasion.

129 inin (alpha-actinin) 4 is critical for tumor cell migration and remodeling of the extracellular matri

130 after KD of Dsc2 revealed delayed epithelial cell migration and repair after scratch-wound healing as

131 in, which is likely to be relevant to cancer cell migration and response to microtubule-modulating th

132 Mutations that impact immune cell migration and result in immune deficiency illustrat

133 choring; however, colonization also requires cell migration and spreading over surfaces.

134 trafficking mechanism required for polarized cell migration and stem cell-driven tissue repair.

135 vidence that FASN activity directly promotes cell migration and supports FASN as a potential therapeu

136 They can directly accelerate malignant cell migration and the formation of metastases.

137 r cells, and knockdown of HSATII RNA reduces cell migration and the rate of cell proliferation.

138 ntrol of the cell cycle, cell proliferation, cell migration and vesicle trafficking.

139 Our findings suggest that cell-migration and proliferation levels can predict pati

140 e show that low U1 AMO doses increase cancer cells' migration and invasion in vitro by up to 500%, wh

141 ctions in the regulation of cell morphology, cell migration, and actin cytoskeleton remodeling.

142 ways linked to acute inflammation and immune cell migration, and activated the NF-kappaB complex alon

143 , such as epithelial-mesenchymal transition, cell migration, and cell invasion.

144 with Slit ligands to mediate axon guidance, cell migration, and cell positioning in development.

145 tions for intracellular signal transduction, cell migration, and differentiation.

146 with cellular response to external stimuli, cell migration, and immune response (inflammation-based)

147 ogical processes such as cell proliferation, cell migration, and morphogenesis.

148 all GTPase 1 signaling, increased epithelial cell migration, and mucosal wound repair.

149 related to myeloid cell activation, myeloid cell migration, and phagocytosis.

150 s and the expression of profibrotic targets, cell migration, and soft agar colony formation stimulate

151 s that control epicardium-derived progenitor cell migration, and the functional contributions of the

152 enhance macropinocytosis negatively regulate cell migration, and vice versa.

153 a number of physiologic processes, including cell migration, angiogenesis, barrier function, and infl

154 s cancer cell adhesion to collagen, promotes cell migration, anoikis resistance, mesothelial clearanc

155 ies, in which cytoskeletal rearrangement and cell migration are altered, such as metastatic cancer.

156 s changes in the actin cytoskeleton to drive cell migration are still unclear.

157 4 and FCW66 were shown to inhibit MDA-MB-231 cell migration as effectively as ST3GALIII-gene knockdow

158 dent and is required for invasive MDA-MB-231 cell migration as well as for gelatin degradation in pri

159 that is not captured in traditional in vitro cell migration assays performed on flat, unconfined two-

160 Invadopodia formation and cell migration assays were performed for invasive breast

161 leton counteracted this regulation in single cell migration assays.

162 ns are also expressed during murine cortical cell migration at earlier developmental stages.

163 echanical confinement can variably influence cell migration behaviors, and it is presently unclear wh

164 ellar-dependent swimming and actin-dependent cell migration, both of which are used by animal cells a

165 class I PI3K mediated oncogenic MET-induced cell migration but not anchorage-independent growth.

166 Talin critically controls integrin-dependent cell migration, but its regulatory role in skin dendriti

167 f 46 protein ligands that induce chemotactic cell migration by activating a family of 23 G protein-co

168 her, the results suggest that Abi1 regulates cell migration by affecting Pfn-1 and N-WASP, but not pV

169 tinct microtubule dynamics regulate amoeboid cell migration by locally promoting the retraction of pr

170 now recognized as an important regulator of cell migration, cancer cell invasion, and vesicular cont

171 discovery rate < 10%), showing enrichment in cell migration, cell adhesion, developmental process, sy

172 proteins, with important regulatory roles in cell migration, cell cycle control, and apoptosis.

173 ures that provide important functions during cell migration, cell division, and cell signaling [1].

174 trol cell division, cell-type specification, cell migration, cellular differentiation, and cell death

175 However, cell migration chromatography, the sorting of large popu

176 l human cancer cell lines and inhibits tumor cell migration, contains an unusual 2-acyl-4-hydroxy-3-m

177 Pase ARL4C participates in the regulation of cell migration, cytoskeletal rearrangements, and vesicul

178 e major driver of lamellipodia formation and cell migration downstream of RAC1 and depends on NCKAP1

179 Directional cell migration drives embryonic development, cancer meta

180 mice, or CRISPR/Cas9 gene editing decreased cell migration due to the longer duration of the station

181 ER-FA contacts, thus promoting FA growth and cell migration during chemotaxis.

182 lved in inflammatory responses (e.g., Saa4), cell migration (e.g., Ccl3, Ccl5, or Cxcl10), APC activa

183 Here, we report a unique mode of cell migration elicited by the lability of integrin liga

184 branched actin filament networks pivotal for cell migration, endocytosis and pathogen infection.

185 Cell migration entails networks and bundles of actin fil

186 ad and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases and is cor

187 l and extracellular matrix changes mediating cell migration, fibrosis, remodeling and regeneration.

188 enhanced cytolytic potential and requires T cell migration from lymph nodes for therapeutic efficacy

189 ne nucleotide exchange factors that regulate cell migration, fusion and viability.

190 lds (EFs) have significant effects on cancer cell migration (galvanotaxis/electrotaxis), however, the

191 veal a requirement for PCP in their oriented cell migration guided by WNT5A.

192 back mechanism, which results in defective T cell migration, impaired T cell function, and loss of ho

193 of IRS2 activated PI3K signaling, promoting cell migration in a PI3K-dependent manner, this did not

194 ism for fine-tuning cell-ECM adhesion during cell migration in development.

195 nes and their receptors are orchestrators of cell migration in humans.

196 eraction energies and lead to enhancement of cell migration in metastatic cholangiocarcinoma.

197 ompliant hydrogels could predict 1D confined cell migration in microfluidic channels.

198 Here we demonstrate, using primordial germ cell migration in mouse as a developmental model, that s

199 ion, anchorage-independent colony formation, cell migration in vitro, and lung metastasis in vivo.

200 IFT20 is implicated in regulating cell migration independently of the primary cilium, but

201 sine-14, as well as suppressed CAV1-enhanced cell migration, invasion and Rac-1 activation in B16F10,

202 Effects on cell migration, invasion, and cytoskeletal organization

203 found that LINC00313 overexpression inhibits cell migration, invasion, and tube formation, and this s

204 Cell migration involves dynamic changes in cell shape.

205 Cell migration is a dynamic process that entails extensi

206 ading to questions about whether directional cell migration is alike or distinct under these differen

207 Collective cell migration is central to many developmental and path

208 Subsequently, cell migration is diminished in stiff environments.

209 Cell migration is driven by local membrane protrusion th

210 Cell migration is driven by pushing and pulling activiti

211 Smooth muscle cell migration is essential for many diverse biological

212 Sustained cell migration is essential for wound healing and cancer

213 Although T cell migration is most frequently defined in the context

214 Cancer cell migration is often guided by cell protrusions, whos

215 l tentacles are significantly shortened, and cell migration is promoted.

216 One of the constraints during cell migration is the diameter of the pores through whic

217 hesive gap closure model in which collective cell migration, large-scale actin-network fusion, and pu

218 ne exchange factor involved in hematopoietic cell migration, lead to immunodeficiency and, paradoxica

219 ium, but how IFT proteins integrate with the cell migration machinery is poorly understood.

220 Targeting the gut microbiota or T cell migration may represent therapeutic strategies for

221 y processes, including inflammation and germ cell migration, means that self-generated gradients are

222 vel role at the basal plasma membrane during cell migration might be an anticancer mechanism.

223 Using the Drosophila border cell migration model, we find that Protein phosphatase 1

224 sults show that nuclear stiffness limits the cell migration more than the ECM rigidity.

225 regulates angiogenesis, actin dynamics, and cell migration/motility.

226 Directional cell migration normally relies on a variety of external

227 the basal plasma membrane during collective cell migration of epithelial sheets.

228 ive regions of cells is important for single-cell migration on two-dimensional surfaces.

229 closely related and underlies the idea that cell migration operates by a common set of physical prin

230 Since LOX is an established player in cancer cell migration, our results imply that Atox1 mediates br

231 Movement is achieved by active cell-on-cell migration: outer cells migrate with apical, centrip

232 ceramide acutely regulates cell adhesion and cell migration pathways with weak connections to commonl

233 that the dynamic SPHARM analysis classifies cell migration patterns more accurately than the static

234 om dynamic SPHARM improves classification of cell migration patterns.

235 lines, we identified and characterized three cell migration phenotypes, where different syndecans are

236 that MAGP1-rich microfibrils support immune cell migration post-injury.

237 ASN, RhoU and Cdc42 that directly influences cell migration potential.

238 ial importance during embryonic neural crest cell migration, proliferation and differentiation.

239 ting important cellular processes, including cell migration, proliferation, and survival.

240 l adhesion, and actin remodeling, as well as cell migration, proliferation, and survival.

241 nd activates signaling pathways that promote cell migration, proliferation, and survival.

242 and increased the tryptophan consumption and cell migration rates in non-tumor cells.

243 emodeling complex PRC2 and downregulation of cell migration-regulating genes.

244 ities and differences in gene expression and cell migration regulation of different glial cell types

245 the mechanisms governing PKA activity during cell migration remain largely unknown.

246 ion and maintenance of EGFR signaling during cell migration remains limited.

247 Individual cell migration requires front-to-back polarity manifeste

248 uency of neutrophil reverse transendothelial cell migration (rTEM).

249 ased the amount of active CDC42 and enhanced cell migration significantly more than WT IQGAP1.

250 The success of the base cell-migration simulation model suggests its future appl

251 Here, we assessed whether a cell migration simulator and associated parameters previ

252 glucocorticoids regulate a dynamic mode of B cell migration specialized for rapid exchange between bo

253 lution the evolving spatiotemporal fields of cell migration speeds, cell shapes, and traction forces

254 ity using a LYCAT mimetic peptide attenuated cell migration, suggesting a novel role for LYCAT activi

255 analysis of cell protrusion formation during cell migration that is regulated by subcellular mitochon

256 cells displayed defects in polarization and cell migration that were rescued by uncoupling VE-cadDEE

257 , short-range lipid signals, regulate single cell migration, their roles in collective migration rema

258 of the copper transporter ATP7A also reduced cell migration, these proteins appear to be on the same

259 se, as well as formation of pancospheres and cell migration; these activities were not observed in ce

260 Cell migration through a three-dimensional (3D) extracel

261 l light-sheet microscope geometry, including cell migration through confined spaces within a microflu

262 s and examine their effects on breast cancer cell migration through exosome-mediated delivery.

263 and deletion of Myo9b in leukocytes impairs cell migration through increased Rho activity.

264 Downstream of PI3K, Rac1 mediated cell migration through its GTPase activity, whereas inde

265 ECM rigidity-determine the effectiveness of cell migration through the dense ECM.

266 als, cell-matrix adhesions are essential for cell migration, tissue organization, and differentiation

267 r cellular function, e.g., in the context of cell migration, tissue organization, and morphogenesis.

268 Tumor cell migration to LECs was inhibited by blocking CXCL11

269 plays multiple critical roles in cells, from cell migration to organelle dynamics.

270 cells, knockout of HuR impaired splenic Th17 cell migration to the CNS and abolished the disease.

271 n-specific CD8 T cells in vivo, induce CD8 T cell migration to the tumor site, delay tumor growth and

272 binding of E-selectin, a central molecule in cell migration, to its glycosylated ligands expressed on

273 rder cells, an established model for in vivo cell migration, to study how chemical and physical infor

274 ve that the inhibitory effect of Tf@pSiNP on cell migration, together with the drug-delivery capabili

275 -EGFR signaling axis coordinates neighboring cell migration toward oncogenic cells and is required fo

276 fficient for regulation of cell adhesion and cell migration under chemotherapeutical stress.

277 Here, we quantify dendritic cell migration under well-defined 2-dimensional confinem

278 ith beta1 integrin in focal adhesions during cell migration using confocal microscopy and total inter

279 dition) over a 9-h time series revealed that cell migration velocity and directionality are significa

280 ion of cell shape and polarity, cytokinesis, cell migration, vesicle trafficking, and receptor signal

281 ults imply that Atox1 mediates breast cancer cell migration via coordinated copper transport in the A

282 xploited for the inhibition of breast cancer cell migration via the exosome-mediated delivery.

283 in-siRNA or ANP-siRNA HK-2 cells on EA.hy926 cell migration was determined by scratch-wound healing a

284 Using an in vitro wound healing assay, cell migration was evaluated 2, 4, 6, and 24 hours after

285 igand for MET, to promote AKT activation and cell migration was significantly greater when IQGAP1-nul

286 Cancer cell migration was then surveyed in the presence of EFs

287 l molecular insights into a putative role in cell migration, we here investigated breast cancer cell

288 itory effects on AQP5 protein expression and cell migration were demonstrated in MDA-MB-231 cells.

289 , and some instances of potential tangential cell migration were noted.

290 P on PC12 cell neurite outgrowth and Schwann cell migration were similar to those caused by other pro

291 Likewise, depletion of TAZ compromised cell migration, whereas its overexpression enhanced migr

292 (PI3K) mediates both cell proliferation and cell migration, whereas the small guanosine triphosphata

293 New work identifies a mechanism of cell migration whereby cellular mechanical forces dissoc

294 Tumor invasion requires efficient cell migration, which is achieved by the generation of p

295 acellular matrix-related gene expression and cell migration, which is relevant to IPF development.Obj

296 matrix-related gene expression and promotes cell migration, which may contribute to the pathogenesis

297 by shRNA reduced human airway smooth muscle cell migration, which was restored by Abi1 rescue.

298 sed transepithelial resistance but increased cell migration, with increased expression of extracellul

299 ecreases F-actin levels and impairs directed cell migration without altering microtubule organization

300 d alpha-smooth muscle actin (alpha-SMA), and cell migration/wound healing.