ライフサイエンスコーパス: cell contact

1 bohydrates over time, induced by endothelial cell contact.

2 tructure and function following de novo cell-cell contact.

3 rized virus assembly and budding at sites of cell contact.

4 s junction maturation following de novo cell-cell contact.

5 romote cancer invasion through direct cancer cell contact.

6 ration to the tips of myofibers through cell-cell contact.

7 te burden through a mechanism independent of cell contact.

8 f Tfh cells from lymph nodes after dendritic cell contact.

9 bacteria exchange toxins via direct cell-to-cell contact.

10 ival through a mechanism partly dependent on cell contact.

11 1 expression, resulting in insufficient cell-cell contact.

12 growth factor receptor (EGFR) in response to cell contact.

13 s that involved the gamma-delta TCR and cell-cell contact.

14 1 structural protein Gag to the site of cell-cell contact.

15 eased by the TGF-beta/Smad3 pathway and cell-cell contact.

16 s inhibit mitogenic signaling in response to cell contact.

17 h Eph receptors is largely dependent on cell-cell contact.

18 polymerization at the site of bacterium-host cell contact.

19 as induced during cell proliferation by cell-cell contact.

20 s such as E-cadherin are present at the cell-cell contact.

21 se in response to apoptotic stimuli and cell-cell contact.

22 ial competition that requires direct cell-to-cell contact.

23 on of the small GTPase RhoA at sites of cell-cell contact.

24 th an egg via a close-range signal or direct cell contact.

25 ed in a very short time and required cell-to-cell contact.

26 signaling proteins directly at sites of cell-cell contact.

27 robust luminescent signal within minutes of cell contact.

28 organization and dynamics near sites of cell-cell contact.

29 sion and arises as a result of intimate cell-cell contact.

30 lls change their direction of migration upon cell contact.

31 fasciculation, and can act independently of cell contact.

32 protein localization, and detection of cell-cell contact.

33 al for the up-regulation of the T3SS on host cell contact.

34 vesicles that move to the synapse on target cell contact.

35 ht that ephrin-Eph signaling requires direct cell contact.

36 ibody, which greatly reduced pilus-dependent cell contact.

37 may contribute to the reinforcement of cell-cell contacts.

38 cardiomyocytes disrupts localization at cell-cell contacts.

39 epithelial polarity, as well as proper cell-cell contacts.

40 atures by perturbing cell-substrate and cell-cell contacts.

41 This HIV-1 transmission was mediated by cell-cell contacts.

42 he existence of oligomeric cadherins at cell-cell contacts.

43 eres with the initiation of sustainable cell-cell contacts.

44 t direct cell-to-cell transmission at immune cell contacts.

45 within the trabecular layer to form new cell-cell contacts.

46 hrough the formation of uropod-mediated cell-cell contacts.

47 ts cell proliferation upon establishing cell-cell contacts.

48 hrough the formation of uropod-mediated cell-cell contacts.

49 tecture through apicobasal polarity and cell-cell contacts.

50 (DC) functions via soluble mediators or cell-cell contacts.

51 Src and stimulates Src signaling along cell-cell contacts.

52 in the cytoplasm at the cell edges and cell-cell contacts.

53 ein CdGAP, a GAP for Rac1 and Cdc42, at cell-cell contacts.

54 PLP1 forms homotypic trans complexes at cell-cell contacts.

55 yosin network, which limits the expansion of cell contacts.

56 ithout a corresponding reinforcement of cell-cell contacts.

57 ogenic stimulus, physical disruption of cell-cell contacts a tolerogenic stimulus.

58 -1) can efficiently spread by direct cell-to-cell contact, a mechanism termed cell-associated HIV tra

59 reduction in cell adhesion, a lack of proper cell contacts, a loss of VE-cadherin, and aberrant actin

60 , Klf4 and Esrrb transcript repression, cell-cell contact abrogation, cell survival in suspension, ST

61 Here we show that in the absence of cell-cell contact, actomyosin contractility suppresses YAP ph

62 , substantiated by a requirement for cell-to-cell contact, aggregation, and FcepsilonRI-dependent sig

63 we present a model in which macrophage/tumor cell contact allows for the transfer of cytoplasmic mole

64 Cell-cell contacts also direct ingression of the cleavage fur

65 was found to be independent of loss of cell-cell contact and Activin/Nodal-dependent pluripotency an

66 . fumigtaus in vitro, which does not require cell contact and can be recapitulated by eosinophil whol

67 was employed to decouple the effects of cell-cell contact and cell-matrix adhesion in TGFbeta1-induce

68 in a larger culture, allowing native cell-to-cell contact and communication even during vigorous acti

69 tion with miR-142-3p mimic inhibited cell-to-cell contact and fusion, decreased protein kinase C alph

70 tory cytokines such as IL-10 and direct cell-cell contact and have been linked to experimental models

71 eling of endosomes occurs within 30 min of T cell contact and involves ligation of HLA-A2 and ICAM-1

72 spindle reorientation is dependent on a new cell contact and on HS and SDN-1.

73 delling to facilitate cadherin-mediated cell-cell contact and promote beta-catenin signalling.

74 f ephrin-Eph signaling independent of direct cell contact and proteolytic cleavage and suggest the pa

75 Notch receptor pathway is responsive to cell-cell contact and regulates keratinocyte growth and diffe

76 pear to be mediated through both direct cell-cell contact and secreted ligands.

77 Furthermore, the importance of cell-to-cell contact and soluble products for gamma9delta2 T cel

78 Requirements for cell contact and specific cell type in ORMDL3 induction

79 In addition to direct cell-to-cell contact and the secretion of soluble factors, EVs f

80 hin 24 hours that were shown to exhibit cell-cell contact and uniform size (201 +/- 2 mum).

81 Syndrome patients strongly destabilize cell-cell contacts and (ii) CdGAP mRNA levels are inversely c

82 epithelium results in disruption of the cell-cell contacts and acquisition of a mesenchymal phenotype

83 pendent growth, reduced ability to form cell-cell contacts and chromosomal aberrations.

84 ant ECM component that forms fibrils through cell contacts and creates directionally biased geometry.

85 ressed adhesion molecule that regulates cell-cell contacts and facilitates leukocyte transendothelial

86 ional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of different

87 , epithelial cell islands rupture their cell-cell contacts and migrate away as single cells on the ex

88 , both infected MDMs and DCs rely on cell-to-cell contacts and nectin-4 to efficiently deliver MeV to

89 the barrier on the dynamic nature of cell-to-cell contacts and perijunctional actin.

90 y some chemotherapeutic agents required cell-cell contacts and proceeded through an endocytic pathway

91 more complete EMT, including disrupted cell-cell contacts and reduced E-cadherin expression, and pro

92 ve guidance does not require persistent cell-cell contacts and strong short range adhesion.

93 whether they do so directly via stable cell-cell contacts and sustained TCR signals.

94 sis requires the formation of stable cell-to-cell contacts and the establishment of apicobasal polari

95 rupted and a tension difference between cell-cell contacts and the free cell surface at gaps of 0.003

96 se they are well positioned to form the cell-cell contacts and to provide the intercellular communica

97 Effector secretion is triggered by host cell contact, and before contact is prevented by a set o

98 was blocked by anti-4-1BBL Ab, required cell-cell contact, and did not require the cytoplasmic signal

99 pression in primary leucocytes required cell-cell contact, and induction was suppressed by plasmacyto

100 h cells move away from each other after cell-cell contact, and it contributes to malignant invasion a

101 the assembly of the LGN/NuMA complex at cell-cell contacts, and define a mechanism that couples cell

102 lial cells lose apicobasal polarity and cell-cell contacts, and gain mesenchymal phenotypes with incr

103 cells, requires the formation of stable cell-cell contacts, and is an active, calcium-dependent proce

104 namic vascular shear stress, and endothelial cell contacts, and it supports high-resolution live-cell

105 stiffness, adhesion ligand density, or cell-cell contacts, and thus strongly influences cell fate.

106 present in Streptococcus intermedius mediate cell contact- and Esx secretion pathway-dependent growth

107 mEF is greater at higher densities when cell-cell contacts are abundant.

108 Furthermore, cell contacts are generated dynamically from positions o

109 n distance and is independent of direct cell-cell contact.ARMMs are extracellular vesicles that bud d

110 n assembly and turnover at newly formed cell-cell contacts as well as for human epithelial lumen form

111 n and transparent diffusion barrier in solar cell contacts, as an intermediate layer in tandem solar

112 luated by using in vitro suppression assays, cell-contact assays, and gene expression panels.

113 ts by sterically interfering with close cell-cell contacts at the NK cell-target cell interface that

114 PGE2 secretion is down-regulated by cell-to-cell contact, attenuating its immunomodulatory potency.

115 to reach their internal position, revealing cell-contact avoidance as an unexplored mechanism drivin

116 on of specific T cells was dependent on cell-cell contact between B cells and moDCs, which was explai

117 occurred rapidly (within 3-4 h) and required cell contact between the iNKT cells and monocytes.

118 e order, with the entry points determined by cell contact between the sensory ganglion cell bodies an

119 ral coculture systems, and found that direct cell contact between the two cell types significantly in

120 The establishment of cell-cell contacts between presynaptic GABAergic neurons and

121 ytokinesis, the remodelling of adhesive cell-cell contacts between the dividing cell and its neighbou

122 At cell-cell contacts, both Elmo2 and Dock1 are essential for th

123 lecular role of E-cadherin not only for cell-cell contact but also for clonal propagation of hPSCs.

124 nt of Tat, (iii) did not require direct cell-cell contact but appeared rather to be mediated by solub

125 Inhibition of cell proliferation in cell-contacted but immature monolayers recapitulated thi

126 cle arrest upon mitogen deprivation and cell-cell contact, but did contribute to RAS(V12)- and radiat

127 mer is not only recruited to the apical cell-cell contacts by binding to Crb but depends on functiona

128 phocytes occurs at retrovirus-induced immune cell contacts called virological synapses (VS).

129 emonstrated that complete disruption of cell-cell contact can promote transforming growth factor (TGF

130 mportant cellular processes involved in cell-cell contact, cell adhesion and motility.

131 by intrinsic cell machineries, such as cell-cell contact, cell polarity, and actin cytoskeleton, as

132 ar and intracellular signals, including cell-cell contact, cell polarity, mechanical cues, ligands of

133 tions to heterogeneity from cell cycle, cell-cell contact, cell stochasticity and heritable morpholog

134 membrane-binding adaptor involved in cell-to-cell contact/communication, to capture the Bro1 domain o

135 he formation of STK11-dependent lateral cell-cell contacts competent for tyrosine kinase signaling pr

136 V infection resulted in aberrant TNT cell-to-cell contact, compromising HIV spread and replication.

137 Neuroepithelial stem cells contact CSF-filled ventricles, proliferate, and di

138 eir suppressive effect appears to be cell-to-cell contact dependent and may involve CTLA-4 signaling

139 DC cross-dressing was cell-contact dependent and unaffected by lipid raft disr

140 ation by FOXP3(+) iNKT cells was found to be cell contact-dependent and was accompanied by a reduced

141 T6SSs are a class of sophisticated cell contact-dependent apparatuses involved in mediating

142 ells were rendered more capable of eliciting cell contact-dependent brain endothelial cell dysfunctio

143 beta pathway on breast cancer cells, we used cell contact-dependent cell growth and clonogenicity ass

144 eripheral blood mononuclear cells elicited a cell contact-dependent expansion of MDSCs.

145 surface of producer cells where it mediates cell contact-dependent killing.

146 d apoptosis of primary murine HSCs in a cell-cell contact-dependent manner, involving Fas-ligand (CD9

147 s by promoting tumor cell intravasation in a cell contact-dependent manner, resulting in elevated num

148 zebrafish by controlling cell polarity in a cell contact-dependent manner.

149 One key competition strategy includes cell contact-dependent mechanisms of interbacterial anta

150 cell density that occurs in these settings, cell contact-dependent mechanisms of interbacterial anta

151 olecules and inhibitory cytokines as well as cell contact-dependent mechanisms.

152 Here we provide evidence for cell contact-dependent orientation of planar cell divisi

153 th bulk cell stiffness and stiffness of cell-cell contacts dictating the invasion pattern.

154 E-cadherin clusters throughout lateral cell-cell contacts display dynamic movements in the plane of

155 interplay between cell polarization and cell-cell contact drives the segregation of these lineages, p

156 Induction of PTPRF by cell-cell contact during cell proliferation quenched the acti

157 Cell contact during CIL requires the participation of th

158 ereby by-passing the requirement for cell-to-cell contact during toxin delivery.

159 cal constriction and the anisotropic loss of cell contacts during NB ingression.

160 n-dependent adaptation of AJs regulates cell-cell contact dynamics and coordinated collective cell mi

161 ix and in vivo, associated with altered DC-T cell contact dynamics and T cell polarization.

162 We surmise, however, that cell-cell contacts enabling HIV-1 fusion with the plasma memb

163 is controlled, the presence of partial cell-cell contacts enhances expression of alphaSMA.

164 ls in social microwells, which allow cell-to-cell contact, exhibited significantly higher levels of I

165 CD73 associated with cell-cell contacts, filopodia, and membrane zippers, indicati

166 the anchoring of cadherin to actin and cell-cell contact fluidity.

167 species induces loss of E-cadherin-mediated cell contact, followed by a regenerative phase, during w

168 the regulation of its production by cell-to-cell contact, followed by the determination of its immun

169 cible T-cell costimulator (ICOS)-ICOS ligand cell contact for Treg cell-mediated ILC2 suppression alo

170 Cell-cell contact formation is a dynamic process requiring th

171 adhesion assay and live cell imaging of cell-cell contact formation revealed that inhibition of Cdc42

172 obust to severe perturbations affecting cell-cell contact formation.

173 alized by active Cdc42 at the external, cell-cell contact-free surfaces of apically constricting cell

174 esis, we found that the expression of a cell-cell contact gene, Desmoplakin, is greatly reduced in No

175 ypes and formation of multiple sites of cell-cell contact, giving rise to nascent fusion pores whose

176 iators, including soluble factors and direct cell contact, have been identified, but roles for the in

177 HLSECs internalized HCV, independent of cell-cell contacts; HCV RNA was translated but not replicated

178 to examine how the presence of partial cell-cell contacts impacts EMT.

179 infection through both cell-free and cell-to-cell contact in a dose-dependent manner.

180 betaII-spectrin colocalize at sites of cell-cell contact in columnar epithelial cells and promote la

181 Therefore, we propose that loss of cell contact in epidermal keratinocytes through reactive

182 or NKG2D-ligand interaction via homotypic NK cell contact in NK cell effector function.

183 hages transfer cytoplasm to tumor cells upon cell contact in vitro.

184 Whether HIV also spreads by cell-cell contact in vivo is a matter of debate.

185 ns in cell morphology, cytoskeleton and cell-cell contacts in a gradient-like manner.

186 ed intramembrane proteolysis to monitor cell-cell contacts in animals.

187 CDH11 mediates cell-cell contacts in both valvular fibroblasts and myofibrob

188 Hakai, an E3 ubiquitin ligase, disrupts cell-cell contacts in epithelial cells and is up-regulated in

189 al cysts, targets the CLC-2 Cl(-) channel to cell contacts in glia and activates CLC-2 currents in vi

190 ow that Elmo2 recruits Dock1 to initial cell-cell contacts in Madin-Darby canine kidney cells.

191 for nonpatterned cells allowed to form cell-cell contacts in monolayer culture.

192 ly contributor to disrupted endothelial cell-cell contacts in the absence of KRIT1.

193 d that GlialCAM clusters all CLC channels at cell contacts in vitro and thus studied GlialCAM interac

194 FF in combination with IL-2 and IL-21 is a T cell contact-independent inducer of human B cell prolife

195 Th cells and the secretion of IFN-gamma in a cell contact-independent manner.

196 ration of effector T cells (Teffs) through a cell contact-independent mechanism.

197 trongly induced the production of IL-10 in a cell-contact-independent manner.

198 Macrophage and tumor cell contact induce RhoA activity in tumor cells, trigge

199 Of interest, cell contact-induced expression of TGF-beta1 and TGF-bet

200 Additionally, we observed that cell-cell contact induces a mitochondrion-dependent increase

201 Here, we show that cell-cell contact induces rapid recruitment of mitochondria t

202 In epithelia, force imbalance at cell contacts induces cell shape changes, such as apical

203 a-secretase inhibitors substantially reduced cell contact induction of PTPRK gene expression.

204 Cell-cell contacts inhibit cell growth and proliferation in p

205 Cell-cell contact inhibition and the mechanical environment o

206 G1 expression resulted in a profound loss of cell contact inhibition, multiple layers of overgrowing

207 Hippo-YAP pathway is a central regulator of cell contact inhibition, proliferation and death.

208 Here we report that cell-contact inhibition of growth through the canonical

209 These cells were defective in cell-contact inhibition with changes in Merlin phosphory

210 etwork and the major regulatory mechanism of cell-contact inhibition.

211 passage required live beta cells in a close cell contact interaction with the phagocytes.

212 through IL-10 production as well as cell-to-cell contact involving CTLA-4.

213 In adult pituitary tissue, direct cell contacts involving gap junctions allowed local spat

214 Furthermore, cell-to-cell contact is an important component of successful MeV

215 on of cell movement with respect to the cell-cell contact is correlated with changes in the average i

216 How the stability of cell-cell contacts is modulated to effect such morphological

217 lthough acquisition of m157 requires cell-to-cell contact, it does not require the expression of the

218 resentation occurs in the context of cell-to-cell contacts, it has the potential for regulation by an

219 omain promotes accumulation in areas of cell-cell contact, leading to enhanced adhesion and inhibitio

220 ctor (TGF)-beta signaling and disassembly of cell contacts leads to nuclear accumulation of MRTFs and

221 ase in DEcad coincides with the reduction of cell contact length and depends on tension anisotropy be

222 th relied on IL-10 secretion as well as cell-cell contact, likely mediated through CD80 and CD86, to

223 lagen matrix unravelled the efficacy of cell-cell contact loosening and 3D emigration into an environ

224 a an intimate coupling with the polarity and cell contact machineries.

225 NKp30-B7-H6 interaction is a novel cell contact mechanism that mediates activation of ILC2

226 To characterize cell-contact mechanisms and soluble factors that contrib

227 ally distinct routes to synaptogenesis: cell-cell contact mediated by adhesion proteins, cell-cell bi

228 Cell-to-cell contact mediated by glycan:glycan interactions have

229 inhibition of these pathways abates the cell-cell contact mediated expression of alphaSMA.

230 f cell-cycle dynamics in bacteria as well as cell-contact mediated phenomena.

231 ly cytoskeletal remodelling and lateral cell-cell contacts, mediated through the RAC1 guanine nucleot

232 This cell contact-mediated decrease in PGE2 secretion down-re

233 Our results illustrate a novel heterotypic cell contact-mediated signaling role for RhoA, as well a

234 lso provide direct evidence that presynaptic cell contact-mediated, clustering of postsynaptic cholin

235 e shaped irregularly with punctuated cell-to-cell contacts, metabolically responsive to environmental

236 crovascular endothelial cells that lack cell-cell contacts migrate in the flow direction.

237 owth factor receptors, adhesion, and cell-to-cell contact molecules.

238 study shows that immediately after bacteria-cell contact, neutrophils rapidly and continuously engul

239 , we characterized the localization and cell-cell contacts of splenic neutrophils at several stages i

240 signaling is mediated either by direct cell-cell contact or by Dll4-containing exosomes from a dista

241 can form gap-junction channels at points of cell contacts or "free HCs" at non-contacting regions.

242 ned spaces, even in the absence of extrinsic cell contacts or antigen recognition.

243 phenomena such as electron transfer in solar-cell contacts or surface reactivity in heterogeneous cat

244 r development of inexpensive, nontoxic solar cell contacting pastes.

245 responding modifications to amino acids at T-cell contact positions modulated the recognition of mult

246 events in the recognition phase of NK-target cell contact rather than events after cytotoxicity has b

247 This rapid spread is based on cell-to-cell contact rather than on particle release and reentry

248 s to epithelial cells also occurs by cell-to-cell contact rather than through cell-free particles.

249 Cell contact rearrangements (Ne/Epi + Ne/Epi --> Ne/Ne +

250 re engaged during natural killer (NK)-target cell contact remains undefined.

251 cytoplasm of neighboring bacteria upon cell-cell contact, resulting in growth inhibition or death un

252 rce as well as the initial direction of cell-cell contact rupture.

253 turbed cells to mitogen deprivation and cell-cell contact seems a better predictor of tumor developme

254 a general platform for generating novel cell-cell contact signaling pathways.

255 uble factors such as morphogen gradients and cell contact signals, eventually resulting in induction

256 secretion of such large granules at the cell-cell contact site.

257 3 patches also exist, which enrich near cell-cell contact sites and fuse with the plasma membrane at

258 when lateral reorganization at the membrane-cell contact sites is physically hindered.

259 le/beta-catenin/E-cadherin complexes to cell-cell contact sites, enhances noncanonical Wnt signals, a

260 eceptor recruitment and distribution at cell-cell contact sites.

261 microenvironment is mediated through direct cell contact, soluble factors, and extracellular vesicle

262 However, whether cell-cell contact specifically induces dynamic T cell remodel

263 zation in cellulo and for its impact on cell-cell contact stability.

264 the immunological synapse, an intimate DC/T cell contact structure that activates T cells.

265 ision was not dependent on septins when cell-cell contacts, such as those with antigen-presenting cel

266 ition of locomotion (CIL), meaning that cell-cell contacts suppress force transduction to the substra

267 ents and repulsive effects arising from cell-cell contact, termed contact inhibition of locomotion (C

268 ions of gamma9delta2 T cells involve cell-to-cell contact that is dependent on CD40-CD40 ligand (CD40

269 ts (3.3 events/min), demonstrating that most cells contact the surface multiple times before transiti

270 auses significant increases in the area of B cells contacting the antigen-presenting membrane and the

271 ligand-receptor interaction in sites of cell-cell contact, the transmembrane domain of an engineered

272 As motile bacteria reach cell-cell contacts they form plasma membrane protrusions that

273 surfaces, myxobacteria glide, and upon cell-cell contact, they can efficiently exchange their OM pro

274 smoplakin (DP) accumulation at sites of cell-cell contact, they play distinct roles in later steps: P

275 n each array and offers tunable control over cell-contact time during long-term culture.

276 stem that typically engages at sites of cell-cell contact to initiate bidirectional signaling.

277 ody without an apparent requirement for cell-cell contact to persist in vivo.

278 HIV-1-infected T cells sense and respond to cell contact to polarize viral egress and promote cell-c

279 taining secretory apparatus to sites of cell-cell contact to support polarized viral assembly and egr

280 r retroviruses in vitro across synaptic cell-cell contacts to uninfected cells, a process called tran

281 this behavior was independent of local cell-cell contact topologies and of position within the tissu

282 for its ability to detect vertices and cell-cell contacts, track cells, and identify mitosis and apo

283 Cell-cell contact triggers active polarization of organelles

284 e hypotheses have been proposed: direct cell-cell contact, tunneling nanotubes, and exosomes.

285 pithelial differentiation and augmented cell-cell contacts underlie the anti-migratory action exerted

286 PIX, which is specifically recruited at cell-cell contacts upon CCM.

287 xonal growth, demonstrating that direct cell-cell contact was not required.

288 Furthermore, direct platelet-EOMA cell contact was required and the proliferation was medi

289 nvolved in proliferation, adhesion, and cell-cell contact, we found that AP-1 repressed the expressio

290 ion reinforcement to stabilize adhesive cell-cell contacts, we propose an alternative mechanosensing

291 s are actively recruited to the site of cell-cell contact where the viral material is efficiently tra

292 , setting in motion E-cadherin-mediated cell-cell contact, which establishes apicobasolateral polarit

293 the specific shortening of mesenchymal cell-cell contacts, which in turn powers cell interdigitation

294 n of capillary-like networks induced by cell-cell contact with vascular smooth muscle cells (vSMCs) a

295 teraction between pUL135 and talin disrupted cell contacts with the extracellular matrix.

296 hepatoblast motility and long-distance cell-cell contacts with the LPM beyond immediate tissue inter

297 at the cell-substratum interface and at cell-cell contacts, with the latter being 10-fold more stable

298 n gate deficient CLC-2 mutant E211V/H816A to cell contacts, without altering its function.

299 lasm and subsequent localization to the cell-cell contact zone, assembly of adherens junction complex

300 cells rapidly drove FMNL2 to epithelial cell-cell contact zones.