ライフサイエンスコーパス: cell contact

1 hich permits irreversible adhesion upon cell-cell contact.

2 TNF signaling via MVs without direct cell-to-cell contact.

3 ditions closely mimicking physiological cell-cell contact.

4 bohydrates over time, induced by endothelial cell contact.

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

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

7 1 expression, resulting in insufficient cell-cell contact.

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

9 lls change their direction of migration upon cell contact.

10 fasciculation, and can act independently of cell contact.

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

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

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

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

15 ing CHIR99021 and concurrent removal of cell-cell contact.

16 ng neighboring cells and signaling this cell-cell contact.

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

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

19 n of ExsD interacts with ExsC following host cell contact.

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

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

22 romote cancer invasion through direct cancer cell contact.

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

24 te burden through a mechanism independent of cell contact.

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

26 ival through a mechanism partly dependent on cell contact.

27 fected to uninfected cells by direct cell-to-cell contact.

28 livered to host cells independent of cell-to-cell contact.

29 rting a critical role of direct T cell-tumor cell contact.

30 and plasmid conjugation both involve cell-to-cell contact.

31 cells kill target cells through direct cell-cell contact.

32 sible factors, but appears to depend on cell-cell contact.

33 ases, and E3 ubiquitin ligase in response to cell contact.

34 to the surface of allogeneic DCs via cell-to-cell contacts.

35 type I PAK, PAK1, does not localize to cell-cell contacts.

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

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

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

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

40 ithout a corresponding reinforcement of cell-cell contacts.

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

42 cardiomyocytes disrupts localization at cell-cell contacts.

43 is yet to be demonstrated at authentic cell-cell contacts.

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

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

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

47 significant role for MAL in viral spread at cell contacts.

48 ry rather than at individual internal border cell contacts.

49 cks keratin filament recruitment toward cell-cell contacts.

50 his keratin population to the region of cell-cell contacts.

51 was observed down to the area of individual cell contacts.

52 haviors of M. xanthus involve extensive cell-cell contacts.

53 easurement of pre-defined parameters at cell-cell contacts.

54 racellular pilus to initiate donor-recipient cell contacts.

55 of PAK1 resulted in its localization to cell-cell contacts.

56 gy and blocked myofibril integration at cell-cell contacts.

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

58 ing early in fetal life, with midget bipolar cells contacting a single cone by mid-gestation and bipo

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 that NK cell proliferation requires cell-to-cell contact, activation of the CD137 axis, and presence

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

63 ation, however, less is known about how cell-cell contacts affect the migratory behavior of leukocyte

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

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

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

67 Similarly organized cell-to-cell contacts also facilitate DC-mediated transfer of HT

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

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

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

71 mutations also localized to regions of cell-cell contact and displayed a punctate staining pattern.

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

73 bit non-polarized morphologies, limited cell-cell contact and indirect migration trajectories.

74 e recognition of antigen by T cells requires cell contact and is associated with changes in T cell sh

75 sk hosts occurs independently of direct cell-cell contact and is mediated by the immunoregulatory cyt

76 ence in surrounding wild-type NSCs in a cell-cell contact and Notch signaling-dependent manner.

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

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

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

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

81 Ag transfer required cell-cell contact and the formation of connexin 43-containing

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

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

84 e bacterial pole and mediated bacterial cell-cell contacts and aggregative growth in the presence of

85 through a separate pathway mediated by cell-cell contacts and allows cells/tissues to switch off nuc

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

87 and myosin colocalize at border cell-border cell contacts and cooperate to transmit directional info

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

89 og proteins are enriched at the site of cell-cell contacts and engage in trans-homophilic interaction

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

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

92 c cells (DCs) promotes the formation of cell-cell contacts and interaction with regulatory T cells (T

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

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

95 , potentially explaining the release of cell-cell contacts and persistent activation of Prkd1.

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

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

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

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

100 , but not sufficient, to direct PAKs to cell-cell contacts and that an N-terminal polybasic sequence

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

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

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

104 er 7, a scaffolding protein involved in cell-cell contacts) and MDH1 (cytosolic Malate dehydrogenase

105 actors, extracellular matrix molecules, cell-cell contact, and favorable substrate stiffness for dire

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

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

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

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

110 downregulation of E-cadherin, loosening cell-cell contacts, and YAP-TRIO-Merlin mediated regulation o

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

112 was also tightly coupled to Treg-endothelial cell contact- and TNFR1-dependent inhibition of angiogen

113 ntrol cellular immune responses through cell-cell contact, antigen presentation, and cytokine product

114 Furthermore, cell contacts are generated dynamically from positions o

115 nature of cell-cell contacts, revealing that cell contacts are highly heterogeneous because of topogr

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

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

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

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

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

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

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

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

124 ate release from Th17 cells upon direct cell-cell contact between Th17 cells and neurons.

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

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

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

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

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

130 vation of myeloid effector cells, close cell-cell contact (between effector and target cell) and form

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

132 due to a lower expression of arnT upon host-cell contact, but do not produce spermidine and are phag

133 transfer was shown to be independent of cell-cell contact, but relied on engulfment within secreted m

134 ce is necessary for PAK1 recruitment to cell-cell contacts, but only if the variable region-mediated

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

136 very of a CdiA-CT domain upon direct cell-to-cell contact can inhibit replication of a susceptible ta

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

138 Here, we explore how cell-cell contacts can affect the directed migration of innat

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

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

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

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

143 ly on TCR dwell time in phosphatase-depleted cell contacts constrained in area by cell topography.

144 el, we show that over time MGCs develop cell-cell contacts containing ZLSs.

145 Mitochondrial transfer to MSC is cell-contact dependent and mediated by HSPC connexin-43

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

147 Using cell fractionation and cell contact-dependent assay, we made the unexpected fin

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

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

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

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

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

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

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

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

156 Like tumor and CD8(+) T cell contact-dependent NKG2D ligand induction, this CD13

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

158 lled by mitotic cell rounding-dependent cell-cell contact disassembly during the last rounds of cell

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

160 Cell contact during CIL requires the participation of th

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

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

163 Further investigation of cell contact dynamics as guidance cues may yield new ins

164 Notably, not all CAR T cell contacts elicited calcium signaling or killing whil

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

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

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

168 Prior to host cell contact, ExsA is inhibited through direct binding o

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

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

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

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

173 effector cell) initiates and stabilizes cell-cell contact for infection.

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

175 tion, thus indicating the importance of cell-cell contacts for the HAX1-mediated effect.

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

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

178 ular and molecular organization and the cell-cell contacts found in vivo.

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

180 fector of DLC1 deficiency-associated loss of cell contact growth inhibition in endothelial cells and

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

182 ic conditions, IGPR-1 is present at the cell-cell contacts; however, under shear stress, it redistrib

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

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

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

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

187 rgeting the bacteria to enhance bacterium-to-cell contacts in a structure- and sequence-dependent fas

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

189 tween motile immune cells to long-lived cell-cell contacts in epithelia.

190 ophilic receptor PTPRK is stabilized at cell-cell contacts in epithelial cells.

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

192 ous string-like structures along endothelial cell contacts in specialized regions of the vascular tre

193 ism, based on a minimal number of four inner-cell contacts in the ICM, which activates Oct4 in the pr

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 s at the developing apical membrane and cell-cell contacts, independently of the Par complex and Crb.

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

200 Cell-cell contact inhibition and the mechanical environment o

201 at YAP is a required effector of the loss of cell contact inhibition of growth manifested by DLC1-def

202 primary endothelial cells causes the loss of cell contact inhibition of growth through incompletely d

203 s increased genome instability, loss of cell-cell contact inhibition, and invasiveness, but also disp

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

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

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

207 of the Hippo signalling pathway involved in cell-contact inhibition.

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

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

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

211 y revealed that the structure of endothelial cell contacts is constantly reorganized and that endothe

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

213 maging showed that CpG-C-activated microglia cells contact, kill, and phagocytize tumor cells in the

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

215 ractility produces transient changes in cell-cell contact lengths, which stabilize to produce lasting

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

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

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

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

220 n is initiated by force transduction on cell-cell contacts mediated by C-cadherin, the mechanism by w

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

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

223 l (Treg)-related elements of suppression are cell contact-mediated.

224 teraction occurs in rat hippocampus via cell-cell contacts, mediating microglial cell branching in th

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

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

227 In some cases, the cell-cell contact must be transient, forming on timescales of

228 hted the variable nature of cell sizes, cell-cell contact networks, and colony arrangement.

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

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

231 as found predominantly along the endothelial cell contacts of the primary arteries and did not overla

232 Cell-cell contacts often underpin signaling between cells.

233 erize stiffness, conventional techniques use cell contact or invasive probes and as a result are low

234 than counteract, tumor malignancy, via cell-cell contact or soluble mediators.

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

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

237 of stem cell-like cancer cells in a cell-to-cell contact- or (at least) proximity-dependent manner i

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

239 nsic signals, such as mechanical force, cell-cell contact, polarity, energy status, stress, and many

240 lining macrophage (SMs) that provide a cell-cell contact portal, which facilitates the uptake of HIV

241 aphorin-5C-Plexin-A interactions at the cell-cell contact, promotes planar polarization and collectiv

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

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

244 agated the competence signal through cell-to-cell contact rather than the classically described quoru

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

246 Target cell contact reduced intracellular GrzB and perforin and

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

248 on of cadherin signaling independent of cell-cell contacts remains unknown.

249 ivate T cells, we speculate that the cell-to-cell contact represents "signal 1," CD137 represents "si

250 racts with ephrin-B2 ligand at sites of cell-cell contact, resulting in bidirectional signaling.

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

252 knowledge, insights into the nature of cell-cell contacts, revealing that cell contacts are highly h

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

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

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

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

257 otch active), revealing a substrate for cell-cell contact support during migrations, a developmental

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

259 onal proteins at sinusoidal endothelial cell-cell contacts, switching capillaries from branching to c

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

261 lockade of autoreactive immune cells by cell-cell contact, Th17 and IL-10 Tr1-like activities, or act

262 Intercalated discs (ICD), specific cell-to-cell contacts that connect adjacent cardiomyocytes, ensu

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

264 of these nanopillar arrays toward bacterial cells contacting the surface; however, with further incr

265 Upon extracellular stimuli such as cell-cell contact, the pathway negatively regulates YAP throu

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

267 proteins that assemble into clusters at cell-cell contacts through cis- and trans- (adhesive) interac

268 Both proteins are co-stabilised at cell-cell contacts through direct interaction.

269 henotype and (ii) FAK_SRC inhibition of cell-cell contacts through the receptor-type tyrosine-protein

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

271 eover, we demonstrate that, with direct cell-cell contact, TME-derived endothelial cells provide the

272 lasma membrane (PM) curvature resulting from cell contact to a surface triggers the initial breakage

273 l remodeling (cwr) checkpoint that acts upon cell contact to assess genetic compatibility and regulat

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

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

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

277 k of claudin strands creates continuous cell-cell contacts to form the intercellular tight junction b

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

279 susceptible to EHV1 infection and that cell-cell contact transmits infectious virus to and from T ly

280 Cell-cell contact triggers active polarization of organelles

281 Host cell contact triggers secretion of ExsE and sequestratio

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

283 Stable cell-cell contacts underpin tissue architecture and organizat

284 in-dependent contractile forces pull on cell-cell contacts until cells release.

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

286 that electron uptake is dependent on direct cell contact via a biofilm on the cathode surface rather

287 e, viral transmission occurs through cell-to-cell contacts via a mechanism that is still poorly under

288 We observed that after cell-cell contact was established between breast cancer cells

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

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

291 Direct cell-to-cell contact was required for N1 to influence microglia

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

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

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

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

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

297 olytic cytotoxic T lymphocytes (CTLs) and NK cell contacts with tumor cells.

298 UR application accompanied by a loss of cell-cell contacts within tumor cell clusters.

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.