ライフサイエンスコーパス: cell-cell contact

1 on using CHIR99021 and concurrent removal of cell-cell contact.

2 sue structure and function following de novo cell-cell contact.

3 herens junction maturation following de novo cell-cell contact.

4 t migration to the tips of myofibers through cell-cell contact.

5 necting neighboring cells and signaling this cell-cell contact.

6 cells that involved the gamma-delta TCR and cell-cell contact.

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

8 increased by the TGF-beta/Smad3 pathway and cell-cell contact.

9 PRF was induced during cell proliferation by cell-cell contact.

10 ecules such as E-cadherin are present at the cell-cell contact.

11 kinase in response to apoptotic stimuli and cell-cell contact.

12 ization of the small GTPase RhoA at sites of cell-cell contact.

13 vers signaling proteins directly at sites of cell-cell contact.

14 bule organization and dynamics near sites of cell-cell contact.

15 ibit the growth of susceptible bacteria upon cell-cell contact.

16 mation of signaling clusters at the sites of cell-cell contact.

17 an be detected during the first minute after cell-cell contact.

18 P-B colocalize with p120-catenin at sites of cell-cell contact.

19 modulates tissue homeostasis in response to cell-cell contact.

20 xic T cells kill target cells through direct cell-cell contact.

21 diffusible factors, but appears to depend on cell-cell contact.

22 GF, which permits irreversible adhesion upon cell-cell contact.

23 invasion and arises as a result of intimate cell-cell contact.

24 VCAM-1 expression, resulting in insufficient cell-cell contact.

25 hrough Eph receptors is largely dependent on cell-cell contact.

26 r conditions closely mimicking physiological cell-cell contact.

27 lular protein localization, and detection of cell-cell contact.

28 hat APLP1 forms homotypic trans complexes at cell-cell contacts.

29 ons without a corresponding reinforcement of cell-cell contacts.

30 ring, may contribute to the reinforcement of cell-cell contacts.

31 d in cardiomyocytes disrupts localization at cell-cell contacts.

32 basal epithelial polarity, as well as proper cell-cell contacts.

33 al features by perturbing cell-substrate and cell-cell contacts.

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

35 of the existence of oligomeric cadherins at cell-cell contacts.

36 nterferes with the initiation of sustainable cell-cell contacts.

37 gh it is yet to be demonstrated at authentic cell-cell contacts.

38 ract within the trabecular layer to form new cell-cell contacts.

39 ing through the formation of uropod-mediated cell-cell contacts.

40 nhibits cell proliferation upon establishing cell-cell contacts.

41 ing through the formation of uropod-mediated cell-cell contacts.

42 architecture through apicobasal polarity and cell-cell contacts.

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

44 inase Src and stimulates Src signaling along cell-cell contacts.

45 enchymal, lacked ruffles but formed abundant cell-cell contacts.

46 for KRIT1 depletion-dependent disruption of cell-cell contacts.

47 nin conformational epitope immunostaining at cell-cell contacts.

48 tion of the RASIP1 protein pool localizes to cell-cell contacts.

49 oA activity, and results in loss of p190B at cell-cell contacts.

50 s ameloblast movement by cleaving ameloblast cell-cell contacts.

51 d blocks keratin filament recruitment toward cell-cell contacts.

52 al filopodia to discrete membrane domains at cell-cell contacts.

53 catenin and the Arp2/3 complex at developing cell-cell contacts.

54 of this keratin population to the region of cell-cell contacts.

55 al behaviors of M. xanthus involve extensive cell-cell contacts.

56 ous measurement of pre-defined parameters at cell-cell contacts.

57 gion of PAK1 resulted in its localization to cell-cell contacts.

58 phology and blocked myofibril integration at cell-cell contacts.

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

60 lated in the cytoplasm at the cell edges and cell-cell contacts.

61 protein CdGAP, a GAP for Rac1 and Cdc42, at cell-cell contacts.

62 immunogenic stimulus, physical disruption of cell-cell contacts a tolerogenic stimulus.

63 Tbx3, Klf4 and Esrrb transcript repression, cell-cell contact abrogation, cell survival in suspensio

64 Here we show that in the absence of cell-cell contact, actomyosin contractility suppresses Y

65 migration, however, less is known about how cell-cell contacts affect the migratory behavior of leuk

66 bjected to serum starvation, allowed to form cell-cell contacts, after microtubule disruption, or inh

67 Cell-cell contacts also direct ingression of the cleavag

68 ormation requires regulation at the level of cell-cell contacts among brain cells.

69 ucing microtubule catastrophe at the site of cell-cell contact and abrogating CIL.

70 ation was found to be independent of loss of cell-cell contact and Activin/Nodal-dependent pluripoten

71 oach was employed to decouple the effects of cell-cell contact and cell-matrix adhesion in TGFbeta1-i

72 three mutations also localized to regions of cell-cell contact and displayed a punctate staining patt

73 us maturation of Swap-70(-/-) DCs depends on cell-cell contact and does not involve beta-catenin sign

74 egulatory cytokines such as IL-10 and direct cell-cell contact and have been linked to experimental m

75 exhibit non-polarized morphologies, limited cell-cell contact and indirect migration trajectories.

76 ow-risk hosts occurs independently of direct cell-cell contact and is mediated by the immunoregulator

77 uiescence in surrounding wild-type NSCs in a cell-cell contact and Notch signaling-dependent manner.

78 remodelling to facilitate cadherin-mediated cell-cell contact and promote beta-catenin signalling.

79 the Notch receptor pathway is responsive to cell-cell contact and regulates keratinocyte growth and

80 ns appear to be mediated through both direct cell-cell contact and secreted ligands.

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

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

83 CCM2) are critical regulators of endothelial cell-cell contact and vascular homeostasis.

84 teral clustering of adhesion receptors after cell-cell contact and, more generally, to the formation

85 liver Syndrome patients strongly destabilize cell-cell contacts and (ii) CdGAP mRNA levels are invers

86 east epithelium results in disruption of the cell-cell contacts and acquisition of a mesenchymal phen

87 at the bacterial pole and mediated bacterial cell-cell contacts and aggregative growth in the presenc

88 tions through a separate pathway mediated by cell-cell contacts and allows cells/tissues to switch of

89 sed the localization of the other protein to cell-cell contacts and altered AJ dynamics and stability

90 esion, Elmo2 and Dock1 no longer localize to cell-cell contacts and are not required subsequently for

91 -independent growth, reduced ability to form cell-cell contacts and chromosomal aberrations.

92 We also determined that cell-cell contacts and cortically associated EB1/beta-ca

93 s, resulting in delocalization of ROCK2 from cell-cell contacts and decreased junctional contractilit

94 at Ihog proteins are enriched at the site of cell-cell contacts and engage in trans-homophilic intera

95 y expressed adhesion molecule that regulates cell-cell contacts and facilitates leukocyte transendoth

96 imensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of diff

97 dritic cells (DCs) promotes the formation of cell-cell contacts and interaction with regulatory T cel

98 ests that RhoA exists as an inactive pool at cell-cell contacts and is recruited to cell-ECM contacts

99 ering, epithelial cell islands rupture their cell-cell contacts and migrate away as single cells on t

100 f Tau, potentially explaining the release of cell-cell contacts and persistent activation of Prkd1.

101 ced by some chemotherapeutic agents required cell-cell contacts and proceeded through an endocytic pa

102 duces more complete EMT, including disrupted cell-cell contacts and reduced E-cadherin expression, an

103 lective guidance does not require persistent cell-cell contacts and strong short range adhesion.

104 iral envelope glycoprotein (Env) establishes cell-cell contacts and subsequently recruits Gag by a pr

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

106 uired, but not sufficient, to direct PAKs to cell-cell contacts and that an N-terminal polybasic sequ

107 y disrupted and a tension difference between cell-cell contacts and the free cell surface at gaps of

108 because they are well positioned to form the cell-cell contacts and to provide the intercellular comm

109 member 7, a scaffolding protein involved in cell-cell contacts) and MDH1 (cytosolic Malate dehydroge

110 tion was blocked by anti-4-1BBL Ab, required cell-cell contact, and did not require the cytoplasmic s

111 hic factors, extracellular matrix molecules, cell-cell contact, and favorable substrate stiffness for

112 L3 expression in primary leucocytes required cell-cell contact, and induction was suppressed by plasm

113 which cells move away from each other after cell-cell contact, and it contributes to malignant invas

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

115 pithelial cells lose apicobasal polarity and cell-cell contacts, and gain mesenchymal phenotypes with

116 et T cells, requires the formation of stable cell-cell contacts, and is an active, calcium-dependent

117 s ECM stiffness, adhesion ligand density, or cell-cell contacts, and thus strongly influences cell fa

118 ated downregulation of E-cadherin, loosening cell-cell contacts, and YAP-TRIO-Merlin mediated regulat

119 ls control cellular immune responses through cell-cell contact, antigen presentation, and cytokine pr

120 (-/-)mEF is greater at higher densities when cell-cell contacts are abundant.

121 Cell-cell contacts are fundamental to multicellular orga

122 cts in distance and is independent of direct cell-cell contact.ARMMs are extracellular vesicles that

123 actin assembly and turnover at newly formed cell-cell contacts as well as for human epithelial lumen

124 ly acts by sterically interfering with close cell-cell contacts at the NK cell-target cell interface

125 eration of specific T cells was dependent on cell-cell contact between B cells and moDCs, which was e

126 We hypothesized that cell-cell contact between plasmacytoid dendritic cells (

127 lutamate release from Th17 cells upon direct cell-cell contact between Th17 cells and neurons.

128 ted with progressive loss of Tregs, impaired cell-cell contact between Tregs and dendritic cells (DCs

129 The establishment of cell-cell contacts between presynaptic GABAergic neurons

130 ial cytokinesis, the remodelling of adhesive cell-cell contacts between the dividing cell and its nei

131 activation of myeloid effector cells, close cell-cell contact (between effector and target cell) and

132 At cell-cell contacts, both Elmo2 and Dock1 are essential f

133 he molecular role of E-cadherin not only for cell-cell contact but also for clonal propagation of hPS

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

135 -binding domains restores cadherin-dependent cell-cell contacts but cannot strengthen intercellular a

136 ll-cycle arrest upon mitogen deprivation and cell-cell contact, but did contribute to RAS(V12)- and r

137 igen transfer was shown to be independent of cell-cell contact, but relied on engulfment within secre

138 thelial barrier dysfunction by disruption of cell-cell contacts, but not CCL20 secretion.

139 equence is necessary for PAK1 recruitment to cell-cell contacts, but only if the variable region-medi

140 through p190RhoGAP-B, which is localized to cell-cell contacts by association with p120-catenin that

141 erodimer is not only recruited to the apical cell-cell contacts by binding to Crb but depends on func

142 ave demonstrated that complete disruption of cell-cell contact can promote transforming growth factor

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

144 ing important cellular processes involved in cell-cell contact, cell adhesion and motility.

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

146 ellular and intracellular signals, including cell-cell contact, cell polarity, mechanical cues, ligan

147 tributions to heterogeneity from cell cycle, cell-cell contact, cell stochasticity and heritable morp

148 hat the formation of STK11-dependent lateral cell-cell contacts competent for tyrosine kinase signali

149 s model, we show that over time MGCs develop cell-cell contacts containing ZLSs.

150 ecular level, little is known about how this cell-cell contact dependent feedback is transmitted at t

151 omoted apoptosis of primary murine HSCs in a cell-cell contact-dependent manner, involving Fas-ligand

152 g, with bulk cell stiffness and stiffness of cell-cell contacts dictating the invasion pattern.

153 ontrolled by mitotic cell rounding-dependent cell-cell contact disassembly during the last rounds of

154 hile, E-cadherin clusters throughout lateral cell-cell contacts display dynamic movements in the plan

155 the interplay between cell polarization and cell-cell contact drives the segregation of these lineag

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

157 crotubule plus ends interact with regions of cell-cell contact during tissue development and morphoge

158 al morphogenetic movements while maintaining cell-cell contacts during embryogenesis and post-embryon

159 ension-dependent adaptation of AJs regulates cell-cell contact dynamics and coordinated collective ce

160 We showed that, without direct cell-cell contact, ECs secrete factors that promoted the

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

162 nhibiting ATE1 disrupted E-cadherin-mediated cell-cell contacts, enhanced formation of actin-rich pro

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

164 CD73 associated with cell-cell contacts, filopodia, and membrane zippers, ind

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

166 ell (effector cell) initiates and stabilizes cell-cell contact for infection.

167 migration, thus indicating the importance of cell-cell contacts for the HAX1-mediated effect.

168 Cell-cell contact formation is a dynamic process requiri

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

170 is robust to severe perturbations affecting cell-cell contact formation.

171 cellular and molecular organization and the cell-cell contacts found in vivo.

172 y localized by active Cdc42 at the external, cell-cell contact-free surfaces of apically constricting

173 ypothesis, we found that the expression of a cell-cell contact gene, Desmoplakin, is greatly reduced

174 ell types and formation of multiple sites of cell-cell contact, giving rise to nascent fusion pores w

175 HLSECs internalized HCV, independent of cell-cell contacts; HCV RNA was translated but not repli

176 static conditions, IGPR-1 is present at the cell-cell contacts; however, under shear stress, it redi

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

178 G and betaII-spectrin colocalize at sites of cell-cell contact in columnar epithelial cells and promo

179 and zebrafish that Par3 is localised to the cell-cell contact in neural crest cells and is essential

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

181 We find that Rab35 accumulates at cell-cell contacts in a cadherin-dependent manner.

182 rations in cell morphology, cytoskeleton and cell-cell contacts in a gradient-like manner.

183 induced intramembrane proteolysis to monitor cell-cell contacts in animals.

184 CDH11 mediates cell-cell contacts in both valvular fibroblasts and myof

185 of cadherin trafficking and stabilization at cell-cell contacts in C2C12 myoblasts and HeLa cells.

186 ns between motile immune cells to long-lived cell-cell contacts in epithelia.

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

188 e homophilic receptor PTPRK is stabilized at cell-cell contacts in epithelial cells.

189 we show that Elmo2 recruits Dock1 to initial cell-cell contacts in Madin-Darby canine kidney cells.

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

191 he only contributor to disrupted endothelial cell-cell contacts in the absence of KRIT1.

192 ells, and morphological changes with loss of cell-cell contacts in the epidermal tissue of zebrafish.

193 ulates at the developing apical membrane and cell-cell contacts, independently of the Par complex and

194 ied E-cadherin as a major contributor to the cell-cell contact-induced osteoblast differentiation.

195 Additionally, we observed that cell-cell contact induces a mitochondrion-dependent incr

196 Here, we show that cell-cell contact induces rapid recruitment of mitochond

197 Cell-cell contacts inhibit cell growth and proliferation

198 e endogenous induction of PXR as a result of cell-cell contact inhibited proliferation and subsequent

199 Cell-cell contact inhibition and the mechanical environm

200 uch as increased genome instability, loss of cell-cell contact inhibition, and invasiveness, but also

201 hat may alter the diffusion dynamics through cell-cell contact interactions.

202 Disruption of endothelial cell-cell contact is a key event in many cardiovascular

203 rection of cell movement with respect to the cell-cell contact is correlated with changes in the aver

204 How the stability of cell-cell contacts is modulated to effect such morpholog

205 ing domain promotes accumulation in areas of cell-cell contact, leading to enhanced adhesion and inhi

206 contractility produces transient changes in cell-cell contact lengths, which stabilize to produce la

207 nd both relied on IL-10 secretion as well as cell-cell contact, likely mediated through CD80 and CD86

208 a collagen matrix unravelled the efficacy of cell-cell contact loosening and 3D emigration into an en

209 The process requires direct cell-cell contact made possible by a multiprotein comple

210 s and may depend on secreted factors, direct cell-cell contact, matrix interactions, or a combination

211 ted by chNKG2D T cells through IFN-gamma and cell-cell contact mechanisms.

212 ceptually distinct routes to synaptogenesis: cell-cell contact mediated by adhesion proteins, cell-ce

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

214 eratin is initiated by force transduction on cell-cell contacts mediated by C-cadherin, the mechanism

215 s early cytoskeletal remodelling and lateral cell-cell contacts, mediated through the RAC1 guanine nu

216 This cell-cell contact-mediated (CCCM) HCV transfer occurs re

217 ia interaction occurs in rat hippocampus via cell-cell contacts, mediating microglial cell branching

218 ty microvascular endothelial cells that lack cell-cell contacts migrate in the flow direction.

219 In some cases, the cell-cell contact must be transient, forming on timescal

220 ghlighted the variable nature of cell sizes, cell-cell contact networks, and colony arrangement.

221 ether the MDSC induction mechanism relies on cell-cell contact of melanoma cells with CD14(+) cells.

222 SLOs), we characterized the localization and cell-cell contacts of splenic neutrophils at several sta

223 Cell-cell contacts often underpin signaling between cell

224 Notch signaling is mediated either by direct cell-cell contact or by Dll4-containing exosomes from a

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

226 extrinsic signals, such as mechanical force, cell-cell contact, polarity, energy status, stress, and

227 sinus lining macrophage (SMs) that provide a cell-cell contact portal, which facilitates the uptake o

228 y Semaphorin-5C-Plexin-A interactions at the cell-cell contact, promotes planar polarization and coll

229 However, how MA targets Gag to sites of cell-cell contact remains unknown.

230 unction of cadherin signaling independent of cell-cell contacts remains unknown.

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

232 o the cytoplasm of neighboring bacteria upon cell-cell contact, resulting in growth inhibition or dea

233 ial cells reduced the level of active Src at cell-cell contacts, resulting in delocalization of ROCK2

234 o our knowledge, insights into the nature of cell-cell contacts, revealing that cell contacts are hig

235 lacement and force redistribution in guiding cell-cell contact rupture during scattering.

236 To explore the role of cell motion and cell-cell contact rupture, we examine the biophysical ch

237 ar force as well as the initial direction of cell-cell contact rupture.

238 n-perturbed cells to mitogen deprivation and cell-cell contact seems a better predictor of tumor deve

239 e as a general platform for generating novel cell-cell contact signaling pathways.

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

241 FMNL3 patches also exist, which enrich near cell-cell contact sites and fuse with the plasma membran

242 s Daple/beta-catenin/E-cadherin complexes to cell-cell contact sites, enhances noncanonical Wnt signa

243 of defects in the molecular architecture of cell-cell contact sites, including the adherens and tigh

244 of receptor recruitment and distribution at cell-cell contact sites.

245 throughout the biofilm where it localizes to cell-cell contact sites.

246 cells determined RhoA/Rho-kinase activity at cell-cell contact sites.

247 However, whether cell-cell contact specifically induces dynamic T cell re

248 omerization in cellulo and for its impact on cell-cell contact stability.

249 l division was not dependent on septins when cell-cell contacts, such as those with antigen-presentin

250 Cs (Notch active), revealing a substrate for cell-cell contact support during migrations, a developme

251 inhibition of locomotion (CIL), meaning that cell-cell contacts suppress force transduction to the su

252 unctional proteins at sinusoidal endothelial cell-cell contacts, switching capillaries from branching

253 gradients and repulsive effects arising from cell-cell contact, termed contact inhibition of locomoti

254 ude blockade of autoreactive immune cells by cell-cell contact, Th17 and IL-10 Tr1-like activities, o

255 scores the complexity of actin regulation at cell-cell contacts that involves actin activators, inhib

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

257 Upon ligand-receptor interaction in sites of cell-cell contact, the transmembrane domain of an engine

258 35 impaired N- and M-cadherin recruitment to cell-cell contacts, their stabilization at the plasma me

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

260 hard surfaces, myxobacteria glide, and upon cell-cell contact, they can efficiently exchange their O

261 of desmoplakin (DP) accumulation at sites of cell-cell contact, they play distinct roles in later ste

262 sion proteins that assemble into clusters at cell-cell contacts through cis- and trans- (adhesive) in

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

264 s demonstrate that RhoA is down-regulated at cell-cell contacts through p190RhoGAP-B, which is locali

265 mal phenotype and (ii) FAK_SRC inhibition of cell-cell contacts through the receptor-type tyrosine-pr

266 Moreover, we demonstrate that, with direct cell-cell contact, TME-derived endothelial cells provide

267 on system that typically engages at sites of cell-cell contact to initiate bidirectional signaling.

268 the body without an apparent requirement for cell-cell contact to persist in vivo.

269 v-containing secretory apparatus to sites of cell-cell contact to support polarized viral assembly an

270 etwork of claudin strands creates continuous cell-cell contacts to form the intercellular tight junct

271 EMT, epithelial cell adhesion switches from cell-cell contacts to mainly cell-ECM interactions, rais

272 ansfer retroviruses in vitro across synaptic cell-cell contacts to uninfected cells, a process called

273 ably, this behavior was independent of local cell-cell contact topologies and of position within the

274 perties could be inferred by the analysis of cell-cell contact topologies, and the nonequilibrium phe

275 eline for its ability to detect vertices and cell-cell contacts, track cells, and identify mitosis an

276 s are susceptible to EHV1 infection and that cell-cell contact transmits infectious virus to and from

277 Cell-cell contact triggers active polarization of organe

278 three hypotheses have been proposed: direct cell-cell contact, tunneling nanotubes, and exosomes.

279 Epithelial differentiation and augmented cell-cell contacts underlie the anti-migratory action ex

280 Stable cell-cell contacts underpin tissue architecture and orga

281 myosin-dependent contractile forces pull on cell-cell contacts until cells release.

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

283 oA activity to be significantly decreased at cell-cell contacts versus cell-ECM adhesions, and, of im

284 2 h or 1-3 days, and in selected experiments cell-cell contact was blocked.

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

286 nce axonal growth, demonstrating that direct cell-cell contact was not required.

287 Jun involved in proliferation, adhesion, and cell-cell contact, we found that AP-1 repressed the expr

288 junction reinforcement to stabilize adhesive cell-cell contacts, we propose an alternative mechanosen

289 lling cell migration and actin regulation at cell-cell contacts, we were interested to investigate th

290 oteins are actively recruited to the site of cell-cell contact where the viral material is efficientl

291 endocytic itinerary of Cx43 is altered upon cell-cell contact, which causes Cx43 to traffic by EEA1-

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

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

294 oma cells required viral replication, direct cell-cell contact with pDCs, and receptor-mediated endoc

295 mation of capillary-like networks induced by cell-cell contact with vascular smooth muscle cells (vSM

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

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

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

299 cytoplasm and subsequent localization to the cell-cell contact zone, assembly of adherens junction co

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