ライフサイエンスコーパス: contact inhibition

1 g capacity density, K, which is a measure of contact inhibition.

2 istinct difference in invasiveness is due to contact inhibition.

3 tial link between the Hippo pathway and cell contact inhibition.

4 growth suppression in a manner dependent on contact inhibition.

5 ration, and cell-to-cell interaction through contact inhibition.

6 ivation of both p53 and pRb attenuates early contact inhibition.

7 zation, and H-ras(V12)/c-myc-induced loss of contact inhibition.

8 o cell density, and is able to overcome cell contact inhibition.

9 that showed rapid proliferation and loss of contact inhibition.

10 red at passage 3 coincident with the loss of contact inhibition.

11 t commissurals apparently maintained through contact inhibition.

12 the plasma membrane rescues these cells from contact inhibition.

13 h by counterbalancing the adverse effects of contact inhibition.

14 es, slow growth kinetics, and restoration of contact inhibition.

15 tial inhibition of their proliferation under contact inhibition.

16 n, increased cell proliferation, and loss of contact inhibition.

17 ion and allowed normal fibroblasts to bypass contact inhibition.

18 ng and growth to a high density with loss of contact inhibition.

19 , nef induced saturation density and loss of contact inhibition.

20 mitotic rate, reduced apoptosis, and reduced contact inhibition.

21 le is part of a molecular switch controlling contact inhibition.

22 sly shown that HIV-infection induces loss of contact inhibition.

23 cluding reduced serum dependence and loss of contact inhibition.

24 tream of DNA damage, cellular senescence and contact inhibition.

25 ch cells have been transiently released from contact inhibition.

26 rol of a single parameter, namely, a form of contact inhibition.

27 ch cells have been transiently released from contact inhibition.

28 1 arrest triggered by TGFbeta, p16INK4a, and contact inhibition.

29 reflect release of the FGF-2 gene from cell contact inhibition.

30 saturating cell density in a process termed contact inhibition.

31 lve symplastic transport or direct cell-cell contact inhibition.

32 HL-negative RCC cells exit the cell cycle by contact inhibition.

33 lattened appearance, and the cells exhibited contact inhibition.

34 G0 by serum and growth factor withdrawal or contact inhibition.

35 te proliferation that is insensitive to cell contact inhibition.

36 ed by enlargement of the cells and increased contact inhibition.

37 ies at transitions between proliferation and contact inhibition.

38 k and the major regulatory mechanism of cell-contact inhibition.

39 as YAP cytoplasmic translocation induced by contact inhibition.

40 hortens population-doubling time and reduces contact inhibition.

41 echanical feedback on the cell cycle akin to contact inhibition.

42 ive chemotaxis rather than chemorepulsion or contact inhibition.

43 t in which cells display hypersensitivity to contact inhibition.

44 anchorage-independent growth and escape from contact inhibition.

45 e studies of molecular mechanisms underlying contact inhibition.

46 SSeCKS in suppressing PKC activation during contact inhibition.

47 -rat fibroblasts display hypersensitivity to contact inhibition, a phenomenon we termed "early contac

48 We propose that coattraction and contact inhibition act in concert to allow cell collecti

49 ative hypotheses about how Wnt signaling and contact inhibition affect proliferation.

50 istent with transformation including loss of contact inhibition, anchorage independence and tumour fo

51 ics of ras transformation, including loss of contact inhibition, anchorage independence, and tumorige

52 mrg1 in Rat1 cells resulted in loss of cell contact inhibition, anchorage-independent growth in soft

53 results in increased proliferation, loss of contact inhibition, anchorage-independent growth, and de

54 oncogenic transformation, including loss of contact inhibition, anchorage-independent survival and p

55 ibit anchorage-independent growth, a lack of contact inhibition and a strong Ewing sarcoma gene expre

56 roblastic morphology, loss of cell polarity, contact inhibition and acquired migratory and invasive p

57 f a transformed phenotype, including loss of contact inhibition and acquisition of anchorage-independ

58 A reduced responsiveness to cell-cell contact inhibition and an increase in E6/E7 activity cor

59 sts expressing this ITAM construct also lost contact inhibition and anchorage dependence.

60 p27 expression is regulated by cell contact inhibition and by specific growth factors, such

61 Assessment of contact inhibition and differentiation-promoting culture

62 nant phenotype, including the acquisition of contact inhibition and diminution of anchorage-dependent

63 In coculture, BCCs exhibit contact inhibition and do not require otherwise needed g

64 of cells to disperse via mechanisms such as contact inhibition and epithelial-to-mesenchymal transit

65 lacking cell adhesion molecules escaped from contact inhibition and exhibited abnormal proliferation

66 ansformed by the following criteria: loss of contact inhibition and formation of foci characteristic

67 t agar and at low serum concentrations, lost contact inhibition and formed tumors after injection int

68 oduction of mutant IDH2 also induced loss of contact inhibition and generated undifferentiated sarcom

69 d provide a mechanism for antagonism between contact inhibition and growth factor action.

70 a transformed phenotype manifest as loss of contact inhibition and loss of dependence on exogenous g

71 of caveolin-1 may be important in mediating contact inhibition and negatively regulating the activat

72 ration rate, but is insufficient for exiting contact inhibition and oncogene-induced anchorage-indepe

73 ent cells is sufficient to restore exit from contact inhibition and oncogenesis.

74 EDTA released cells from contact inhibition and promoted proliferation in corneal

75 cquire transformed features such as impaired contact inhibition and reduced serum dependence.

76 Contact inhibition and reduction in serum concentration

77 ithelial cell line is sufficient to overcome contact inhibition and results in the formation of cellu

78 yte physiologic growth arrest in response to contact inhibition and serum starvation in vitro, sugges

79 previously unrecognized link between BMI-1, contact inhibition and the Hippo-YAP pathway and suggest

80 Cell-cell contact inhibition and the mechanical environment of cel

81 se intercellular contacts, causing a loss of contact inhibition and the rapid initiation of healing.

82 us-to-cytoplasm translocation of YAP1 during contact inhibition and thus inhibits YAP1 transactivatio

83 s of several of the kinases leads to loss of contact inhibition and to anchorage-independent growth,

84 (INK4a/b) expression is induced during early contact inhibition and upon a variety of stresses such a

85 urthermore, we demonstrate that the onset of contact-inhibition and the timing of spatial patterns in

86 r gene that functions in cell proliferation, contact inhibition, and angiogenesis.

87 the cells used in experiments can lose their contact inhibition, and can therefore pile up on top of

88 ade deficient in VASP by RHKO showed loss of contact inhibition, and consequently, continued cell div

89 s) underwent reversible cell cycle arrest by contact inhibition, and determined whether increases in

90 epithelial phenotype, TSC astrocytes outgrew contact inhibition, and monolayers sporadically generate

91 stimulated proliferative potential, loss of contact inhibition, and multilayer fibroblastic cells.

92 n a reduction of growth rate, restoration of contact inhibition, and suppression of both soft agar cl

93 with anchorage-independent growth, defective contact inhibition, and the ability to form metastatic t

94 dence, loss of anchorage dependence, loss of contact inhibition, and tumor formation in immunocomprom

95 , PRC17 induced growth in low serum, loss of contact inhibition, and tumor formation in nude mice.

96 on of stable cell-cell contacts, implicating contact inhibition as an important mechanism of growth a

97 include cytoskeletal reorganization, reduced contact inhibition at confluence and accelerated tumour

98 , which is driven by the stress of prolonged contact inhibition at confluence, occurs far more freque

99 to amplify cell-cell interactions, we induce contact-inhibition at a higher threshold level of EGF.

100 have limited proliferative capacity due to "contact-inhibition" at G1 phase.

101 f p16(Ink4a) and p27(Kip1) in the control of contact inhibition became temporally separated in this s

102 are insufficient to quantify the effects of contact inhibition because they focus on data describing

103 and increased exogenous SDF-1alpha prevented contact inhibition between BCCs and BM stroma.

104 h inhibition may not be solely attributed to contact inhibition but may involve the redistribution of

105 The Pak1 kinase mutants perturb contact inhibition by a mechanism that depends on the Pa

106 that cadherins are involved in regulation of contact inhibition by controlling the function of the Pa

107 locking the ability of E-cadherin to mediate contact inhibition by either antagonistic antibodies or

108 rters, and the endothelium was released from contact inhibition by producing a 2-mm scrape wound.

109 suggesting that silencing of BMI-1 restored contact inhibition by restoring normal activation of the

110 Such contact-inhibition can be delayed from Day 21 to Day 42

111 Cells arrested by contact inhibition, chemical arresting agents, or termin

112 The term contact inhibition (CI) encompasses the cellular changes

113 During cell cycle arrest caused by contact inhibition (CI), cells do not undergo senescence

114 ct inhibition, a phenomenon we termed "early contact inhibition." Contact inhibition is a key antican

115 layer of protection conferred by two-tiered contact inhibition contributes to the remarkable tumor r

116 erhaps by regulating cell proliferation by a contact inhibition-dependent mechanism.

117 provides a quantitative characterization of contact inhibition dynamics on tissue-wide and single ce

118 timing of its formation, can be explained by contact inhibition dynamics within the geometry of the D

119 ic expression of ING4 suppressed the loss of contact inhibition elicited by either MYCN or MYC but ha

120 a screen for genes that suppress the loss of contact inhibition elicited by overexpression of the pro

121 nchorage independent growth and release from contact inhibition (focus formation).

122 Drosophila macrophages (haemocytes) require contact inhibition for their uniform embryonic dispersal

123 ssing SYF cells are transformed and overcome contact inhibition, form colonies in transformation assa

124 ke the parental RIE cells, RIE-Tr cells lost contact inhibition, formed foci in culture, grew in soft

125 Furthermore, they lost contact inhibition, had enhanced anchorage-independent g

126 Contact inhibition has been implicated as an important a

127 This quantitative model of contact-inhibition has direct implications for how tissu

128 egative Rac blocks PAK-mediated release from contact inhibition, implying that PAK functions upstream

129 Inhibition of YAP function restores contact inhibition in a human cancer cell line bearing d

130 re, AMOTL2 knockdown results in loss of cell contact inhibition in a manner dependent on the function

131 strate that cyclin D1b specifically disrupts contact inhibition in a manner distinct from cyclin D1a.

132 o-YAP pathway and suggest that resistance to contact inhibition in BMI-1 overexpressing cancer cells

133 at high levels of BMI-1 confer resistance to contact inhibition in ESFT cells.

134 Contact inhibition in human and mouse is triggered by th

135 iating the cleavage of RPTPmu in response to contact inhibition in HUVEC.

136 In contrast, early contact inhibition in naked mole-rat is associated with

137 l Wnt signaling is essential for the loss of contact inhibition in NF2-deficient cells.

138 d and remains inappropriately high in during contact inhibition in pVHL-deficient cell lines.

139 to anchorage-independent growth and loss of contact inhibition in rat fibroblasts.

140 admium-transformed cells exhibited a loss of contact inhibition in vitro and rapidly formed highly in

141 ost abundant cell of the CNS and demonstrate contact inhibition in which a nonproliferative, nonmotil

142 ferative changes in vitro, including reduced contact inhibition, increased beta-catenin expression, a

143 lial cells (evidenced by decreased cell-cell contact inhibition, increased proliferation and apoptosi

144 Stratification and contact inhibition induced by elevated Ca2+ are dependen

145 roliferation of transit-amplifying cells via contact inhibition-induced up-regulation of p27/kip1 pro

146 The mechanism by which Muc4 disrupts contact inhibition involves a Muc4-induced relocalizatio

147 Contact inhibition is a central feature orchestrating ce

148 Our measurements and analysis show that contact inhibition is a consequence of mechanical intera

149 Deficient contact inhibition is a hallmark of invasive cancer cell

150 omenon we termed "early contact inhibition." Contact inhibition is a key anticancer mechanism that ar

151 merical simulations demonstrate that loss of contact inhibition is a sufficient mechanism, appropriat

152 from this laboratory, strongly suggest that contact inhibition is an important mechanism responsible

153 ning tissues, whereas abnormal regulation of contact inhibition is associated with pathological condi

154 Under normal conditions, contact inhibition is associated with the proper functio

155 human umbilical vein endothelial cells from contact inhibition is blocked by an unphosphorylatable f

156 porally separated in this species: the early contact inhibition is controlled by p16(Ink4a), and regu

157 ion is controlled by p16(Ink4a), and regular contact inhibition is controlled by p27(Kip1).

158 This abrogation of contact inhibition is dependent on the number of mucin r

159 This demonstrates that the loss of contact inhibition is due to a direct effect of HIV-1.

160 Thus, the requirement of Akt for exiting contact inhibition is mediated by the induction of Skp2

161 blot studies in cultured cells indicate that contact inhibition is mediated, in large part, through t

162 Contact inhibition is often antagonized by mitogenic gro

163 we have gleaned little understanding of how contact inhibition is regulated and only lately observed

164 authors also have shown that the process of contact inhibition is reversible, which may explain part

165 ns epithelial tissue growth, and the loss of contact-inhibition is a hallmark of cancer cells.

166 ncreases the threshold level of EGF at which contact-inhibition is triggered.

167 vitro assays, FAP or FSM expression restored contact inhibition, led to cell cycle arrest at G0/G1 ph

168 s, they acquired new characteristics such as contact inhibition loss, telomerase activity, anchorage-

169 several hallmarks of transformation-reduced contact inhibition, lower dependence on serum for growth

170 Muc4-induced abrogation of contact inhibition may be an important mechanism by whic

171 pression resulted in a profound loss of cell contact inhibition, multiple layers of overgrowing cells

172 s was true whether quiescence was induced by contact inhibition (NIH 3T3 mouse cells), growth factor

173 The contact inhibition observed in the alpha5 myoblasts is m

174 Cx43 induced contact inhibition of cell growth but in contrast to oth

175 It mediates contact inhibition of cell growth downstream of cadherin

176 Contact inhibition of cell growth is essential for embry

177 erin function leads to the density-dependent contact inhibition of cell growth.

178 the regulation of cell adhesion and possibly contact inhibition of cell growth.

179 F2 knockout mouse embryonic fibroblasts lost contact inhibition of cell proliferation and contained s

180 asts, by growth factor withdrawal but not by contact inhibition of cell proliferation.

181 This contact inhibition of cell spreading was blocked by disr

182 g confluency (day 8), and eventually undergo contact inhibition of growth (day 10).

183 Merlin regulates contact inhibition of growth and controls the availabili

184 ions as part of the Hippo pathway to promote contact inhibition of growth and tumor suppression by ph

185 of Merlin and indicate that Merlin mediates contact inhibition of growth by suppressing recruitment

186 ations based on staining that confluency and contact inhibition of growth can cause a small increase

187 induction of goblet cell differentiation by contact inhibition of growth depended on the loss of Jag

188 ton protein necessary for the maintenance of contact inhibition of growth in cells.

189 p21 function was not sufficient to overcome contact inhibition of growth nor for tumor formation in

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

191 -dependent chord-like phenotype, the loss of contact inhibition of growth, and an inhibition of pro-a

192 sruptions of the actin cytoskeleton, lack of contact inhibition of growth, and anchorage-independent

193 expressed in adherent Rat1A cells decreased contact inhibition of growth, and expression of AML1/MDS

194 h exhibit both adhesion-dependent growth and contact inhibition of growth, showed that the effects ar

195 nt to release primary endothelial cells from contact inhibition of growth.

196 estoration of type I collagen expression and contact inhibition of growth.

197 rowth rates in complete medium and both show contact inhibition of growth.

198 ive guidance factor Semaphorin 4D and induce contact inhibition of locomotion (CIL) in osteoblasts th

199 Contact inhibition of locomotion (CIL) is a multifaceted

200 There is growing evidence that contact inhibition of locomotion (CIL) is essential for

201 Contact inhibition of locomotion (CIL) is the process th

202 lar matrix molecules and effectively abolish contact inhibition of locomotion (CIL) of the cells.

203 tween cell softness, cell-cell adhesion, and contact inhibition of locomotion (CIL) yields structures

204 l property of neural crest (NC) migration is contact inhibition of locomotion (CIL), a process by whi

205 rate and on each other, and interact through contact inhibition of locomotion (CIL), meaning that cel

206 these cell-cell interactions, which include contact inhibition of locomotion (CIL), micropatterned s

207 fects arising from cell-cell contact, termed contact inhibition of locomotion (CIL).

208 own phenomenological cell behaviors, such as contact inhibition of locomotion and force-induced cell

209 non-canonical Wnt signalling abolishes both contact inhibition of locomotion and the directionality

210 However, the molecular basis of contact inhibition of locomotion and whether it also occ

211 n likened to malignant invasion, demonstrate contact inhibition of locomotion both in vivo and in vit

212 ework, we explain how cells characterized by contact inhibition of locomotion can display coherent co

213 These results provide the first example of contact inhibition of locomotion in vivo, provide an exp

214 l Abercrombie first described the process of contact inhibition of locomotion more than 50 years ago

215 Contact inhibition of locomotion was discovered by Aberc

216 se results show a role for N-cadherin during contact inhibition of locomotion, and they reveal a mech

217 y mechanisms on rotational motion, including contact inhibition of locomotion, neighbor alignment, an

218 meets another cell type, it fails to display contact inhibition of locomotion; instead, it invades th

219 N-cadherins all implicate N-cadherin in the contact inhibition of migration.

220 ctable phenotypes in the developing animals, contact inhibition of proliferation and cell-substrate a

221 ppo pathway is involved in the regulation of contact inhibition of proliferation and responses to var

222 ppo signaling pathway has been implicated in contact inhibition of proliferation as well as organ siz

223 ral tumor-suppressor genes and regulates the contact inhibition of proliferation in cultured cells.

224 ropose that acetylated microtubules regulate contact inhibition of proliferation through the Hippo pa

225 either reduced cell-cell adhesion or reduced contact inhibition of proliferation triggers cyst induct

226 onents are required for E-cadherin-dependent contact inhibition of proliferation.

227 sites was required for the establishment of contact inhibition of proliferation.

228 ntage in the urothelium by overcoming normal contact inhibition of proliferation.

229 owth of tumors is characterized by a loss of contact inhibition of proliferation.

230 n overlap with the region that mediates cell contact inhibition of the FGF-2 promoter.

231 y multiple mechanisms, including chemotaxis, contact-inhibition of locomotion and cell sorting.

232 Contact-inhibition of proliferation constrains epithelia

233 ire monolayers-that combines both vertex and contact-inhibition-of-locomotion models to include cell-

234 effects of cell migration, compression, and contact inhibition on the growth of tumor cell clusters

235 1 in transformation assays measuring loss of contact inhibition or anchorage-independent growth.

236 s a paralysis and retraction of protrusions (contact inhibition or collapse) when the medial surface

237 e to cues inherent in release from cell-cell contact inhibition or presented by denuded substratum, b

238 insensitive to G(1) arrest signals following contact inhibition or serum starvation.

239 cells to escape G(1)/G(0) arrest induced by contact inhibition or serum withdrawal.

240 be opposed in crowded cell cultures through contact-inhibition or by autocrine release of antiprolif

241 ells rendered quiescent by serum starvation, contact inhibition, or differentiation.

242 ed for Src to increase growth rate, suppress contact inhibition, or suppress anchorage dependence.

243 es a novel signaling cascade regulating cell contact inhibition, organ size control, cell growth, pro

244 es a novel signaling cascade regulating cell contact inhibition, organ size control, cell growth, pro

245 Contact inhibition penalizes clumped cells by halting th

246 We discovered that the loss of contact inhibition plays a critical role in the initiati

247 Here, to investigate the role that contact inhibition plays in the patterning of haemocyte

248 Bronchial Cdc42 loss destroys contact inhibition potentially through cell polarity dis

249 E-cadherin to mediate cell-cell contact and contact inhibition presumably accounts for its antitumor

250 ptible to transformation, however, prolonged contact inhibition progressively selects mutants that fa

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

252 of IMR90 cells in G1 by serum starvation and contact inhibition reduced transduction.

253 Contact inhibition refers to a reduction in the rate of

254 ight junction proteins through endosomes and contact-inhibition-regulated cell growth.

255 Thus, the Hippo pathway links contact-inhibition regulation to miRNA biogenesis and ma

256 We demonstrate that early contact inhibition requires the activity of p53 and pRb

257 sting loss of anchorage-dependent growth and contact inhibition, respectively.

258 The normal cell contact inhibition response is mediated, in large part,

259 Growth arrest of normal diploid cells by contact inhibition resulted in an induction of p27(kip1)

260 the classic immortalization and loss of cell contact inhibition seen when the Rb1 pathway is lost.

261 repare to exit the cell cycle in response to contact inhibition, serum starvation, or replicative sen

262 grow in circular colonies that densify until contact inhibition takes place.

263 The Hippo signaling pathway imposes the cell contact inhibition that establishes organ size and tissu

264 ocytomas and provide a model for the loss of contact inhibition that may broadly apply to understandi

265 d by others arise predominantly by decreased contact inhibition, that is, increased proliferation.

266 ng epithelial cell cultures and is known as "contact inhibition." The study presented here provides a

267 Further, during contact inhibition, there is more p21 associated with cy

268 sk the importance of parameters that control contact inhibition through scaling arguments.

269 tic growth equation as a caricature model of contact inhibition to make recommendations as to how to

270 rin T567A, but not wild-type ezrin, restores contact inhibition to Net- and Dbl-transformed cells, an

271 cell cycle progression, and it imposes cell contact inhibition to suppress tumor outgrowth.

272 Cancer cells often lose contact inhibition to undergo anchorage-independent prol

273 42 failed to achieve such reprogramming when contact inhibition transitioned to senescence with nucle

274 Contact inhibition was restored with low SDF-1alpha leve

275 in MCDB 402 in 2% CS in successive rounds of contact inhibition was uniform increases in saturation d

276 A levels remained relatively constant during contact inhibition, whereas immunoblotting showed that t

277 p2 mRNA and protein are induced upon exiting contact inhibition, which enables entry into mitosis.

278 hypersensitivity of naked mole rat cells to contact inhibition, which is associated with induction o

279 expression restored junctions, polarity, and contact inhibition while suppressing migration and metas

280 measured in cells that attain G1 arrest upon contact inhibition, wild-type p53 was inactive, and only

281 These cells were defective in cell-contact inhibition with changes in Merlin phosphorylatio