ライフサイエンスコーパス: cell matrix

1 man olfactory neurosphere-derived stem (ONS) cell matrix.

2 These activities lead to a loss of normal cell matrix adherent junctions and correlate with invasi

3 mount for dynamic cellular functions such as cell matrix adhesion and mechanotransduction.

4 al protein and plays a critical role in cell-cell matrix adhesion in the skin; however, its other bio

5 the first direct evidence that BP180, a cell-cell matrix adhesion molecule, possesses antitumor funct

6 ntrolled by signal-mediated cytoskeletal and cell matrix adhesion remodeling.

7 TK) with key roles in integrating growth and cell matrix adhesion signals, and FAK is a major driver

8 gh a cell required coordinated modulation of cell-matrix adhesion and actomyosin contractility in the

9 m1 and that the PDZ domain has a function in cell-matrix adhesion and cell migration.

10 This proposes that integrin-dependent cell-matrix adhesion and cell spreading are independentl

11 e, including small proteoglycans involved in cell-matrix adhesion and collagen fibrillogenesis.

12 t the expression of proteins associated with cell-matrix adhesion and cytoskeletal tension is regulat

13 ls, resulting in increased cell motility and cell-matrix adhesion and decreased cell-cell adhesion an

14 IP6K2 acts by enhancing cell-matrix adhesion and decreasing cell-cell adhesion.

15 Notch inhibited cells demonstrated decreased cell-matrix adhesion and enhanced lamellipodia formation

16 Reversible modulation of integrin-regulated cell-matrix adhesion and epithelial (E)-cadherin-mediate

17 We were also able to selectively restore cell-matrix adhesion and heart progenitor induction thro

18 hese data suggest that the interplay between cell-matrix adhesion and intercellular adhesion is an im

19 L), polymerizes actin at FAs, which promotes cell-matrix adhesion and mechanosensing.

20 nificance of this, demonstrating that cancer cell-matrix adhesion and outgrowth were markedly inhibit

21 in D1 and FAK, leading to enhanced survival, cell-matrix adhesion and proliferation of schwannoma.

22 lacking p38delta also displayed an increased cell-matrix adhesion and reduced cell detachment.

23 t Gas6 is mitogenic and increases schwannoma cell-matrix adhesion and survival acting via Axl in schw

24 P(C) contributes to increased proliferation, cell-matrix adhesion and survival in schwannoma cells ac

25 Integrins regulate cell-cell and cell-matrix adhesion and thereby play critical roles in

26 nal antagonism between Ddr/Intbeta1-mediated cell-matrix adhesion and Vegfr signaling appears to modu

27 Specifically, for sufficiently strong cell-matrix adhesion and/or sufficiently weak cell-cell

28 s that regulate alterations in cell-cell and cell-matrix adhesion are deregulated to promote the earl

29 derlying schwannomas basal proliferation and cell-matrix adhesion are not understood.

30 ing metastasis by facilitating cell-cell and cell-matrix adhesion as well as anchorage-independent ce

31 acoustofluidic device for parallel profiling cell-matrix adhesion at single-cell level.

32 rowth factor receptor and ErbB2/3, increased cell-matrix adhesion because of the overexpression of in

33 Targeted disruption of pre-cardiac cell-matrix adhesion blocked heart progenitor induction.

34 r distinction between cell-cell adhesion and cell-matrix adhesion by showing that type IV collagen is

35 anize the ECM and regulate its engagement by cell-matrix adhesion complexes (CMACs) are therefore ess

36 RAP1 activation is required for cell-matrix adhesion confirmed by adhesion to fibronecti

37 a, depression and schizophrenia, its role in cell-matrix adhesion could have implications for neural

38 , and genetic alterations that perturb local cell-matrix adhesion drove cell translocation.

39 n unexpected role of a classical cadherin in cell-matrix adhesion during cell migration.

40 tempers evoked Ca(2+) signals, and regulates cell-matrix adhesion during migration.

41 nal changes in extracellular compartment and cell-matrix adhesion genes but not in cell-cell adhesion

42 or cell surface adhesion receptors mediating cell-matrix adhesion in animals.

43 Given the importance of integrin-mediated cell-matrix adhesion in development of multicellular ani

44 ecouple the effects of cell-cell contact and cell-matrix adhesion in TGFbeta1-induced EMT.

45 odel of cancer invasion, where cell-cell and cell-matrix adhesion is accounted for through non-local

46 Cell-matrix adhesion is essential for building animals,

47 Profiling the kinetics of cell-matrix adhesion is of great importance to understan

48 d in basal keratinocytes, and functions as a cell-matrix adhesion molecule in the dermal-epidermal ju

49 Mechanistically, the tension sensing cell-matrix adhesion molecule, vinculin, and the Rho/ROC

50 erization triggered by specific cell-cell or cell-matrix adhesion molecules propelled invasive cell m

51 otein family serves to connect cell-cell and cell-matrix adhesion molecules to the intermediate filam

52 utants, we establish which components of the cell-matrix adhesion network are coordinated through dir

53 in this setting by modulating cell-cell and cell-matrix adhesion of endothelial cells.

54 velopment is the regulation of cell-cell and cell-matrix adhesion programmes.

55 n that mutant FGFR3 alters the cell-cell and cell-matrix adhesion properties of urothelial cells, res

56 gulation of genes encoding for cell-cell and cell-matrix adhesion proteins, and in the upregulation o

57 dation of the surrounding ECM accompanied by cell-matrix adhesion pulls the cells into the surroundin

58 d locally, rapidly, and correctly as diverse cell-matrix adhesion sites?

59 analyses of cell motion, membrane dynamics, cell-matrix adhesion status and F-actin organization, th

60 strength, epithelial cell mitosis rate, and cell-matrix adhesion strength.

61 Cell-matrix adhesion strongly influences developmental s

62 Hemidesmosomes are specialized cell-matrix adhesion structures that are associated with

63 blastin (Ambn) has the potential to regulate cell-matrix adhesion through familiar cell-binding domai

64 action couples with actin polymerization and cell-matrix adhesion to regulate cell protrusions and re

65 dings show that RAP1 has a prominent role in cell-matrix adhesion via extracellular matrix molecule f

66 hat Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac1 activi

67 When cell-matrix adhesion was reduced (in poly(2-hydroxyethyl

68 ha subunits and participate in cell-cell and cell-matrix adhesion, all with important implications fo

69 small GTPase regulating cell-cell adhesion, cell-matrix adhesion, and actin rearrangements, all proc

70 ch play critical roles in matrix deposition, cell-matrix adhesion, and actin stress fibers.

71 ar reactive oxygen species (ROS) production, cell-matrix adhesion, and cellular protrusions at the le

72 pled S1P receptors to regulate cell-cell and cell-matrix adhesion, and thereby influence cell migrati

73 dy, we determine that CD82 expression alters cell-matrix adhesion, as well as integrin surface expres

74 loss, namely multipolar morphology, enhanced cell-matrix adhesion, focal adhesion and, most important

75 ated that these compounds strongly inhibited cell-matrix adhesion, migration, and invasion of U87-MG

76 Its function, other than cell-matrix adhesion, remains unclear.

77 nabled and enhanced by altered cell-cell and cell-matrix adhesion, the cancerous mass can invade the

78 anied by fibronectin deposition and stronger cell-matrix adhesion, the transition to leader-cell phen

79 other matrices and integrins are involved in cell-matrix adhesion, this model system gives us a limit

80 al rearrangements required for cell-cell and cell-matrix adhesion.

81 enes implicated in networks of cell-cell and cell-matrix adhesion.

82 close to genes involved in intercellular and cell-matrix adhesion.

83 bited IEC migration while promoting enhanced cell-matrix adhesion.

84 vity, we were able to manipulate pre-cardiac cell-matrix adhesion.

85 tations in EXPH5 have significant defects in cell-matrix adhesion.

86 tin cytoskeleton to facilitate cell-cell and cell-matrix adhesion.

87 hat plays a major role in integrin-dependent cell-matrix adhesion.

88 potentiating schwannoma's proliferation and cell-matrix adhesion.

89 1, which is required for matrix assembly and cell-matrix adhesion.

90 emble podosomes, a specialized structure for cell-matrix adhesion.

91 ing to the relative strength of cell-cell to cell-matrix adhesion.

92 -Smad signaling independently of its role in cell-matrix adhesion.

93 r) cooperates with Integrin-beta1 to promote cell-matrix adhesion.

94 Here we report a novel role for 5-HT(2A) in cell-matrix adhesion.In HEK293 cells, which are loosely

95 al tumors where alterations in cell/cell and cell/matrix adhesion are early steps in tumor disseminat

96 barrier dysfunction and suggest that common cell-matrix-adhesion pathways are involved in the progre

97 sions and that they are the modular units of cell matrix adhesions.

98 ocess dependent on dynamic turnover of focal cell-matrix adhesions (FAs).

99 ced and confinement-induced EMT work through cell-matrix adhesions and cytoskeletal polarization, res

100 s suggest TRPV4 activity regulates forces at cell-matrix adhesions and is critical to aligned collage

101 which affects talin and vinculin dynamics in cell-matrix adhesions and results in the formation of ta

102 is a novel mechanism by which cell-cell and cell-matrix adhesions are coordinated.

103 In animals, cell-matrix adhesions are essential for cell migration,

104 Cell-matrix adhesions are exquisite sensors of physiolog

105 sion in the cleft region and increased cleft cell-matrix adhesions are required for cleft progression

106 and intercellular stresses that tend to pull cell-matrix adhesions away from the boundary.

107 somes represent a class of integrin-mediated cell-matrix adhesions formed by migrating and matrix-deg

108 iple function of lamellipodia is to organize cell-matrix adhesions in a spatially coherent manner.

109 ion, actomyosin contractility, cell-cell and cell-matrix adhesions on cleft progression, and it was u

110 Cell-cell and cell-matrix adhesions play essential roles in the functi

111 eves its distinct functions at cell-cell and cell-matrix adhesions remains unanswered.

112 While increased mechanical loading at cell-matrix adhesions results in focal adhesion growth,

113 Cooperative cell-cell and cell-matrix adhesions that sculpt the emerging tissue ar

114 Hemidesmosomes (HDs) are epithelial-specific cell-matrix adhesions that stably anchor the intracellul

115 Integrins are components of cell-matrix adhesions, and function as scaffolds for var

116 version of epithelial cell-cell adhesions to cell-matrix adhesions, but the mechanisms of cleft forma

117 lobal regulator of endothelial cell-cell and cell-matrix adhesions, CD151 is needed for the optimal f

118 Many of these are involved in cell-matrix adhesions, cytoskeleton, and transcriptional

119 n was not required for vinculin functions in cell-matrix adhesions, including integrin-induced cell s

120 Examples include cell-cell and cell-matrix adhesions, nucleoprotein bodies, and cell si

121 tion of forces from intercellular tension to cell-matrix adhesions, which break down the cadherin jun

122 t low-dose, disrupts the integrity of TJ and cell-matrix adhesions, with indicators of cellular stres

123 , and both have been shown to signal through cell-matrix adhesions.

124 s underlies the architecture and function of cell-matrix adhesions.

125 their microenvironment through cell-cell and cell-matrix adhesions.

126 recruited and/or activated in cell-cell and cell-matrix adhesions.

127 M-1) at cell-cell junctions and integrins at cell-matrix adhesions.

128 antioxidant, it has been reported to affect cell-matrix adhesions.

129 g protein thought to reinforce cell-cell and cell-matrix adhesions.

130 d probe its mechanical properties by forming cell-matrix adhesions.

131 phosphorylated at Y822 in cell-cell, but not cell-matrix, adhesions.

132 umber of innovative methods exist to measure cell-matrix adhesive forces, but they have yet to accura

133 Although cell-matrix adhesive interactions are known to regulate

134 Many cell-cell and cell-matrix adhesive interactions maintain and regulate

135 d to play an important role in mediating the cell-matrix adhesive properties of epithelial cells.

136 p1-Radil signaling, integrin activation, and cell-matrix adhesiveness required for tumor progression.

137 ers, lowered RhoA activities and compromised cell-matrix adhesiveness.

138 cosylation, which is important to ensure the cell/matrix anchor of muscle fibers.

139 n cytokines and their receptors, and over 30 cell matrix and adhesion molecules were found to be expr

140 of metabolites and electrolytes between the cell matrix and mitochondria.

141 sduction pathways, yet FGF functions such as cell-matrix and cell-cell adhesion remained unaffected,

142 anization, in conjunction with disruption of cell-matrix and cell-cell adhesion.

143 are integral membrane proteins that mediate cell-matrix and cell-cell adhesion.

144 suggest that the cooperative balance between cell-matrix and cell-cell adhesions in the heart is guid

145 Knowing how epithelial cells regulate cell-matrix and cell-cell adhesions is essential to unde

146 Although cell-matrix and cell-cell adhesions reorganize during de

147 ired for branching morphogenesis to regulate cell-matrix and cell-cell adhesions that are required fo

148 sion rate could be altered by modulating the cell-matrix and cell-cell adhesions.

149 e results suggest that mechanical forces via cell-matrix and cell-cell interactions are crucial in sp

150 Recapitulation of developmental cell-matrix and cell-cell interactions are of critical i

151 tural 3D settings, to better explore complex cell-matrix and cell-cell interactions, and to facilitat

152 strand-like microstructure through increased cell-matrix and cell-cell interactions, while compact de

153 d highlight a role for Rap1GAP in regulating cell/matrix and cell/cell adhesion.

154 iated with increased stress fiber formation, cell-matrix, and cell-cell adhesion in the shRNARelB (sh

155 the formation of 3-dimensional FAP-positive cell matrix, as demonstrated by reducing the fibronectin

156 rticle in this issue describes a rapid whole-cell matrix-assisted laser desorption ionization-time of

157 combination of shotgun proteomics and whole-cell matrix-assisted laser desorption ionization-time-of

158 Single-cell matrix-assisted laser desorption/ionization (MALDI)

159 turn is required for the active turnover of cell-matrix associations, cell migration, and wound clos

160 SRF-related decreases in vasomotor tone and cell-matrix attachment increase arterial elasticity in l

161 ine the role of talin, an adapter protein at cell-matrix attachment sites, in outside-in signaling.

162 uction, which are known to alter DNA repair, cell-matrix attachments, angiogenic process, and epithel

163 al relationship between apoE and endothelial cell matrix because the deregulation of these molecules

164 nd acquired valve abnormalities; and (c) the cell/matrix biology of degeneration in replacement tissu

165 size and shape depend on cell shape changes, cell-matrix communication, and apical membrane growth.

166 Cell-cell and cell-matrix communications play important roles in both

167 A cell-matrix composite was constructed by applying fibrin

168 ificantly decreased the force exerted by the cell-matrix constructs in a tensiometer testing platform

169 Initial FN nanofibrils form within <5 min of cell-matrix contact and subsequently extend at a rate of

170 y locally facilitates the destabilization of cell-matrix contact sites.

171 Here, we analyze matrix forces after initial cell-matrix contact, when early rigidity-sensing events

172 en cell death and survival following loss of cell-matrix contact.

173 s cellular movement is driven by progressive cell-matrix contacts and actively translocates prospecti

174 llagen gels when seeded at low density, when cell-matrix contacts dominate, whereas contractility of

175 d the integrity of endothelial cell-cell and cell-matrix contacts in vivo.

176 nd inside-out signaling that maintains tumor cell-matrix contacts required for cell invasion.

177 olves extensive remodelling of cell-cell and cell-matrix contacts.

178 agonist Yoda1 increasing the number of focal cell-matrix contacts.

179 tifaceted regulation that includes important cell-matrix derived interactions.

180 tability, along with improved diffusion from cell matrix due to microwave-induced sorghum cell wall d

181 These studies support a model wherein cell-matrix engagement regulates the functional integrit

182 ates the dynamic assembly and disassembly of cell-matrix focal adhesions (FAs), which is essential fo

183 ent upon local anisotropies generated by the cell-matrix force balance.

184 neurysm, new knowledge on the involvement of cell-matrix forces could lead to elucidation of disease

185 1) and hibernation decreased (P<0.01) in the cells+matrix group only.

186 nd wall motion abnormalities improved in the cells+matrix group.

187 that generates high yields of an osteogenic cell-matrix (ihOCM) in vitro.

188 ation, lineage determination, cell adhesion, cell-matrix interaction and cytoskeleton remodeling.

189 rful model system to study integrin-mediated cell-matrix interaction in an in vivo context, as it is

190 that IGF signaling is masked by signals from cell-matrix interaction in anchorage-dependent condition

191 We provide evidence that integrin-mediated cell-matrix interaction is a key player in pluripotency

192 dation, a minimal network model of a dynamic cell-matrix interaction is proposed.

193 ing of ITGB6 resulting in either compromised cell-matrix interaction or compromised ITGB6 activation

194 The defect is associated with an altered cell-matrix interaction that is evident by morphologic c

195 GF) is a matricellular protein that mediates cell-matrix interaction through various subtypes of inte

196 defy anoikis, cell death caused by a lack of cell-matrix interaction, and grow in an anchorage-indepe

197 es associated with glycolysis, angiogenesis, cell-matrix interaction, epithelial to mesenchymal trans

198 To acquire information on this cell-matrix interaction, we developed a technique for co

199 lar mechanism and function of Ambn in enamel cell-matrix interaction.

200 oproteins in vertebrates that broadly affect cell-matrix interaction.

201 f collagen fibrils play an important role in cell-matrix interactions and are a manifestation of thei

202 es (ECMs), providing new pathways to explore cell-matrix interactions and direct cell fate under phys

203 s and the extracellular matrix (ECM) through cell-matrix interactions and ECM remodelling.

204 These findings have provided insights into cell-matrix interactions and how these interactions diff

205 and myocardial dysfunction, but the role of cell-matrix interactions and integrins in this process h

206 nctions, including maintenance of epithelial cell-matrix interactions and intestinal homeostasis.

207 he inhibition of the AGE-RAGE axis to resume cell-matrix interactions and maintain tissue integrity.

208 or cells (LEPC) that incorporate the in vivo cell-matrix interactions are essential to enhance LEPC e

209 Together, our data suggest that defective cell-matrix interactions are linked to Wnt signaling and

210 Cell-matrix interactions are made possible by integrins,

211 These results show that alterations in cell-matrix interactions are sufficient to initiate and

212 alloproteinase ADAM9 modulates cell-cell and cell-matrix interactions as well as ectodomain shedding

213 differentiation is likely to involve altered cell-matrix interactions but the mechanism is not known.

214 er, our results suggest that Tmem2 regulates cell-matrix interactions by affecting both ECM organizat

215 an Arg-Gly-Asp (RGD) motif needed to mediate cell-matrix interactions by binding to cell-surface inte

216 Mechanical cell-matrix interactions can drive the innate immune res

217 our of mono-dispersed epithelial cells where cell-matrix interactions dominate and hinder formation o

218 AI and further highlights the importance of cell-matrix interactions during enamel formation.

219 impact of transmembrane protein 2 (tmem2) on cell-matrix interactions during muscle morphogenesis in

220 Our recent efforts have focused on the tumor cell-matrix interactions essential to tumor cell activat

221 vidence that Nck directs the polarization of cell-matrix interactions for efficient migration in thre

222 ydrogels to recapitulate the composition and cell-matrix interactions found in the native microenviro

223 onnective tissues, and the key to unraveling cell-matrix interactions in diseases.

224 Whether and how cell-matrix interactions influence virus particle uptake

225 faces, these fibrous materials recapitulated cell-matrix interactions observed with collagen matrices

226 By reproducing physiological cell-cell and cell-matrix interactions of the native niche environment

227 as the regulatory influence of cell-cell and cell-matrix interactions on signaling outcomes.

228 Cdc42 deficiency leads to a defect in global cell-matrix interactions reflected by a decrease in coll

229 derstanding the molecular mechanisms whereby cell-matrix interactions regulate liver regeneration may

230 sustain oncogenic signals in the absence of cell-matrix interactions remains poorly understood.

231 oenvironment with a balance of cell-cell and cell-matrix interactions supports distinctive phenotypes

232 These effects are opposite to cell-matrix interactions that are strengthened by proton

233 TG2) and fibronectin (FN) is involved in the cell-matrix interactions that regulate cell signaling, a

234 single-cell migration with matrix fibers and cell-matrix interactions through contact guidance and ma

235 rlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adh

236 les, but rather regulate matrix proteins and cell-matrix interactions to influence normal cellular fu

237 ignaling by growth factors and cell-cell and cell-matrix interactions to prevent apoptosis, senescenc

238 Relevance of matrix viscoplasticity to cell-matrix interactions was established through a quant

239 l the cell type, organization, and cell-cell/cell-matrix interactions within these systems.

240 of how context, in particular cell-cell and cell-matrix interactions, affects endothelial cell respo

241 t a variety of stimuli, including cytokines, cell-matrix interactions, and challenge with foreign mat

242 gnaling critical to intercellular junctions, cell-matrix interactions, and cytoskeletal regulation.

243 events, including cell-cell communications, cell-matrix interactions, and response to environmental

244 on, cytoskeleton organization, cell-cell and cell-matrix interactions, apoptosis, cell cycle, and oxi

245 d in a wide range of cell-cell signaling and cell-matrix interactions, both in vitro and in vivo in i

246 Embryogenesis is guided by cell-cell and cell-matrix interactions, but it is unclear how these ph

247 ILK is involved in cell-matrix interactions, cytoskeletal organization, and

248 ion to the well-recognized, force-regulated, cell-matrix interactions, forces also tune the interacti

249 integrin-linked kinase (ILK), a mediator of cell-matrix interactions, is indispensable for retinal a

250 Many factors, including cell-matrix interactions, play a role in the development

251 de-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tum

252 lly isotropic matrix via locally reinforcing cell-matrix interactions.

253 ating physiologically relevant cell-cell and cell-matrix interactions.

254 th the integrity of extracellular matrix and cell-matrix interactions.

255 ember of the proteoglycan family involved in cell-matrix interactions.

256 that early and late amelogenesis depend upon cell-matrix interactions.

257 sion-related genes, disrupting cell-cell and cell-matrix interactions.

258 n domains capable of mediating cell-cell and cell-matrix interactions.

259 time of cuticle secretion and remodeling of cell-matrix interactions.

260 une system functioning through cell-cell and cell-matrix interactions.

261 ar differentiation through its modulation of cell-matrix interactions.

262 of uPA overexpression on cell migration and cell-matrix interactions.

263 sion molecules that direct key cell-cell and cell-matrix interactions.

264 as key regulators of cellular functions and cell-matrix interactions.

265 the cells it carries, promoting advantageous cell-matrix interactions.

266 of adherens junctions, tight junctions, and cell-matrix interactions.

267 hat must be accounted for when interrogating cell-matrix interactions.

268 extracellular cues, including cell-cell and cell-matrix interactions.

269 Although it is known that cell/matrix interactions are essential for directional m

270 sion/growth-regulatory galectins within cell-cell/matrix interactions.

271 Nanoscale properties at the cell-matrix interface that appear to affect adherent ste

272 al a link between filopodia formation at the cell-matrix interface, in collectively invading cells an

273 ation of DDR1 cleavage and activation at the cell-matrix interface.

274 ock face-scanning electron microscopy of the cell-matrix interface.

275 laminin by redistributing alpha3beta1 at the cell-matrix interface.

276 librate and visualize cellular forces at the cell-matrix interface.

277 sults in a tunable stiffness gradient at the cell-matrix interface.

278 However, studies on cell/matrix interplay are impossible to perform due to d

279 f tightly controlled cell-cell adhesions and cell-matrix junctions between lens epithelial (LE) cells

280 Cell-cell and cell-matrix junctions transmit mechanical forces during

281 nked to the plasma membrane at cell-cell and cell-matrix junctions.

282 ural and signaling proteins at cell-cell and cell-matrix junctions.

283 rplay between the mechanical environment and cell/matrix kinetics, ultimately dictating changes in th

284 -) mice had intercellular gaps below TJs and cell matrix loosening.

285 Cell-cell and cell-matrix mechanical interactions through membrane rec

286 yalocytes, contractile myofibroblasts, glial cells, matrix metalloproteinases-2 and -9, and collagen

287 ith cells to generate three-dimensional (3D) cell-matrix microtissue arrays.

288 The measurements were independent of the cell matrix or the cell lysis buffer and were not affect

289 cell adhesion molecules that mediate either cell-matrix or cell-cell interactions.

290 This provided unique perspectives of live cell-matrix organization and a means of assaying tissue

291 rangements in SMC morphology, cell-cell, and cell-matrix relationships, including disruption of the e

292 Cross talk between cell-cell and cell-matrix signaling is crucial for regulating these tr

293 ling transducers that regulate cell-cell and cell-matrix signals across the membrane.

294 nd that this event depends on subendothelial cell matrix stiffness.

295 TV bioprostheses demonstrate "growth" and a cell-matrix structure similar to mature NVs while mainta

296 In contrast to other cell-matrix systems in which cells migrate along fibers,

297 owed that translocation of this complex from cell-matrix to cell-cell adhesion sites was required for

298 aling assay that was associated with reduced cell-matrix traction forces, decreased levels of integri

299 ir endogenous TGF-beta2 expression and their cell-matrix traction stresses.

300 homeostasis of the intervertebral disc (IVD) cell matrix, with physiologic and nonphysiologic loads l