ライフサイエンスコーパス: cell matrix

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

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

3 ion of E-cadherin would affect expression of cell matrix adhesion receptors.

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

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

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

7 ion receptors such as integrins that mediate cell-matrix adhesion and also transduce signals into cel

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

9 f galectin-3 expression, resulted in reduced 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 nificance of this, demonstrating that cancer cell-matrix adhesion and outgrowth were markedly inhibit

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

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

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

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

24 in the cellular control of integrin-mediated cell-matrix adhesion and that loss of this interaction l

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

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

27 Cell-cell and cell-matrix adhesion are crucial during many stages of e

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 nery to promote cell edge protrusions during cell-matrix adhesion are unclear.

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

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 Cell-matrix adhesion complexes (CMACs) play fundamental

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

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

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

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

41 Our results show that a spondin maintains cell-matrix adhesion in multiple tissues.

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

43 ant model shows that integrin beta1-mediated cell-matrix adhesion is a major determinant of the mural

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

45 Cell-matrix adhesion is essential for building animals,

46 Cell-matrix adhesion is essential for the development an

47 Loss of cell-matrix adhesion is often associated with acute epit

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

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

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

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

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

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

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

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

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

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

58 Cell-matrix adhesion strongly influences developmental s

59 somes and are thought to be more involved in cell-matrix adhesion than invadopodia [2-4].

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

61 The impact of cAMP on cell-matrix adhesion was followed by immunostaining of f

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

63 g the effects of both cell-cell adhesion and cell-matrix adhesion, along with cell growth and proteol

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

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

66 lating cells, eventual loss of cell-cell and cell-matrix adhesion, and dose-dependent failure of blas

67 Reversible modulation of cell-cell adhesion, cell-matrix adhesion, and proteolytic activity plays a c

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

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

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

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

72 Although many cells generally require cell-matrix adhesion, our results demonstrate that CRKL

73 n MIG-2-null colon cancer cells strengthened cell-matrix adhesion, promoted focal adhesion formation,

74 These findings, perturbed and up-regulated cell-matrix adhesion, suggest possible mechanisms for th

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

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

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

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

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

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

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

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

83 1, which is required for matrix assembly and cell-matrix adhesion.

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

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

86 I and their different roles in cell-cell and cell-matrix adhesion.

87 the trafficking machinery, and cell-cell and cell-matrix adhesion.

88 ls also showed defects in both cell-cell and cell-matrix adhesion.

89 ion and development as well as cell-cell and cell-matrix adhesion.

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

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

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

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

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

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

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

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

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

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

100 Cell-matrix adhesions are exquisite sensors of physiolog

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

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

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

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

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

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

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

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

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

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

111 Shc orchestrates signals from cell-cell and cell-matrix adhesions to elicit flow-induced inflammator

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

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

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

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

116 e regulation of the F-actin cytoskeleton and cell-matrix adhesions, involve previously unrecognized c

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

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

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

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

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

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

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

124 activated and associates with cell-cell and cell-matrix adhesions.

125 1 is an important regulator of cell-cell and cell-matrix adhesions.

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

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

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

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

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

131 Although cell-matrix adhesive interactions are known to regulate

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

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

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

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

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

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

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

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

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

141 ign of biomaterials intended to support both cell-matrix and cell-cell adhesion.

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

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

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

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

146 generation of mechanical forces at sites of cell-matrix and cell-cell contact.

147 ses, have consequences well beyond classical cell-matrix and cell-cell interactions and motility, and

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

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

150 larly suitable for studies on the effects of cell-matrix and cell-cell interactions on cell migration

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

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

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

154 n cell adhesion (P <or= 10(-57)), especially cell-matrix as opposed to cell-cell adhesion.

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 peptides in the nervous system using single cell matrix-assisted laser desorption/ionization mass sp

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 es and fibronectin fibril growth at discrete cell-matrix attachment sites.

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

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

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

166 onsiderations in replacement and repair (eg, cell/matrix biology of tissue valve substitutes and thei

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

168 A cell-matrix composite was constructed by applying fibrin

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 lial polarity in the absence of cell-cell or cell-matrix contacts.

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

179 e of Maspin, as is the case with most cancer cells, matrix degradation proceeds unrestricted, thus fa

180 This finding suggests that the increased cell-matrix engagement inherent to a 3D matrix architect

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 gh multiple mechanisms, including effects on cell matrix interaction.

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 decorin modulates cell-matrix interaction in this context by stimulating c

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 However, several mediators of cell-matrix interaction were reduced in the Tgfbr2(derma

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

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

199 ss after liver injury, involves considerable cell-matrix interaction.

200 duced by anticancer agents via disruption of cell-matrix interaction.

201 The role of integrin/cell matrix interactions between the RPE and the basemen

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

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

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

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

206 zation of cells into tissues, and defects in cell-matrix interactions are an important element in man

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

208 Cell-matrix interactions are frequently mediated by the

209 Cell-matrix interactions are made possible by integrins,

210 CM), yet the pathogenic mechanisms involving cell-matrix interactions are poorly understood.

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

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

218 dulatory proteins are important effectors of cell-matrix interactions during tissue remodeling and re

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

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

221 to overcome difficulties in tracking stromal cell-matrix interactions for several days in live mice.

222 ithelial cells are dependent on cell-cell or cell-matrix interactions for survival and undergo apopto

223 s achieved, in part, via protection of renal cell-matrix interactions from damage by a variety of RCS

224 Cell-matrix interactions have critical roles in regenera

225 beta signaling that influences cell-cell and cell-matrix interactions in the developing nervous syste

226 lts suggest that TGFBIp may modulate scleral cell-matrix interactions in vivo, thereby affecting scle

227 ch regulated interplay between cell-cell and cell-matrix interactions is likely to have wide relevanc

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

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

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

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

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

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

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

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

238 ithin the integrin-based adhesome that links cell-matrix interactions with the tissue-specific functi

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

240 athogenic viral strains alters cell-cell and cell-matrix interactions, affecting extracellular matrix

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

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

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

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

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

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

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

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

249 ing septation may cause loss of cell-cell or cell-matrix interactions, resulting in apoptosis (anoiki

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

251 unctions that involve numerous cell-cell and cell-matrix interactions, which ultimately mediate the h

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

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

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

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

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

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

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

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

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

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

262 cell proliferation, and altered cell-cell or cell-matrix interactions.

263 in growth factor signaling and cell-cell and cell-matrix interactions.

264 matrix proteins and interference with renal cell-matrix interactions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 ravasation, possibly via (1) promoting tumor cell matrix invasion and (2) facilitating development of

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

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

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

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

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

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

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

287 volved in keratinocyte integrity, as well as cell-matrix or cell-cell adhesion.

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

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

290 In lon2 cotyledon cells, matrix proteins were localized to peroxisomes in

291 ellular matrix molecules and integrin family cell-matrix receptors may regulate this phenotypic trans

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

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

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

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

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

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

298 expression profiles (which we call the 'stem cell matrix') that enables the classification of culture

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

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