ライフサイエンスコーパス: ECM

1 ECM ligand concentration was derived from LC-MS/MS quant

2 ECM-related transcriptional changes were induced by the

3 identified and assayed the abundance of 113 ECM proteins, which revealed robust ECM protein signatur

4 A total of 151 ECM and ECM-associated proteins were identified by mass

5 rowth speeds in ECs cultured on compliant 2D ECMs but promotes slow MT growth speeds in ECs cultured

6 Furthermore, we find that 3D ECM engagement uncouples MCAK-mediated regulation of MT

7 We believe this innovative vascular 3D ECM system can be used to provide novel insights into ce

8 rowth speeds in ECs cultured on compliant 3D ECMs, and these effects are myosin-II dependent.

9 clinical implications, little is known about ECM changes post-stent implantation.

10 (HTS) models to identify molecules affecting ECM accumulation are limited in their relevance or throu

11 nt of integrin receptors, locally amplifying ECM input to internal signaling cascades.

12 icroparticulate layers were integrated by an ECM-based biological glue to form thick 3D cardiac patch

13 ry and, in association with HA, generates an ECM that promotes leukocyte infiltration and adhesion.

14 proteases that degrade basement membrane, an ECM barrier surrounding all epithelial tissues.

15 ic spines by triggering MMP-9 activation and ECM remodelling.

16 sition of understory invaders between AM and ECM dominant forests.

17 ges between the relative abundance of AM and ECM trees and microbial functioning in three hardwood fo

18 d shell formation model including chitin and ECM-related proteins.

19 The cation/Cl(-) cotransporters and ECM metalloproteinases may be particularly druggable tar

20 force transfer between the cytoskeleton and ECM-integrin complexes.

21 oliferation, rearrangement, deformation, and ECM dynamics have varied roles in driving budding versus

22 ted cell proliferation, differentiation, and ECM deposition resulting in AF-like tissue features base

23 A total of 151 ECM and ECM-associated proteins were identified by mass spectrom

24 tigating the collaborative effect of EMT and ECM in the metastatic process reveals increased collagen

25 glomerulosclerosis, mesangial expansion, and ECM protein (collagen IV and fibronectin) accumulation a

26 ypotheses for how intracellular (GTPase) and ECM signaling jointly regulate lamellipodial dynamics.

27 ant connection between energy metabolism and ECM assembly.

28 hibit increased proliferation, migration and ECM synthesis.

29 chness increased plant root productivity and ECM root tips but decreased hyphal length, whereas inter

30 nthesis contributes to GMC proliferation and ECM accumulation under high glucose conditions.

31 Moreover, proliferation and ECM production in high glucose-challenged GMCs were atte

32 UII-induced GMC proliferation and ECM protein synthesis were dependent on TRPC4 channel-me

33 Unique interactions between ECM cells and collagen cables were also observed and rec

34 the potential for functional overlap between ECM and saprotrophic fungi.

35 The relationship between ECM mechanics and cell behavior is dynamic, as cells rem

36 Soils dominated by ECM trees had higher F : B ratios and more standing fung

37 enes with saprotrophic function expressed by ECM fungi when in symbiosis?

38 ls of Rac and Rho, (2) activation of RhoA by ECM signaling, and (3) feedback from lamellipodial growt

39 hematopoietic compartment, IFN-gamma causes ECM by acting redundantly or by targeting non-T cell or

40 eficient mice, we show that IFN-gamma causes ECM by signaling within both the hematopoietic and nonhe

41 w interdependence between cell-cell and cell-ECM adhesions is important in regulating cell behaviors,

42 the embryo, requires both cell-cell and cell-ECM adhesions.

43 trix (ECM), lamellipod growth increases cell-ECM contact area and enhances engagement of integrin rec

44 l-cell adhesion caused up-regulation of cell-ECM adhesion, leading to reduced cell deformation and fo

45 lamellipodial growth or contraction to cell-ECM contact area and therefore to the ECM signaling leve

46 ides in high-throughput without using cells, ECM-proteins, or antibodies.

47 the budding yeast Saccharomyces cerevisiae, ECM remodeling refers to sequential formations of the pr

48 Combinatorial ECMs composed of collagen IV + heparan sulfate + laminin

49 hese data suggest that optimal combinatorial ECMs enhance endothelial differentiation, compared to ma

50 mified macrophages emerged in the contracted ECM of recovering colons and mainly expressed M2 macroph

51 In contrast, ECM detachment of cells lacking alpha6beta4 is sufficien

52 F signaling, as well as in genes controlling ECM structure and disassembly.

53 Conversely, ECMs isolated from omental fat and lung did not redirect

54 hyaluronidase, an enzyme that degrades core ECM components.

55 y the bone forming cells, are novel coupling ECM components that control bone mass through sequestrat

56 The resulting condensed, highly crosslinked ECM impeded drug permeation, protecting tumor cells from

57 e established that TGFbeta is required for D-ECM production but dispensable for D-ECM-induced naive f

58 d for D-ECM production but dispensable for D-ECM-induced naive fibroblast-to-CAF activation, which de

59 and self-sustaining extracellular matrix (D-ECM), is a puzzling feature of pancreatic ductal adenoca

60 MPC-dependent ECM remodeling during the first week of a growth stimulu

61 As, and this was consistent across different ECM stiffness and cytoskeletal tension states.

62 sylvestris) seedlings colonized by different ECM fungal isolates, in monocultures and mixtures, enabl

63 f CD8 T cells to initiate brain edema during ECM.

64 Ectomycorrhizal (ECM) symbioses have evolved a minimum of 78 times indepe

65 scular mycorrhizal (AM) and ectomycorrhizal (ECM) trees.

66 ecology study of the model ectomycorrhizal (ECM) genus Laccaria was performed using herbarium materi

67 he identity and richness of ectomycorrhizal (ECM) fungi at the intra- and interspecific levels affect

68 Temperate ectomycorrhizal (ECM) fungi show segregation whereby some species dominat

69 to control orderly formation of the elastin ECM, thereby driving alveolar septa formation to increas

70 induces a synthetic phenotype with elevated ECM production; and 3) progressive matrix stiffening, mo

71 ired for dissemination in vivo, but enhanced ECM-mediated signaling, LUAD cell survival, and micromet

72 ferentiated state, characterized by enhanced ECM production, that established a pro-metastatic fibron

73 However, excessive ECM remodeling can cause fibrosis of the TM as in primar

74 is, in fibrogenic cells to prevent excessive ECM deposition.

75 rm not only provides strategies to fabricate ECM-like interfaces for medical devices, but also offers

76 ferentiation, compared to many single-factor ECMs, in part through an integrin beta3-mediated pathway

77 xpression of CD31, compared to single-factor ECMs.

78 niche components, including growth factors, ECM, and immune cells, and intrinsic stem cell propertie

79 near fibronectin features to mimic fibrillar ECM and elucidate the mechanisms of contact guidance.

80 a the engagement of integrins with fibrillar ECM proteins.

81 re and composition of wild-type and fibrotic ECM, we show that collagen in the ECM is organized into

82 Mathematical models for ECM-integrin binding kinetics that were developed incorp

83 lathrin-mediated endocytosis is required for ECM-dependent STAT5 activation.

84 These data reveal a novel role for ECM-driven endocytosis in the positive regulation of cyt

85 Have ECM fungi retained genes with lignocellulolytic potentia

86 from LC-MS/MS quantification of the hepatic ECM from mice exposed to chronic carbon tetrachloride (C

87 oming increasingly accepted that the hepatic ECM proteome (i.e., matrisome) responds dynamically to s

88 An extraction method to enrich the hepatic ECM was characterized.

89 tics of integrin receptor binding to hepatic ECM proteins.

90 nsional (3D), and structurally heterogeneous ECM environments such as occur in vivo.

91 and have used this system to investigate how ECM microstructural properties influence epithelial cell

92 However, it is not understood how ECM accumulation leads to TM dysfunction and IOP elevati

93 Fibronectin (FN) is an important ECM component that forms fibrils through cell contacts a

94 y for drusen formation, COL4 accumulation in ECM, and complement pathway gene alteration, it impacted

95 rious molecular perturbations and changes in ECM signaling modulate the fraction of cells exhibiting

96 typically quantified based on an increase in ECM collagen.

97 e IL-10R during P. berghei ANKA infection in ECM-resistant BALB/c mice leads to amplified T cell acti

98 creased accumulation of COL4 was observed in ECM isolated from control vs. patient hiPSC-RPE cultures

99 peptidases, which plays an important role in ECM remodelling.

100 Enzyme stoichiometry in ECM soils shifted to higher investment in extracellular

101 usly, we observed that genetic variations in ECM genes are associated with an increased risk of weigh

102 ally release active collagenase (to increase ECM porosity) and PDGF-AB (to attract endogenous cells)

103 st-mortem TM tissues, we show that increased ECM accumulation leads to endoplasmic reticulum (ER) str

104 cer cell activity and cell-migration-induced ECM and collagen remodeling and realigning dynamics.

105 ated cancer cells can coopt the inflammatory ECM to persist, leading to brain metastatic outgrowths.

106 ion of the mechanical properties of integrin-ECM links, which may be harnessed by cells to control ad

107 ent with impaired PHEX activity having local ECM effects in XLH.

108 ntitative understanding of the role of local ECM size and arrangement in cell emergence-based migrati

109 Experimental cerebral malaria (ECM) is a gamma interferon (IFN-gamma)-dependent syndrom

110 acting across a fibrous extracelluar matrix (ECM).

111 ll adhesions, and cell-extracellular matrix (ECM) adhesions.

112 Aligned fibers of extracellular matrix (ECM) affect the direction, efficiency, and persistence o

113 ant remodelling of the extracellular matrix (ECM) and increased local invasion from the primary tumou

114 xcessive deposition of extracellular matrix (ECM) and larger smooth muscle mass are correlated with i

115 ng cells on underlying extracellular matrix (ECM) and test possible therapeutic inhibitors.

116 ent affinities for the extracellular matrix (ECM) and the coreceptor NRP1, which leads to distinct va

117 ing cell migration and extracellular matrix (ECM) assembly.

118 BM) is a thin layer of extracellular matrix (ECM) beneath nearly all epithelial cell types that is cr

119 eposition of fibrillar extracellular matrix (ECM) components and high expression of lysyl oxidases.

120 nsing modifications in extracellular matrix (ECM) composition and mechanics.

121 ls to characterize the extracellular matrix (ECM) composition of normal lung, fibrotic lung, lung tum

122 The extracellular matrix (ECM) consists of diverse components that work bidirectio

123 , we observed that the extracellular matrix (ECM) constructed by AKAP12+ colon mesenchymal cells (CMC

124 ch as stiffness of the extracellular matrix (ECM) contribute to MSC phenotype in cancer remains poorl

125 vily influenced by the extracellular matrix (ECM) density and composition of the surrounding tumour m

126 hich entails excessive extracellular matrix (ECM) deposition and tissue remodeling by activated myofi

127 In addition, extracellular matrix (ECM) detachment is a physiologic trigger of ferroptosis,

128 The liver extracellular matrix (ECM) expands with high-fat (HF) feeding.

129 onsible for defects in extracellular matrix (ECM) formation and mineralization.

130 hyphae with the dried extracellular matrix (ECM) from the fungus, and Ca oxalate crystals.

131 nt anions, polyanionic extracellular matrix (ECM) glycoproteins, and plasmalemmal Cl(-) transporters

132 odeling of the stromal extracellular matrix (ECM) has a crucial, but incompletely understood role dur

133 e density of the local extracellular matrix (ECM) in conjunction with releasing chemoattractive signa

134 poorly differentiated extracellular matrix (ECM) in MDA-MB-231 tumors relative to T-47D tumors.

135 e physical role of the extracellular matrix (ECM) in vascular homeostasis in the basal chordate Botry

136 in aligned collagenous extracellular matrix (ECM) is a critical enabler of breast cancer disseminatio

137 d or organized fibrous extracellular matrix (ECM) is a crucial precursor to collective cell migration

138 The extracellular matrix (ECM) is a dynamic, bioactive structure critical to organ

139 The extracellular matrix (ECM) is a fibrillar protein-based network, the physical

140 mic remodelling of the extracellular matrix (ECM) is a key feature of cancer progression.

141 The extracellular matrix (ECM) is an oft-overlooked component of the interface bet

142 ated attachment to the extracellular matrix (ECM) is required to combat the induction of programmed c

143 s architectures in the extracellular matrix (ECM) is the strong and directional interaction between b

144 on and accumulation of extracellular matrix (ECM) leading to glomerulosclerosis.

145 3-dimensional model of extracellular matrix (ECM) mineralization.

146 Interactions with the extracellular matrix (ECM) occur through focal adhesions or hemidesmosomes via

147 eoglycans (PGs) in the extracellular matrix (ECM) play vital roles in axon growth and navigation, pla

148 via interaction of the extracellular matrix (ECM) protein cochlin with the cell surface bound and str

149 dynamically expressed extracellular matrix (ECM) protein with critical functions in cardiovascular d

150 esis and deposition of extracellular matrix (ECM) proteins in the trabecular meshwork (TM) is associa

151 essive accumulation of extracellular matrix (ECM) proteins.

152 that produce excessive extracellular matrix (ECM) proteins.

153 essive accumulation of extracellular matrix (ECM) proteins.

154 The extracellular matrix (ECM) regulates cell migration and sculpts organ shape.

155 ies cell migration and extracellular matrix (ECM) remodeling and is thus an essential aspect of compl

156 Extracellular matrix (ECM) remodeling contributes to in-stent restenosis and t

157 Localized extracellular matrix (ECM) remodeling is thought to stabilize the cleavage fur

158 critical regulator of extracellular matrix (ECM) remodeling through its availability and stepwise po

159 an enzyme involved in extracellular matrix (ECM) remodelling and synaptic plasticity.

160 Extracellular matrix (ECM) rigidity sensing by integrin adhesions has been wel

161 llagen arrangement and extracellular matrix (ECM) stiffness.

162 TRACT: Skeletal muscle extracellular matrix (ECM) structure and organization are not well understood,

163 mice showed decreased extracellular matrix (ECM) structure-related gene expression, whereas Tsc1 con

164 sduction signal in the extracellular matrix (ECM) to coordinate the cross-talk between the LRP4-MuSK

165 with basement membrane extracellular matrix (ECM) via beta1 integrins which activate both ILK and Rac

166 of invadopodia to the extracellular matrix (ECM) with their ability to degrade the ECM in breast tum

167 is known about how the extracellular matrix (ECM), and particularly the mechanical information in the

168 d the formation of the extracellular matrix (ECM), and stimulates reepithelialization by keratinocyte

169 ical attributes of the extracellular matrix (ECM), are known to drive cell branching and shape change

170 connective tissues and extracellular matrix (ECM), are significantly and irreversibly remodeled by ce

171 lasts to accumulate an extracellular matrix (ECM), enriched in hyaluronan (HA) and its binding partne

172 ated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TA

173 l migrates through its extracellular matrix (ECM), lamellipod growth increases cell-ECM contact area

174 ned to the complement, extracellular matrix (ECM), lipid, cell survival, immune system, metabolism, o

175 t with the surrounding extracellular matrix (ECM), remodeling ECM fiber network structure by condensi

176 l cells to the stromal extracellular matrix (ECM), which is distinct from the ECM within the normal e

177 e aspects of the brain extracellular matrix (ECM), which is relatively enriched in hyaluronic acid (H

178 , we characterized the extracellular matrix (ECM), with a focus on collagen IV and its variant, spong

179 ant biomolecules on an extracellular matrix (ECM)-like substrate with arbitrary micropatterns.

180 analysis revealed that extracellular matrix (ECM)-receptor interaction and metabolic pathways were th

181 connect a cell to its extracellular matrix (ECM).

182 hanical strains in the extracellular matrix (ECM).

183 esistance within their extracellular matrix (ECM).

184 nts to the surrounding extracellular matrix (ECM).

185 on domain of a brain's extracellular matrix (ECM).

186 ts and the surrounding extracellular matrix (ECM).

187 lls, stromal cells and extracellular matrix (ECM).

188 diated adhesion to the extracellular matrix (ECM).

189 exerting forces on the extracellular matrix (ECM).

190 eins that comprise the extracellular matrix (ECM).

191 between cells and the extracellular matrix (ECM).

192 icating defects in the extracellular matrix (ECM).

193 ypes of cells with the extracellular matrix (ECM).

194 characteristics of the extracellular matrix (ECM).

195 major component of the extracellular matrix (ECM).

196 splay higher vascularization and less mature ECM, significantly enhancing tumor response to TSLDox an

197 Using this method to measure ECM accumulation in a kidney cell model, we demonstrated

198 ic lung fibroblasts from SSc patients modify ECM during migration but remain growth factor dependent

199 ing how the tumor microenvironment modulates ECM homeostasis control.

200 The skeletal muscle ECM substrates enhanced fiber formation leading to the e

201 d (i.e. containing smooth or skeletal muscle ECM) and used to culture MPCs in vitro.

202 These results demonstrate that the muscle ECM is more highly organized than previously reported.

203 The Neotropical ECM tree Dicymbe corymbosa forms monodominant stands and

204 other pre-clinical reports have not observed ECM-mediated skeletal muscle regeneration.

205 ally related to the observed accumulation of ECM in the kidneys.

206 Analysis of ECM alignment over time revealed that tissues rapidly re

207 omplete chemo-mechanical characterization of ECM proteins such as fibronectin (FN) is lacking.

208 CM remodeling via transcriptional control of ECM proteins.

209 fect of CD44, which is imposed downstream of ECM-mechanosensing and determines if cells couple or unc

210 gated the relation between the expression of ECM genes during WL and a period of weight stabilization

211 ion about matrix organisation: the extent of ECM accumulation was unaffected by the BMP antagonist Gr

212 With time-lapse imaging of ECM micro-fiber morphology, the local alignment vector c

213 to the brain, and an increased incidence of ECM.

214 om electron acceptor-dependent inhibition of ECM production.

215 ted before it is certain that any lineage of ECM fungi actively expresses extracellular enzymes in or

216 idence that not all evolutionary lineages of ECM have retained the genetic potential to produce extra

217 Dex) increased the secretory protein load of ECM proteins in the ER of TM cells, inducing ER stress.

218 Manipulation of ECM density was associated with an altered migration pat

219 been analyzed extensively, the mechanisms of ECM remodeling remain poorly understood.

220 akes into account the sliding and merging of ECM fibers.

221 (when cancer cells are exposed to periods of ECM detachment), cancer cells must alter their metabolis

222 neration of myofibroblasts and production of ECM proteins during chlamydial infection.

223 stromal surrounds that comprised a range of ECM densities, composition and stromal cell populations.

224 ta (TGF-beta) is an established regulator of ECM remodeling via transcriptional control of ECM protei

225 duction of fibronectin, a major regulator of ECM structure, prevented ER stress in Dex-treated TM cel

226 iquely regulate the continuous remodeling of ECM in the normal TM.

227 chanical stress and continuous remodeling of ECM is crucial to maintain normal aqueous humor drainage

228 igration is essential to deliver a subset of ECM components evenly throughout the embryo.

229 esulting in AF-like tissue features based on ECM deposition and morphology, indicating potential for

230 Primary human TM cells grown on ECM derived from Dex-treated TM cells induced ER stress

231 stallization and represent chitin related or ECM related proteins.

232 en-coupled stiff or compliant polyacrylamide ECMs to examine the effects of MCAK expression on MT gro

233 d 93% of tissue's DNA, generally preserving ECM's components and microarchitecture.

234 rils are the primary component in primordial ECM and, as such, FN assembly is a critical component in

235 a-SMA)-positive myofibroblasts that produced ECM proteins, including collagen types I and III and fib

236 Under elevated productivity, ECM trees enhanced decomposition more than AM trees via

237 terstitial fibrogenic cells to ensure proper ECM deposition and optimal muscle remodeling in response

238 e found persistent degradation of protective ECM structures called perineuronal nets (PNNs) around fa

239 Neutrophils undergo a rapid, ECM-dependent mechanism of homotypic aggregation and NET

240 oma contains fewer CAFs and exhibits reduced ECM deposition.

241 hrombosis, followed by changes in regulatory ECM proteins.

242 nding extracellular matrix (ECM), remodeling ECM fiber network structure by condensing, degrading, an

243 e of 113 ECM proteins, which revealed robust ECM protein signatures unique to fibrosis, primary tumor

244 e biology of maculopathies affecting the RPE-ECM interface.

245 as used to evaluate the origin of Laccaria's ECM ecology.

246 subcellular mechanisms by which cells sense ECM geometry and translate it into changes in shape and

247 It is also interesting that several ECM proteins responded similarly to both stresses, sugge

248 the first demonstration of a tissue specific ECM driving differentiation of cells to form a functiona

249 rusion dynamics and find that the structured ECM orients cellular protrusions parallel to the ECM.

250 ngiogenic therapy by concomitantly targeting ECM-modifying enzymes.

251 rons were completely susceptible to terminal ECM.

252 The ECM did not affect the secretion of tissue inhibitors of

253 3.75; 95% CI, 1.79-7.86; P < 0.001), and the ECM pathway and more severe levels in the AREDS Extended

254 tions of inflammation, angiogenesis, and the ECM to both "healthy" and "unhealthy" AT expansion.

255 The link between the ECM component fibronectin (fn) and integrin alpha5beta1

256 n oscillation and, importantly, broadens the ECM stiffness range over which FAs can accurately adapt

257 trix (ECM) with their ability to degrade the ECM in breast tumor cells.

258 lar matrix (ECM), which is distinct from the ECM within the normal epithelial microenvironment.

259 h that 2) local strains are generated in the ECM and 3) cells preferentially extend protrusions along

260 d fibrotic ECM, we show that collagen in the ECM is organized into large bundles of fibrils, or colla

261 kably, HUVEC cells naturally migrated in the ECM scaffold and spontaneously repopulated the lining of

262 rticularly the mechanical information in the ECM, guides these cellular decisions.

263 enerated HA-enriched cable structures in the ECM, providing a substrate for monocytic cells in vitro,

264 l tumor cells by crosslinked collagen in the ECM.

265 from the tumor spheroids and invade into the ECM.

266 on results suggest that the evolution of the ECM ecology was a key innovation in the evolution of Lac

267 This manuscript reviews the role of the ECM in cardiac repair and remodeling and discusses matri

268 Excessive remodeling of the ECM is a hallmark of a variety of inflammatory condition

269 guidance, the fibrillar architecture of the ECM promotes an elongated cell shape and migration along

270 f this work were to validate analysis of the ECM proteome and compare the impact of 6 weeks of ethano

271 The complexity of the ECM taking care of many essential properties has inspire

272 armacology model captures the ability of the ECM to regulate isoform-specific growth factor distribut

273 osis should consider the organization of the ECM to target the structures and cells contributing to f

274 a process critical for the remodeling of the ECM.

275 eedback, where: 1) cells apply forces on the ECM, such that 2) local strains are generated in the ECM

276 iled to efficiently deposit and organize the ECM in two and three dimensions.

277 xts (e.g., hepatic fibrosis), changes to the ECM are well recognized and understood.

278 nature and magnitude of these changes to the ECM in liver injury are poorly understood.

279 CM attachment to the ECM is mediated by integrin complexes localized at the m

280 o cell-ECM contact area and therefore to the ECM signaling level.

281 ape elongation and migration parallel to the ECM, or contact guidance.

282 orients cellular protrusions parallel to the ECM.

283 ecretion of MMP-1 and -10 on adhesion to the ECM.

284 N1 which, once secreted, associates with the ECM and the cell surface and tightly controls the bidire

285 rganization are not well understood, yet the ECM plays an important role in normal tissue homeostasis

286 To understand this ECM plasticity, we develop a computational model that ta

287 Recapitulating tissue ECM composition and stromal cell composition enhanced ca

288 tatic maintenance that likely contributes to ECM pathology.

289 of myosin light chain), which are coupled to ECM signaling that is modulated by protrusion/contractio

290 ational upregulation of molecules related to ECM remodeling and the persistent breakdown of PNNs arou

291 determinant of cell mechanics in response to ECM cues.

292 heir proliferative and motility responses to ECM stiffness.

293 Similar to ECM proteins, matrix-bound chemokines, cytokines, and gr

294 A determining factor is the tumor ECM, which strongly influences the effect of anti-VEGF t

295 ion and partial digestion, different urethra ECM-derived coating substrates were formulated (i.e. con

296 ed a urethra bioscaffold that retained vital ECM proteins and was liable to cell repopulation, a cruc

297 To date, the way in which ECM binding alters the distribution of isoforms of VEGF

298 acquired of wood cell walls and hyphae with ECM.

299 actile connections to discrete points within ECM during cell migration, and provides a plausible mean

300 beta-glucan or to C. albicans hyphae without ECM.