ライフサイエンスコーパス: ECM

1 ECM degradation requires metalloproteases, but whether o

2 ECM differences suggest that glomerular sclerosis in cFS

3 ECM fungi, however, originate from diverse saprotrophic

4 ECM remodeling was reduced by surgery alone, with an add

5 (hMSCs) for 96 h on a three-dimensional (3D) ECM-based microgel platform.

6 bone marrow-derived extracellular matrix (3D-ECM), which contains many of the matrix components prese

7 Of 58 ECM proteins that differed in abundance between cFSGS an

8 we examined the hypothesis that an abnormal ECM-integrin receptor axis contributes to BM megakaryocy

9 differential upregulation of aforementioned ECM genes/proteins with new ones emerging (collagen-I, t

10 e response to loss of vascular tension after ECM disruption-requires functional force sensing machine

11 P control, while ablation results in altered ECM repair/homeostasis and conventional outflow physiolo

12 Glutathione S-transferase omega-1, an ECM-modifying enzyme, was significantly increased in the

13 local dissociation of ECM ligands creates an ECM ligand gradient below the cell body that guides cell

14 ronment will provide a rational basis for an ECM-based approach for tendon repair.

15 ing a finger-like protrusion, adhering to an ECM node, and pulling the cell body forward) and 'rear-s

16 se-like 2-4, tissue transglutaminase-2), and ECM turnover genes/enzymes (matrix metalloproteinases-MM

17 arbored a similar signature of adenosine and ECM profiles; high expression of A(2B) adenosine recepto

18 ssociated with pathways of cell adhesion and ECM-receptor interactions, and MPC trajectories to carti

19 ype); and subgroup 3 showed a high ARMS2 and ECM GRS, RPD, and extrafoveal atrophy.

20 h the ECM by contracting the cell cortex and ECM at the cell rear).

21 s contractile force, nuclear elasticity, and ECM rigidity-determine the effectiveness of cell migrati

22 , Osr1 (encodes a transcription factor), and ECM-related genes.

23 x (ECM) through cell-matrix interactions and ECM remodelling.

24 uirements associated with cell mechanics and ECM remodelling, implicating a reciprocal crosstalk betw

25 al interstitial myofibroblast population and ECM deposition.

26 alone did not resolve insulin resistance and ECM remodeling.

27 erials, with the goal of matching tissue and ECM mechanics for in vitro tissue models and application

28 complex mechanical behaviours of tissues and ECMs, discuss the effect of ECM viscoelasticity on cells

29 rogen gas flux (NO(y) = NO, NO(2) , HONO) as ECM tree abundance increases.

30 -free approach to mathematically model basal ECM turnover during embryogenesis by exploiting our abil

31 cells + HUVECs in an HLF-laden, fibrin-based ECM within our microfluidic device optimally (1) enhance

32 an cortical cells in the soft, biocompatible ECM, Matrigel.

33 offer sustained sequential delivery of bone ECM chemical cues and offer an ideal stabilized 3D micro

34 their post-translational modifications, but ECM proteomics remains challenging owing to the extremel

35 sponse to increased inorganic nutrients, but ECM tree growth was suppressed when compared with the co

36 o experiments clarified pathological cardiac ECM prevents cell homing, thus providing further hints t

37 We identified the postnatal cardiac ECM as a nonpermissive environment for cardiomyocyte cyt

38 ppreciated that these changes in the cardiac ECM result in altered mechanical properties of ischemic

39 identify consistent modifications to cardiac ECM structure and mechanics that contribute to HF and (2

40 m berghei NK65 (PbNK65), that does not cause ECM, differ in only 21 single nucleotide polymorphysims

41 Cell-ECM (extracellular matrix) interactions play essential r

42 Cell-ECM interactions regulated by integrin alpha5beta1 and F

43 However, the relationship between cell-ECM adhesions and sarcomeres assembling de novo remains

44 iated adapter protein talin coordinates cell-ECM adhesion during melanoblast migration in vivo Specif

45 rted by the extracellular matrix (ECM), cell-ECM and cell-cell adhesion complexes influence metabolic

46 show that coordinated integrin-mediated cell-ECM attachment is essential for melanoblast migration an

47 ryonic migration processes that require cell-ECM attachment are dependent on the integrin family of a

48 Taken together, our results show that cell-ECM adhesions mediate coupling between the substrate and

49 an important mechanism for fine-tuning cell-ECM adhesion during cell migration in development.

50 CTSV had been predicted to cleave ECM proteins in the AMR glomeruli.

51 The mouse model of CM, experimental CM (ECM), induced by infection with the rodent parasite, Pla

52 tion of human and murine ECM (decellularized ECM) and then analyzed the pathological changes occurrin

53 The analysis of HF decellularized ECM resulting from ischemic or dilated cardiomyopathy, a

54 ological changes occurring in decellularized ECM during HF by atomic force microscopy, 2-photon micro

55 Knockdown of Smad7 alleviated deficient ECM production in SA fibroblasts in response to TGFbeta.

56 tiveness of cell migration through the dense ECM.

57 clear how they can travel through the dense ECM.

58 teractions through a novel exosome-dependent ECM deposition mechanism.

59 to a greater extent than mouse cell derived ECM.

60 Yet, the contribution of cancer cell-derived ECM and tumor mechanics to drug adaptation and therapy r

61 rate when cultured on postnatal cFb-derived ECM compared with embryonic cFb-derived ECM.

62 ived ECM compared with embryonic cFb-derived ECM.

63 ate VSMC migration and adhesion to different ECM proteins and regulate cellular stiffness and cytoske

64 lial phenotype in CRC cells while disordered ECM drove a mesenchymal phenotype, similar to well and p

65 Infiltration of activated PECs may disrupt ECM remodeling in cFSGS.

66 emodeling but also the generation of distant ECM-enriched stromal niches in vivo.

67 ruli and tubulointerstitium identified early ECM remodeling, which may represent a new therapeutic op

68 tion; RAP, an inhibitor of LRP1 blocked eCRT ECM induction.

69 Ectomycorrhizal (ECM) fungi are integral to boreal and temperate forest e

70 zal (AM) to the alternative ectomycorrhizal (ECM) or nonmycorrhizal (NM) associations.

71 colonized ericoid (ERM) and ectomycorrhizal (ECM) shrub roots and occurred below the maximum rooting

72 d by trees associating with ectomycorrhizal (ECM) fungi.

73 mutualistic symbiosis with ectomycorrhizal (ECM) fungi.

74 rved for species possessing ectomycorrhizas (ECM) and not arbuscular mycorrhizal (AM) fungi.

75 d a switch from a promigratory to an elastic ECM drive valve leaflet elongation.

76 These data demonstrate that embryonic ECM undergoes constant replacement, which is likely nece

77 uncovered novel functions for the embryonic ECM proteins SLIT2 and NPNT (nephronectin) in promoting

78 ns through inhibition of the Fli-1/HSPB1/EMT/ECM remodeling protein networks.

79 This Azo-enabled ECM proteomics strategy will streamline the analysis of

80 n and identified potent maturation-enhancing ECMs through this simple and rapid assay.

81 We found that 2 embryonically enriched ECM proteins, SLIT2 and NPNT (nephronectin), promote cyt

82 Cav1-driven exosomal ECM deposition not only promotes local stromal remodelin

83 This provided a favored ECM reorganization that promoted tolerance to BRAF inhib

84 llular disulfide bonds and are essential for ECM degradation.

85 gn principle of separable contributions from ECM prestrain and actomyosin tension during epithelial o

86 mal adipocytes alter their fate and generate ECM-producing myofibroblasts within wounds.

87 cross species, and especially within a given ECM species, on function and interactions with the envir

88 omics to test the hypothesis that glomerular ECM composition in collapsing FSGS (cFSGS) differs from

89 As compared with healthy heart, HF ECM exhibited aligned, flat, and compact fiber bundles,

90 High ECM stiffness leads to ligand-independent phosphorylatio

91 Whether and how ECM regulates epigenetic alterations to influence cancer

92 eased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, implicating CatA as a

93 ased proteomics is an ideal tool to identify ECM proteins and characterize their post-translational m

94 ix (ECM) and that its loss leads to impaired ECM engulfment and a concomitant accumulation of ECM pro

95 together, these data suggest that changes in ECM stiffness can modulate the morphology, cytoskeletal

96 for parasite strain-specific differences in ECM phenotypes.

97 ing of the different roles of fibroblasts in ECM biology, wound healing, diseases, and aging.

98 esentation of dysregulated genes involved in ECM organization, or being connected to TGFbeta1 (transf

99 nted at mechanosensor YAP as a key player in ECM remodeling in the diseased heart via transcriptional

100 In breast cancer, increased ECM stiffness promotes epithelial-to-mesenchymal transit

101 agen fiber alignment, a marker of increasing ECM stiffness.

102 s neither necessary nor sufficient to induce ECM and thus cannot account for parasite strain-specific

103 as an obligatory factor for TGF-beta-induced ECM synthesis as well as differentiation and survival of

104 Silencing HE4 inhibited hypoxia-induced ECM deposition and alleviated fibrosis in UUO mice in vi

105 Whereas eCRT strongly induces ECM and integrin alpha5 proteins in K41 wild-type mouse

106 itor metalloproteinases 1, which may inhibit ECM degradation through inhibition of matrix metallopept

107 phic technology to pattern single cells into ECM sheets that are >10x larger than previously describe

108 proteins within rat Achilles tendon and its ECM phases.

109 cin-C (TNC) was identified as one of the key ECM markers in the lung epithelial-mesenchymal interface

110 Tumours leverage ECM remodelling to create a microenvironment that promot

111 the aryl hydrocarbon receptor (AHR) to limit ECM accumulation in vitro.

112 bridges are abundant in connective and liver ECM.

113 cent NSCs are the main source of their local ECM, including the multi-functional enzyme transglutamin

114 ntributing to experimental cerebral malaria (ECM) mortality.

115 Because of the "smart" material ECM, this scaffold may have the potential for providing

116 rmodynamically-stable extra-cellular matrix (ECM), (3) preserved collagen composition and crosslinkin

117 ion of the provisional extracellular matrix (ECM) (Tnc, Postn, Spon2, Thbs2) as a key lung morphogene

118 component of the cell-extracellular matrix (ECM) adhesion machine that is frequently overexpressed i

119 by cell-cell and cell-extracellular matrix (ECM) adhesions and is modulated by cell tension and tiss

120 ndant component in the extracellular matrix (ECM) and a fundamental element to the architecture and t

121 Both the extracellular matrix (ECM) and DNA epigenetic regulation are critical for main

122 asion is suppressed by extracellular matrix (ECM) and programmed cell death (PCD) along the embryonic

123 EC numbers as well as extracellular matrix (ECM) and SMC disorganization.

124 lial engulfment of the extracellular matrix (ECM) and that its loss leads to impaired ECM engulfment

125 ting links between the extracellular matrix (ECM) and the TRNs but could not detect any differences i

126 ar organization of the extracellular matrix (ECM) and to defining the cellular microenvironment.

127 tant for breaching the extracellular matrix (ECM) and visceral muscle.

128 The native extracellular matrix (ECM) can exhibit heterogeneous nano-sequences periodical

129 stromal cells secrete extracellular matrix (ECM) components that remodel the tissue and lead to fibr

130 adhere to immobilized extracellular matrix (ECM) components, exhibited a diverse range of ligand spe

131 ing and non-permissive extracellular matrix (ECM) components.

132 ical properties of the extracellular matrix (ECM) critically influence tumor progression, but the mol

133 MMPs), that are key in extracellular matrix (ECM) degradation.

134 Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of

135 Hypoxia-induced extracellular matrix (ECM) deposition is an important cause of renal fibrosis

136 tracting vessels under extracellular matrix (ECM) disruption.

137 s has established that extracellular matrix (ECM) elasticity, or stiffness, affects fundamental cellu

138 consisting of aligned extracellular matrix (ECM) fibers and ordered micro-architecture induced an ep

139 es abundant neo-dermal extracellular matrix (ECM) formation by 3 days post-wounding.

140 betaRII(LysM)) affects extracellular matrix (ECM) formation in tumor tissue, specifically increasing

141 The extracellular matrix (ECM) has force-responsive (i.e., mechanochemical) proper

142 The abundant extracellular matrix (ECM) in PDAC comprises a major fraction of the tumor mas

143 The extracellular matrix (ECM) is a complex and dynamic meshwork of cross-linked p

144 The extracellular matrix (ECM) is a polymer network hypothesized to form a stable

145 ring tumor growth, the extracellular matrix (ECM) is degraded and substituted with a tumor-specific c

146 tic nanoparticles, the extracellular matrix (ECM) is of crucial importance because it acts as a barri

147 abecular meshwork (TM) extracellular matrix (ECM) may induce ocular hypertensive phenotypes in human

148 ane proteins that bind extracellular matrix (ECM) molecules on one side and connect to the actin cyto

149 natural decellularised extracellular matrix (ECM) obtained by whole thymus perfusion.

150 t do not represent the extracellular matrix (ECM) of brain tissue.

151 between tumors and the extracellular matrix (ECM) of the surrounding tissues have profound effects on

152 n-neoplastic cells and extracellular matrix (ECM) on drug resistance in glioblastoma (GBM) cells.

153 proteomic changes and extracellular matrix (ECM) organization over time in a mouse model of CAC.

154 e proteins involved in extracellular matrix (ECM) organization, angiogenesis and cell migration.

155 , lipid metabolism, or extracellular matrix (ECM) pathways and ARMS2 also were included, and genetic

156 ast contractile force, extracellular matrix (ECM) production, chemotaxis, and wound healing.

157 atal stem cell derived extracellular matrix (ECM) promotes hiPSC-CM maturation to a greater extent th

158 Basement membrane and extracellular matrix (ECM) proteins were significantly decreased in both AMR c

159 eptidases that degrade extracellular matrix (ECM) proteins, and reveal tripeptide Arginine-Glycine-As

160 in the degradation of extracellular matrix (ECM) proteins.

161 through regulation of extracellular matrix (ECM) remodeling and epithelial mesenchymal transition (E

162 y/repair response, and extracellular matrix (ECM) remodeling in the partially resected glands.

163 Extracellular matrix (ECM) remodeling is a hallmark of the pathology of gastro

164 drive inflammation and extracellular matrix (ECM) remodelling.

165 d collagens leading to extracellular matrix (ECM) stabilization.

166 dy is to elucidate the extracellular matrix (ECM) structure, composition, and biomechanical function

167 creased decorin in the extracellular matrix (ECM) surrounding epithelial cells, and we observed that

168 e, we present a tumour extracellular matrix (ECM) targeting ROS nanoscavenger masked by pH sensitive

169 ions of scaffold-based extracellular matrix (ECM) technologies as alternatives to autogenous soft tis

170 diverse assemblies of extracellular matrix (ECM) that can be separated by micron-scale gaps.

171 long with an extensive extracellular matrix (ECM) that is rich in hyaluronan, plays an integral role

172 tease signaling in the extracellular matrix (ECM) through beta3-integrin to activate focal adhesion k

173 resident cells and the extracellular matrix (ECM) through cell-matrix interactions and ECM remodellin

174 pertrophic growth, the extracellular matrix (ECM) undergoes remodeling, and the heart loses regenerat

175 three-dimensional (3D) extracellular matrix (ECM) underlies important physiological phenomena and is

176 upon engagement of the extracellular matrix (ECM) via focal adhesion kinase.

177 nd accumulation of the extracellular matrix (ECM) was notably impaired in tumors grown in the Ifnar1(

178 llular adhesion to the extracellular matrix (ECM) with inhibition of ciliation in both normal and can

179 rometry to analyze the extracellular matrix (ECM), a critical component of metastatic niches, in meta

180 al cues exerted by the extracellular matrix (ECM), cell-ECM and cell-cell adhesion complexes influenc

181 essive accumulation of extracellular matrix (ECM), is a leading cause of mortality worldwide.

182 , including changes in extracellular matrix (ECM), is critical for normal processes such as developme

183 fibroblasts (CAFs) and extracellular matrix (ECM), which plays a critical role in tumor initiation, p

184 ry of stem cells on an extracellular matrix (ECM)-based platform alters cell behavior, including migr

185 tial of MRL/MpJ tendon extracellular matrix (ECM)-derived coatings to regulate scar-mediated healing.

186 llular tethers and the extracellular matrix (ECM).

187 lycans of the vascular extracellular matrix (ECM).

188 changes in the cardiac extracellular matrix (ECM).

189 nd detachment from the extracellular matrix (ECM).

190 heroids embedded in an extracellular matrix (ECM).

191 ween lysosomes and the extracellular matrix (ECM).

192 es EVs to traverse the extracellular matrix (ECM).

193 s of connective tissue extracellular matrix (ECM).

194 e cytoskeleton and the extracellular matrix (ECM).

195 ss to collagen stiffening and force-mediated ECM remodeling through activation of actin-dependent mec

196 An electrochemical metallization (ECM) memory(4,5), typically based on silicon (Si), has d

197 Here, using micropatterned ECMs, we identify T-Plastin, one of the most ancient act

198 Ipsilateral gastrulation was lost by midline ECM and PCD inhibition but restored with exogenously ind

199 ctrometry proteomics and identified multiple ECM glycoproteins whose expression and function in IgAN

200 formed decellularization of human and murine ECM (decellularized ECM) and then analyzed the pathologi

201 te the hyaluronic acid (HA)-rich, nanoporous ECM of the brain, a problem with fundamental implication

202 a photo-crosslinkable formulation of native ECM (extracellular matrix) proteins and used this bioink

203 exploiting our ability to live image de novo ECM development in Drosophila to quantify production fro

204 engulfment and a concomitant accumulation of ECM proteins in contact with synapses.

205 ics strategy will streamline the analysis of ECM proteins and promote the study of ECM biology.

206 and tumor cells produced a diverse array of ECM-associated proteins, including secreted factors and

207 membrane protrusions and enables bridging of ECM gaps.

208 However, the contribution of ECM proteins to early metastatic onset in the peritoneal

209 The local dissociation of ECM ligands creates an ECM ligand gradient below the cel

210 t this mutualism and reduce the diversity of ECM fungi.

211 s of tissues and ECMs, discuss the effect of ECM viscoelasticity on cells, and describe the potential

212 anscription factor Sox9 drives expression of ECM components and that laminin 211 increases BP prolife

213 ype, characterized by enhanced expression of ECM, focal adhesion and cytoskeletal genes and suppressi

214 esponse characterized by increased levels of ECM deposition, sustained Ki67 levels in stromal cells,

215 es, clinical application, and limitations of ECM-based scaffold technologies in periodontal and peri-

216 C-MS/MS) post-translational modifications of ECM proteins, including glycosylation, phosphorylation,

217 tein interaction modules found in a range of ECM proteins.

218 ls through non-cell-autonomous regulation of ECM-integrin interactions and soluble molecules.

219 ic approach has highlighted repercussions of ECM remodeling on cell homing, cardiac fibroblast activa

220 Secretion of ECM protein fibronectin (FN) by BM stromal cells from PM

221 rafficked to invadosomes, which are sites of ECM degradation.

222 sis of ECM proteins and promote the study of ECM biology.

223 s as well as differentiation and survival of ECM-producing myofibroblasts.

224 t of MMP transport and its overall impact on ECM remodeling.

225 Indeed, collagen and other ECM components have been observed to facilitate beta(2)m

226 as been shown to affect the binding of other ECM components to collagen.

227 Melanoma cells secrete their own ECM proteins, an event that is promoted by oncogenic BRA

228 Instead, passive ECM pre-strain serves to maintain the shape independent

229 By producing ECM-remodelling enzymes-in particular the ECM protease A

230 he autocrine remodeling of a drug-protective ECM.

231 nts, and detect the HSF1-dependent proteomic ECM signature in human colorectal cancer.

232 ue compositional cues in MRL/MpJ provisional-ECM have the therapeutic capability to motivate canonica

233 ablished targets identified as co-regulated 'ECM organisation' genes and miR-22-3p which is highly co

234 Combined evaluation of collagen-related ECM remodeling and inflammatory activity was the most ac

235 reported about their function in remodeling ECM in health and disease, their trafficking across the

236 lectively in D1-expressing neurons requiring ECM stimulation of beta3-integrin-mediated phosphorylati

237 stituted with a tumor-specific collagen-rich ECM.

238 ich) and interfascicular (glycoprotein-rich) ECM phases of tendon.

239 tical contraction cannot deform a near-rigid ECM, but then the contraction of the cortex has to be ab

240 ix metalloproteinases (MMPs) degrade several ECM components and are crucial modulators of cell invasi

241 its emerging contractile nature; similarly, ECM lining blood vessels is highly elastic in order to s

242 We conclude that cuticle, a specialized ECM, impinges on DBL-1/BMP expression and signaling.

243 dditively upregulated myofibroblast-specific ECM genes independent of topography, but only fibroblast

244 fibers and expressed myofibroblast-specific ECM genes like Postn (periostin).

245 astasis, suggesting that some niche-specific ECM proteins may be involved in metastatic tropism.

246 reduced expression of Osr1 and PMC-specific ECM genes.

247 ular and molecular crosstalk between stroma, ECM and thymocytes, and offer practical prospects for tr

248 ells produced predominantly core, structural ECM proteins and tumor cells produced a diverse array of

249 d with overexpression/activity of structural ECM genes (fibronectin, collagen IV, collagen VI, myocil

250 ave the ability to adhere to the surrounding ECM through integrin receptors, we examined the hypothes

251 other growth factors (GFs) within the tendon ECM microenvironment will provide a rational basis for a

252 Here we report that ECM through laminin-integrin alpha6 upregulates ten-elev

253 Linear mixed effects modeling shows that ECM tree abundance, microbial process rates, and geograp

254 The ECM of the developing heart has unique properties create

255 The ECM protein fibronectin circulates in the blood as a glo

256 at act as a buffer between the tumor and the ECM, which in turn mediates all cell-tissue mechanics.

257 e Isl1 lineages showed that signaling by the ECM regulates aortic arch artery morphogenesis at multip

258 ive diseases such as Alzheimer's, causes the ECM in the CNS to be remodeled.

259 the majority of COL1A1 expression during the ECM remodeling phase of healing.

260 l pathways, including those derived from the ECM.

261 In addition, we discuss how the ECM helps to regulate tissue morphology during embryonic

262 nd influence the hyaluronan synthesis in the ECM on the other.

263 the stochastic search process of CTLs in the ECM should strongly be influenced by a dynamically chang

264 s an active role in TGFbeta signaling in the ECM.

265 ellular proteins (MCP) are secreted into the ECM.

266 on and revealed abnormal organization of the ECM and altered formation of the coronary vasa vasorum.

267 t, leading to an extensive remodeling of the ECM and an increased infiltration of CD8+ T cells.

268 ptomic analyses reveal downregulation of the ECM gene fibulin-5, which when overexpressed in ECs amel

269 the role, function, and basic biology of the ECM in both heart development and in the adult.

270 plications for understanding the role of the ECM in diseases such as fibrosis and cancer, and suggest

271 y demonstrates that these alterations of the ECM not only affect the structural properties of the isc

272 for deposition of bioactive peptides of the ECM, and their intrinsic biophysical properties make lam

273 is usually larger than the mesh size of the ECM, it is not clear how they can travel through the den

274 owing to the extremely low solubility of the ECM.

275 g on the cell type and the properties of the ECM.

276 rents were observed following removal of the ECM/glycocalyx, replacement of these glycosylated aspara

277 urated proteomic data from 17 studies on the ECM of 15 different normal tissue types, six cancer type

278 ng ECM-remodelling enzymes-in particular the ECM protease ADAMTS4-and inflammatory cytokines, damage-

279 e migration of tumour cells, and remodel the ECM in distant organs to allow for metastatic progressio

280 ness limits the cell migration more than the ECM rigidity.

281 queezing' (pushing the cell body through the ECM by contracting the cell cortex and ECM at the cell r

282 nciple, they may provide a connection to the ECM that facilitates vascular responsiveness contributin

283 While the ECM can undergo acute remodeling during embryogenesis, i

284 a1 activity and enhanced TGFbeta1 within the ECM of obese mammary tissue may enhance breast cancer ri

285 ractions and modulating stiffness within the ECM.

286 bs inhibit cardiomyocyte cytokinesis through ECM modulation rather than by secreting diffusible facto

287 Thus, ECM- integrin alpha6-STAT3-TET3 axis regulates hydroxyme

288 of extracellular peptides may contribute to ECM remodeling and left ventricular (LV) dysfunction.

289 CFs differentially express genes related to ECM maturation at P7 and immune crosstalk at P30.

290 opy numbers, respectively, in AM relative to ECM soil.

291 rst demonstration of replicating human tumor ECM architecture in ex vivo and in vivo cultures.

292 The collagen density of this tumor ECM has been associated with poor patient prognosis but

293 An underappreciated mediator of tumor-ECM interactions is the glycocalyx, the sugar-decorated

294 ion, but the molecular mechanisms underlying ECM layering are poorly understood.

295 A total of 173 and 225 unique ECM proteins from mouse mammary tumors have been identif

296 nt progress in our understanding of vascular ECM.

297 methylsiloxane (PDMS) elastomers coated with ECM proteins are widely used to assess the role of stiff

298 ysis, naive murine eosinophils cultured with ECM enriched in TNC significantly induced expression of

299 and NFAT5, which have targets enriched with ECM associated genes.

300 miR-22-3p which is highly co-expressed with ECM genes and may regulate these genes indirectly by tar