ライフサイエンスコーパス: tenascin-C

1 s an established downstream target promoter (tenascin-c).

2 ctor SOX4 and extracellular matrix component tenascin C.

3 ascular endothelial growth factor (VEGF) and tenascin C.

4 eractions between the aggrecan G3 domain and tenascin-C.

5 ggrecan as well as articular markers such as tenascin-C.

6 ed the presence of the target protein, human tenascin-C.

7 rite outgrowth by itself and also as part of tenascin-C.

8 ion of syndecan-4 circumvents the effects of tenascin-C.

9 extracellular matrix ligands osteopontin and tenascin-C.

10 e other alpha9beta1 ligands, osteopontin and tenascin-C.

11 een control cells and cells transfected with tenascin-C.

12 duction of brain natriuretic peptide but not tenascin-C.

13 xtracellular matrix proteins osteopontin and tenascin-C.

14 all three alternatively spliced isoforms of tenascin-C.

15 tical for neutrophil migration on VCAM-1 and tenascin-C.

16 lobulin, Rab geranylgeranyl transferase, and tenascin-C.

17 lfonate significantly inhibited induction of tenascin-C.

18 that hair cells supply at least part of the tenascin-C.

19 ding to the alternatively spliced regions of tenascin-C.

20 n AP chimera, interacts strongly with native tenascin-C.

21 N-CAM, tenascin-C, FGF-5, or both N-CAM and tenascin-C.

22 action with the proteoglycan binding site on tenascin-C.

23 oximately 12 nM) as to native or recombinant tenascin-C.

24 on of proliferating cell nuclear antigen and tenascin-C.

25 ased EMT protein markers, SMA, vimentin, and tenascin-c.

26 levels under the control of the promoter for tenascin-C.

27 egulation of anti-adhesive molecules such as tenascin-C.

28 pha9beta1-mediated adhesion and migration on tenascin-C.

29 (5.8-fold versus control, P:<0.05, n=3) and tenascin-C (7.0-fold, P:<0.02) mRNA expression by strain

30 Tenascin-C, a developmentally regulated matrix protein,

31 Tenascin-C, a matrix protein induced upon tissue damage

32 mechanical strain on the gene expression of tenascin-C, a prominent extracellular molecule in active

33 Induction of tenascin-C, a proproliferative and promigratory extracel

34 Syndecan-4 is also required for tenascin-C action.

35 Inhibition of syndecan-4 function suppresses tenascin-C activity and overexpression of syndecan-4 cir

36 Tenascin C-adhering cells remained round, whereas they s

37 by immunocytochemistry, the distribution of tenascin-C along neural growth pathways in the developin

38 The presence of tenascin-C along the growth routes of nerve fibers, part

39 stains in the rodent heart demonstrated that tenascin-C also colocalizes with EPCs homing to sites of

40 and media-lumen ratio and overexpression of tenascin C, an extracellular matrix glycoprotein that co

41 (EGFR) found within the EGF-like repeats of tenascin-C, an antiadhesive matrix component present dur

42 Tenascin-C, an extracellular matrix protein involved in

43 CD44, tenascin C and fibrillin-1 mRNA levels were reduced by 4

44 s such as SPARC, thrombospondin 1 and 2, and tenascin C and X subserve important functions in extrace

45 ie, production of collagen, fibronectin, and tenascin-C and accumulation of myofibroblasts).

46 ronment consisting of the highly upregulated tenascin-C and chondroitin sulfate proteoglycans (CSPGs)

47 Newly characterized Ets target genes such as tenascin-C and collagen type I suggest their role in dis

48 ectin type III repeats 1-2, A, B, and 6-8 of tenascin-C and fibronectin type III repeats 1-2 and 6-8

49 ith matrices representative of transitional (tenascin-C and fibronectin) and differentiated environme

50 nts of this dynamic matrix, hyaluronic acid, tenascin-C and fibronectin, differentially direct cellul

51 ograft model of advanced human osteosarcoma, tenascin-C and its receptor integrin alpha9beta1 were de

52 Full length tenascin-C and longer fragments containing this repeat d

53 hesion assays showed the interaction between tenascin-C and newborn cells to be predominantly RGD-ind

54 t binding of alpha9beta1-expressing cells to tenascin-C and osteopontin, respectively, had no effect

55 The functional importance of stromal Tenascin-C and S100A4(+) fibroblast-derived VEGF-A in me

56 In this way, tenascin-C and syndecan-4 work together to control fibro

57 d in the developing brain: the glycoproteins tenascin-C and tenascin-R and the chondroitin sulfate pr

58 extracellular domain of the beta2 subunit to tenascin-C and tenascin-R in vitro.

59 ls to extracellular matrix molecules such as tenascin-C and tenascin-R may play a crucial role in loc

60 sion proteins containing various segments of tenascin-C and tenascin-R were purified, digested with t

61 eract with the extracellular matrix proteins tenascin-C and tenascin-R.

62 binds to the extracellular matrix molecules tenascin-C and tenascin-R.

63 ta1- and FGF-2-induced de novo expression of tenascin-C and the downregulation of alpha3(IV) collagen

64 alpha7beta1 integrin mediates a response to tenascin-C and the first to demonstrate a functional rol

65 M molecules and growth factors, particularly Tenascin-C and VEGF-A.

66 s for cell adhesion/motility (syndecan-4 and tenascin-C) and hyaluronan (HA) signaling.

67 Bone matrix markers (biglycan, COL1A1, tenascin C, and fibronectin) and low-density lipoprotein

68 (N-CAM), an extracellular matrix component, tenascin-C, and a soluble growth factor, fibroblast grow

69 hed with vascular endothelial growth factor, tenascin-C, and activated matrix metalloproteinase-9, fa

70 ether, these results demonstrate that N-CAM, tenascin-C, and FGF-5 are dispensable for major aspects

71 transitional matrix rich in hyaluronic acid, tenascin-C, and fibronectin controls muscle cell behavio

72 We could validate phosphacan, tenascin-C, and L1-CAM as major LeX carrier proteins pre

73 n, matrix metalloproteinases (MMPs) 2 and 9, tenascin-C, and osteopontin, revealed that MMP-9 and ten

74 vascular cell adhesion molecule 1 (VCAM-1), tenascin-C, and osteopontin.

75 lly expresses neural cell adhesion molecule, tenascin-C, and other molecules.

76 00 were induced >2.5-fold: cyclooxygenase-1, tenascin-C, and plasminogen activator inhibitor-1.

77 TSP1, tenascin-C, and SPARC induce the intermediate adhesive s

78 regulated matricellular proteins TSP1 and 2, tenascin-C, and SPARC.

79 tracellular matrix proteins, fibronectin and tenascin-C, and the basement membrane components, lamini

80 several MMPs, TGF-beta signaling molecules, Tenascin-C, and VEGF-A, while pro-fibrotic molecules, in

81 In addition, the expression of tenascin C, another marker of the mammary mesenchyme, is

82 Tenascin-C-AR modified cells aggregated to cells in a te

83 stem cell (HSC) mimics were modified with a tenascin-C-AR to improve the homing of HSC after an auto

84 Levels of tenascin-C are elevated in SSc skin biopsy samples, and

85 iated by the alternatively spliced region of tenascin-C are separable events that can be independentl

86 n alpha8 beta1-fibronectin, vitronectin, and tenascin-C-are not appropriately localized to mediate al

87 s performed and led to the identification of tenascin-C as a candidate protein.

88 valuate the contribution of the glycoprotein tenascin-c as a key mediator of smooth muscle cell growt

89 Together, our data highlight the role of tenascin-C as a microenvironmental regulator of cardiac

90 Thus, we have identified tenascin-C as a novel endogenous activator of TLR4-media

91 These results identify tenascin-C as an endogenous danger signal that is upregu

92 Our study revealed midkine, CYR61, and tenascin-C as endogenous substrates for KLK7.

93 the physiologically relevant presentation of tenascin-C as hexabrachion, and suggesting an increase i

94 lts show that trimers are an intermediate of tenascin-C assembly and that Cys-64 is essential for for

95 p21 loss, elevated NF-kappaB expression and tenascin C-associated rigidity, with p-Mypt1 inactivatio

96 ted epithelial cells with alpha9 integrin, a tenascin-C-binding integrin, led to a large increase in

97 adhesion modulatory proteins, fibulin-1 and tenascin-C, both of which bind to the C-terminal heparin

98 ype mice or mice with a targeted deletion of tenascin-C by assessing cell maturation, cytokine synthe

99 ha(v)beta(3), suggesting that fibrinogen and tenascin C C-terminal domains interact with alpha(v)beta

100 We also found that tenascin C C-terminal fibrinogen-like domain specificall

101 Using live-cell imaging, we found softer tenascin-C-coated substrates significantly enhanced migr

102 cells preferentially migrated and colonized tenascin-C-coated trabecular bone xenografts in a novel

103 In the spiral lamina, tenascin-C coexists in a region where nerve bundles arbo

104 f age, there were fewer condylar superficial tenascin-C/Col1-positive cells and more numerous apoptot

105 ges in netrin 4, fibroblast growth factor 2, tenascin C, collagen 1, meprin 1-alpha, and meprin 1-bet

106 Total levels of tenascin C, collagen type XII, and CD44 mRNA were increa

107 top 10 results (collagen, type III, alpha-1; tenascin C; collagen, type VI, alpha-3; thrombospondin 2

108 ation of thick fibronectin fibrils, to which tenascin C colocalized.

109 The effects of tenascin-C combined with its location around the wound b

110 PGE(2) but more PGI(2) and expressed reduced tenascin-C compared with wild-type cells.

111 The region of tenascin-C containing only alternately spliced fibronect

112 We have found that the region of tenascin-C containing only alternately spliced fibronect

113 ons were observed only to short fragments of tenascin-C containing the third fibronectin type III rep

114 We conclude that tenascin C contributes to the generation of a stem cell

115 ciated KLKs), whereas others (e.g. CYR61 and tenascin-C) could be digested by several KLKs.

116 Tenascin-C deficiency resulted in minor structural diffe

117 Tenascin C-deficient mice also have altered numbers of C

118 -C, and osteopontin, revealed that MMP-9 and tenascin-C demonstrated reduced expression both in vitro

119 nipin reduced the levels of collagen type I, tenascin C, elastin and versican.

120 Select EGF-like repeats of tenascin-C elicited mitogenesis and EGFR autophosphoryla

121 Tenascin-C (encoded by Tnc) is an extracellular matrix g

122 ltured on osteo-mimetic surfaces coated with tenascin C exhibited enhanced adhesion and colony format

123 Using portions of tenascin-C expressed as recombinant proteins in human fi

124 The permissive guidance cues of large tenascin-C expressed by cells were mapped to fnA-D.

125 C-AR modified cells aggregated to cells in a tenascin-C expressing stem cell niche model better than

126 a correlation of IL-17+ T cell numbers with tenascin C-expressing cells and MMP-9+ eosinophils was a

127 PGE(2) and augmentation of PGI(2) attenuate tenascin-C expression and vascular smooth muscle cell pr

128 showed both retention of alpha9 integrin and tenascin-C expression at the anterior stromal-epithelial

129 Tenascin-C expression begins with adventitial myofibrobl

130 Among these cells, tenascin-C expression is most highly induced in activate

131 Suppression of GTPase activation allows tenascin-C expression to act as a regulatory switch to r

132 Tenascin-C expression, however, did not persist in this

133 nregulated both TGF-beta1- and FGF-2-induced tenascin-C expression, ROCK inhibition was found to down

134 pathologic remodeling with aberrant Prx1 and Tenascin-C expression.

135 eased proliferating cell nuclear antigen and tenascin-C expression.

136 after vascular injury, in part by regulating tenascin-C expression.

137 ons in homozygous mutant mice lacking N-CAM, tenascin-C, FGF-5, or both N-CAM and tenascin-C.

138 infant but not the adult DM was positive for tenascin-C, fibrillin-1, SPARC, and laminin-332.

139 Here, we report that, like tenascin-C, fibulin-1 inhibits fibroblast spreading and

140 kers, including collagen types I and III and tenascin-C, fostered statistically significant cell alig

141 ey cellular regulators, such as EGFR, HSP70, Tenascin C, Frizzled-5, Patched-1, and Delta-like 1.

142 s indicated that mechanical strain increases tenascin-C gene transcription by activating nuclear fact

143 nents (fibrillar type I and III collagen and tenascin-C) had no effect.

144 Tenascin-C has been implicated in regulation of both neu

145 shown previously that a particular region of tenascin-C has powerful neurite outgrowth-promoting acti

146 ssibility that growth cone interactions with tenascin-C helps to guide nerve fibers in the cochlea.

147 Dendritic cells that did not express tenascin-C, however, produced lower levels of inflammato

148 show dynamic spatial and temporal changes in tenascin-C, hyaluronic acid, and fibronectin ECM distrib

149 Faint tenascin-C immunolabeling of normal hair cells, strong t

150 At the age when most neural growth ceases, tenascin-C immunoreactivity disappears.

151 Mg2+ increased newborn cell adhesion to tenascin-C in a concentration-dependent manner, whereas

152 s demonstrate that mechanical strain induces tenascin-C in cardiac myocytes through a nuclear factor-

153 To determine the importance of tenascin-C in cardiac neovascularization, we used an est

154 ted to bind to fibronectin, vitronectin, and tenascin-C in cell adhesion or neurite outgrowth assays.

155 diated induction of procollagen type III and tenascin-C in isolated cardiac fibroblasts was dependent

156 cts, interstitial deposition of collagen and tenascin-C in the remodeling myocardium was markedly red

157 ults illuminate how tumor cell deposition of tenascin-C in the tumor microenvironment promotes invasi

158 te how the extracellular matrix glycoprotein tenascin-C in the tumor microenvironment promotes invasi

159 aim of this study was to examine the role of tenascin-C in this cell type.

160 In contrast to their interactions with tenascin-C, in which binding was decreased by approximat

161 otion of neurite outgrowth by fnD as well as tenascin-C, indicating that this peptide sequence is fun

162 SCCs exhibited increased NF-kappaB and novel tenascin C, indicative of elevated rigidity; yet despite

163 n in vivo in mice, and addition of exogenous tenascin-C induces cytokine synthesis in explant culture

164 ia of individuals with rheumatoid arthritis, tenascin-C induces synthesis of proinflammatory cytokine

165 Functionally, tenascin-C inhibits cardiac endothelial cell spreading a

166 including VEGF, IL-6, VEGF-C, HB-EGF, CTGF, tenascin C, integrin alpha5, and Eph receptor A2.

167 Here, we report that tenascin C is expressed in the bone endosteum and is ass

168 Tenascin C is highly expressed in the SVZ, and transgeni

169 igands, implying that the RGD site in native tenascin-C is a cryptic binding site for this integrin,

170 Tenascin-C is a glycoprotein of the extracellular matrix

171 Tenascin-C is a large extracellular matrix glycoprotein

172 Tenascin-C is a large, multimeric extracellular matrix p

173 The extracellular matrix protein tenascin-C is a multidomain protein that regulates cell

174 By embryonic day 16, tenascin-C is abundant on the pillar side of the inner h

175 Tenascin-C is an arthritogenic extracellular matrix glyc

176 Tenascin-C is an extracellular matrix molecule that driv

177 Tenascin-C is an extracellular matrix protein that regul

178 We show that tenascin-C is anti-adhesive for retinal pigmented epithe

179 The inhibitory effect of tenascin-C is circumvented by downstream activation of R

180 This demonstrates for the first time that tenascin-C is essential for postnatal cardiac angiogenic

181 Tenascin-C is expressed in response to balloon injury.

182 Tenascin-C is expressed in the vessel wall after vascula

183 Tenascin-C is expressed transiently during wound repair

184 peptide sequence this integrin recognizes in tenascin-C is highly homologous to the sequence recogniz

185 These data demonstrate that tenascin-C is important in DC-mediated polarization of T

186 position of the extracellular matrix protein tenascin-C is part of the reactive stroma response, whic

187 Here we show that tenascin-C is produced by type-B cells and forms a layer

188 The extracellular matrix glycoprotein tenascin-C is widely expressed in the vertebrate central

189 , laminin, and nidogen, as well as the large tenascin-C isoform, fibronectin, and type I gelatin in v

190 of proangiogenic genes, such as osteopontin, tenascin C, KGF, angiopoietin, HIF-1alpha, and PDGFRbeta

191 Tenascin-C levels and tumor uptake were studied in a var

192 In the organ of Corti, tenascin-C lines the neural pathways along pillar and De

193 Here, we report that tenascin-C markedly altered cell phenotype on a three-di

194 , vimentin, discoidin domain receptor 2, and tenascin C, markers of fibroblasts and components of the

195 Cells surrounded by a fibrin-FN+tenascin-C matrix are unable to induce matrix contractio

196 to facilitate colonization, whereas stromal Tenascin-C may provide protection from apoptosis.

197 model and showed that unlike wild-type mice, tenascin-C-/- mice fail to vascularize cardiac allograft

198 As with the intact tenascin-C molecule, adherent cells remained round, and

199 cated near the carboxyl-terminal part of the tenascin-C molecule.

200 Mechanical strain induced tenascin-C mRNA (3.9 +/- 0.5-fold, p < 0.01, n = 13) and

201 Tenascin-C mRNA expression was detected in epithelial, s

202 SMA, vimentin, and tenascin-c mRNAs were decreased by 60%, 40%, and 49%, re

203 A in metastasis was established by examining Tenascin-C null mice and transgenic mice expressing Cre

204 Moreover, tenascin-C-null mice displayed ablated levels of interle

205 Dendritic cells derived from tenascin-C-null mice exhibited no defects in maturation;

206 NS and other organs have been found in adult tenascin-C-null mice, raising the question of whether th

207 Despite multiple effects of tenascin-C on cell behaviour in culture, no structural a

208 ed by expressing an integrin that recognizes tenascin-C, one of the components of glial scar tissue,

209 rat aorta to investigate the interaction of tenascin-C or its various domains with these cells using

210 association of the alpha7beta1 integrin with tenascin-C peptides containing the VFDNFVLK sequence but

211 co-localizing with the fibrillar fibronectin/tenascin-C/periostin structures that characteristically

212 Truncated tenascin-C promoter-reporter assays using dominant negat

213 utonomous signaling mechanism explaining how tenascin-C promotes cancer cell migration in the tumor m

214 Tenascin-C promotes growth of axons if they express a te

215 Intra-articular injection of tenascin-C promotes joint inflammation in vivo in mice,

216 as occurs in the presence of the ECM protein tenascin-C, promotes a motile phenotype; FAK and Rho sig

217 Analysis of human coronary thrombi revealed tenascin-C protein expression colocalized with the endot

218 RNA (3.9 +/- 0.5-fold, p < 0.01, n = 13) and tenascin-C protein in an amplitude-dependent manner but

219 Cells on fibrin-FN+tenascin-C redistribute their actin to the cell cortex,

220 demonstrating the potential applicability of tenascin-C regions as therapeutic reagents.

221 ansgenic approach, we have demonstrated that tenascin-C regulates both cell proliferation and migrati

222 f the provisional matrix, we have found that tenascin-C regulates cell responses to a fibrin-FN matri

223 anding how the extracellular matrix molecule tenascin-C regulates neuronal growth.

224 se of MMPs was accompanied by an increase in tenascin-C release.

225 aling by competitive binding of fibulin-1 or tenascin-C represents a shared mechanism of adhesion mod

226 21-associated differentiation in wdSCCs; yet tenascin C retention in connective tissue extracellular

227 um channels on microtiter plates coated with tenascin-C revealed saturable and specific binding with

228 dorsal root ganglia regenerated through the tenascin-C-rich dorsal root entry zone into the dorsal c

229 (+)) preceded K14.ROCK(er)-mediated (p-Mypt1/tenascin C/rigidity) malignant conversion.

230 Of these, "FD" and "FV" are conserved in tenascin-C sequences derived from all the species availa

231 ssed in the SVZ, and transgenic mice lacking tenascin C show delayed acquisition of the EGF receptor.

232 Mice lacking tenascin-C show attenuation of skin and lung fibrosis, a

233 Here we show that mice that do not express tenascin-C show rapid resolution of acute joint inflamma

234 we show that the regenerative ECM component tenascin-C significantly increases newt cardiomyocyte ce

235 erexpressed the largest but not the smallest tenascin-C splice variant when given a choice between co

236 as indicated by inappropriate expression of tenascin-C starting by day 6 of pregnancy.

237 Exogenous tenascin-C stimulates collagen gene expression and myofi

238 he desmoplastic extracellular matrix protein tenascin C, suppressing tumor outgrowth, and improving h

239 e utilized the extracellular matrix molecule tenascin-C (tenascin) and an antibody (Ab) to the cell a

240 born cells were three times more adherent to tenascin-C than adult cells.

241 Here we map three sites within tenascin-C that directly and cooperatively interact with

242 llular deposits of eosinophil peroxidase and tenascin C, the effects not seen with placebo.

243 taining the fibronectin type III domain D of tenascin C, the long NC3 isoform of collagen type XII, t

244 e effective than laminin-1, L1-Fc, or intact tenascin-C, thus demonstrating the potential applicabili

245 For cyclinD1, fibulin 2, tenascin C, TIMP1, and aquaporin-4, correlations were si

246 Tenascin-C (TN) is an extracellular matrix protein that

247 Enhanced expression of tenascin-C (TN-C) at the invasive edges of glioblastoma

248 Intense matrix metalloproteinase (MMP-2) and tenascin-C (TN-C) expression were seen in the proximity

249 h vascular disease, colocalizing to sites of tenascin-C (TN-C) expression.

250 To determine the potential role of tenascin-C (TN-C) in the pathophysiology of atherosclero

251 Tenascin-C (TN-C) is an extracellular matrix (ECM) prote

252 Tenascin-C (TN-C) is an extracellular matrix protein tha

253 Tenascin-C (TN-C) is expressed in embryogenesis, tissue

254 To address this question, we focused on tenascin-C (TN-C), a stromal extracellular matrix glycop

255 icipates in network formation, we focused on tenascin-C (TN-C), an extracellular matrix (ECM) protein

256 dy was performed to test the hypothesis that tenascin-C (TN-C), an extracellular matrix (ECM) protein

257 Tenascin-C (TN-C), an extracellular matrix glycoprotein

258 PDGF-BB also stimulates the expression of tenascin-C (TN-C), an extracellular matrix glycoprotein

259 vation of FAK and cellular interactions with tenascin-C (TN-C).

260 ed the expression of the profibrotic factors tenascin C (TNC) and connective tissue growth factor (CT

261 Tenascin C (TNC) is a matricellular glycoprotein whose e

262 catenin signaling led to marked induction of tenascin C (TNC), an established promoter of cancer meta

263 of multiple metastasis effectors, including Tenascin C (Tnc), Jagged1 (Jag1), and Epiregulin (Ereg).

264 ranscriptional regulation of the ECM protein tenascin C (Tnc), which was necessary and sufficient for

265 ), mapped within the gene coding sequence of Tenascin C (TNC).

266 metastasis-initiating ability by expressing tenascin C (TNC).

267 ctive tissue growth factor (Ctgf, P = 0.04), tenascin C (Tnc, P = 0.035), Collagen Ialpha1 (Col1a1, P

268 tified the extracellular matrix glycoprotein tenascin-C (TNC) as an important regulator of ENCC devel

269 o determine the temporospatial expression of tenascin-C (TnC) in balloon-injured rat and porcine arte

270 pattern of the extracellular matrix molecule tenascin-C (Tnc) in the developing mouse olfactory bulb

271 Tenascin-C (TNC) is a highly conserved matricellular pro

272 Tenascin-C (TNC) is a mechano-regulated, morphogenic, ex

273 Tenascin-C (Tnc) is an extracellular matrix protein (ECM

274 Tenascin-C (TNC) is highly expressed in melanoma; howeve

275 r mPIN used the extracellular matrix protein Tenascin-C (TNC) to inhibit T-cell receptor-dependent T-

276 Here we provide evidence that tenascin-C (TNC), an extracellular matrix protein promin

277 Tenascin-C (TnC), an extracellular matrix protein, is tr

278 ral S100 proteins, including Fibronectin and Tenascin-C (Tnc), in primary lung tumors and associated

279 Tenascin-C (TNC), overexpressed in invasive growths, has

280 or alpha-smooth muscle actin (alpha-SMA) and tenascin-C (TNC).

281 y HIV-1-neutralizing protein in breast milk, Tenascin-C (TNC).

282 th at least three members: tenascin-X (TNX), tenascin-C (TNC, or cytotactin) and tenascin-R (TN-R, or

283 ne signature identified five common targets: tenascin-C(TNC), matrix metalloprotease-2, collagen-6-A1

284 ctin (fnFN10) and the 3rd FN-III domain from tenascin-C (tnFN3) have 27% sequence identity and the sa

285 EDGIHELFP(48)) resembles the sequence within tenascin-C to which the integrin alpha(9)beta(1) binds.

286 nD to an eight amino acid sequence unique to tenascin-C, VFDNFVLK, and showed that the amino acids FD

287 ha-smooth muscle actin were reduced, whereas tenascin C was increased, suggesting that P15-1 promoted

288 sis of PAH such as serotonin transporter and tenascin-C was elevated in distal arteries and had a hig

289 Fibroblast response to fibulin-1, similar to tenascin-C, was dependent on expression of the heparan s

290 aptamer to the extracellular matrix protein tenascin-C, was prepared in fluorescent and radiolabeled

291 nction relationships of different domains of tenascin-C, we used recombinant full-length fibronectin-

292 remodeling such as MMP-9, procollagen-3, and tenascin C were observed in all acute eczematous lesions

293 Increased apoptosis and immunoreactivity for tenascin-C were observed in mutant muscle fibers.

294 istribution of molecular markers (SHH, NCAM, Tenascin-C) were characteristic of feather buds.

295 pha-smooth muscle actin (SMA), vimentin, and tenascin-c, were measured in archived human HCC tissues

296 ar degeneration-affected Bruch's membrane is tenascin-C which we confirm is present at high levels in

297 ulation of the extracellular matrix protein, tenascin C, which affords a scaffold for VSMC migration.

298 Calcific leaflets also exhibit tenascin-C, which may facilitate inflammatory cell migra

299 nderstanding the mechanism of interaction of tenascin-C with smooth muscle cells and a framework for

300 milarity with the fibrinogen domain of human tenascin-C, with a human C-type serum lectin, and with p