ライフサイエンスコーパス: metalloproteinase

1 ns, and suppressed the expressions of matrix metalloproteinases.

2 ases or extracellularly by plasmin or matrix metalloproteinases.

3 epidermal growth factor receptor mediated by metalloproteinases.

4 ration, and reduced the expression of matrix metalloproteinases.

5 collagens, profibrotic cytokines and matrix metalloproteinases.

6 and is mediated by specific proteases, e.g. metalloproteinases.

7 ution of the vertebrate tissue inhibitors of metalloproteinases.

8 brane by regulating the expression of matrix metalloproteinases.

9 mics that of endogenous tissue inhibitors of metalloproteinases.

10 nd superfamily member 13B (TNFSF13B), matrix metalloproteinase 1 (MMP-1), MMP-2, and MMP-3.

11 Matrix metalloproteinase 1 (MMP1) is required in tracheal cells

12 pproach that would allow tissue inhibitor of metalloproteinase 1 (TIMP-1), the endogenous inhibitor o

13 Higher levels of tissue inhibitor of matrix metalloproteinase 1 and soluble ST2 at baseline and incr

14 lsartan decreased tissue inhibitor of matrix metalloproteinase 1 by 8% (95% confidence interval [CI]:

15 al fibroblast cultures confirmed that matrix metalloproteinase 1 mRNA, MMP1, increased with aging, wh

16 thase 2 was highly expressed, whereas matrix metalloproteinase 1 was elevated in the dermal papilla a

17 ma-glutamyl transferase, tissue inhibitor of metalloproteinase 1, C-reactive protein, and bile acids

18 llagen I and III, tissue inhibitor of matrix metalloproteinase 1, carboxyl-terminal telopeptide of co

19 en type I alpha 1 chain, tissue inhibitor of metalloproteinase 1, platelet-derived growth factor c, t

20 C-reactive protein (CRP) degraded by matrix metalloproteinases 1 and 8 (CRPM) from baseline to week

21 roteinase-8) and TIMP-1 (tissue inhibitor of metalloproteinases 1); false discovery rate q < 0.05 for

22 NF-kappaB upregulated tissue inhibitor metalloproteinases 1, which may inhibit ECM degradation

23 hesis and inducing TIMP (tissue inhibitor of metalloproteinases)-1.

24 ility of AHR to control expression of matrix metalloproteinase-1 (MMP1) was analyzed.

25 recruited to intron 1 of tissue inhibitor of metalloproteinase-1 (TIMP1) gene and modulated its expre

26 , -2, -3, -7, and -8 and tissue inhibitor of metalloproteinase-1 and -2; and depressed active and tot

27 nal telopeptide of collagen type-I to matrix metalloproteinase-1 ratio) and with excessive myocardial

28 cellular matrix-modifying enzymes and matrix metalloproteinase-1.

29 Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a pleiotropic protein,

30 and downstream mediator tissue inhibitor of metalloproteinases-1 (TIMP-1).

31 A disintegrine and metalloproteinase 10 (ADAM10) is implicated in synaptic

32 ted the role of macrophage-associated matrix metalloproteinase 12 (MMP12) in the regulation of CCL2 a

33 growth/differentiation factor 15, and matrix metalloproteinase 12.

34 Matrix metalloproteinase-12 (MMP-12) is highly upregulated in s

35 es causing aberrant expression of the matrix metalloproteinase-12 (MMP-12).

36 rentiation 40, apolipoprotein(a), and matrix metalloproteinase-12.

37 fish model to show that the epidermal matrix-metalloproteinase 13 (MMP-13) induces degeneration of un

38 Here, we reported that matrix metalloproteinase 14 (MMP14), a key pericellular collage

39 A Disintegrin and Metalloproteinase-15 (ADAM15) is a transmembrane protein

40 ion, the metalloproteinase A disintegrin and metalloproteinase 17 (ADAM17) sheds L-selectin from the

41 ved by the metalloprotease a disintegrin and metalloproteinase-17 upon stimulation.

42 The matrix metalloproteinase 2 (MMP2) gene has been identified as a

43 inase JNK mediate the accumulation of matrix metalloproteinase 2 (Mmp2), damaging the BM, which recru

44 Collagen deposition and metalloproteinase 2 and 9 (MMP2-9) activity were compare

45 h correlated with a decrease in MMP2 (matrix metalloproteinase 2), MMP9, and ADAM10 (ADAM metallopept

46 ng requires mesenchymal expression of matrix metalloproteinase 2, which is necessary for branch exten

47 tor receptor-1, protein kinase C, and matrix metalloproteinase 2.

48 eration, migration, and production of matrix metalloproteinase 2; treatment with MDM2 inhibitors repr

49 cells by modulating the activities of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).

50 o tumor-associated proteases, such as matrix metalloproteinases 2 and 9, the coiled-coil peptides are

51 ng collagen 1 and 3, fibronectin, and matrix metalloproteinases 2 and 9, were up-regulated in PH rat

52 tor (VEGF), Interleukin 6 (IL-6), and matrix metalloproteinase-2 (MMP-2) were measured using an enzym

53 A matrix metalloproteinase-2 (MMP2) sensitive self-assembling pep

54 native activation, iii) cytokine, iv) matrix metalloproteinase-2 activity, v) fibrosis, and vi) cardi

55 pneic group showed significantly less matrix metalloproteinase-2 and -9 activity.

56 oclonal antibody was raised against a matrix metalloproteinase-2 and -9 specific cleavage site of COL

57 cycle arrest biomarkers tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-bindi

58 r admission, and urinary tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-bindi

59 s connective tissue growth factor and matrix metalloproteinase-2 expression.

60 Pathogenic rise of collagenolytic matrix metalloproteinase-2 in biofilm-infected wound-edge tissu

61 Levels of IL-10, IL-6, and matrix metalloproteinase-2 were significantly increased, wherea

62 enal resistive index and tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

63 The performance of tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

64 Urinary tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

65 f the urinary biomarker, tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

66 Urinary tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

67 luate the performance of tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding

68 with sham, and its activation induced matrix metalloproteinase-2, which enhanced GB pathogenesis.

69 ulation of its downstream target gene matrix metalloproteinase-2.

70 the relationship between tissue inhibitor of metalloproteinases-2 ([TIMP-2]) and insulin growth facto

71 Urinary tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth fa

72 tractile myofibroblasts, glial cells, matrix metalloproteinases-2 and -9, and collagen type I, II, an

73 bit an increased urinary tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-bind

74 Absolute changes in [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

75 t was change in urinary [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

76 tioning could stimulate [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

77 on absolute changes in [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

78 significantly increased [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

79 ning to induce required [tissue inhibitor of metalloproteinases-2]*[insulin-like growth factor-bindin

80 nvestigate the role of proteolysis by matrix metalloproteinase 20 (MMP20) in regulating the initial f

81 rthermore, this study elucidated that matrix metalloproteinase-20 is a critical regulator of the enam

82 Tissue inhibitor of metalloproteinase 3 (TIMP3) and cytoplasmic polyadenylat

83 so increased the levels/activation of matrix metalloproteinase 3 and 9.

84 une activation, in particular YKL-40, matrix metalloproteinase 3, macrophage inflammatory protein 1be

85 r repair (matrix metalloproteinase 7, matrix metalloproteinase 3, the integrins beta6 and beta8, and

86 cardiac fibroblasts, suppressing MMP (matrix metalloproteinase)-3 and MMP-8 synthesis and inducing TI

87 vitro that a variant of tissue inhibitor of metalloproteinase-3 ([-1A]TIMP3) inhibits ADAMTSs but no

88 Matrix metalloproteinase-3 (MMP-3) participates in normal extra

89 used by mutations in the Tissue Inhibitor of Metalloproteinase-3 (TIMP3) gene.

90 iated with epithelial barrier repair (matrix metalloproteinase 7, matrix metalloproteinase 3, the int

91 Identifying no significantly changes in metalloproteinase-7 (MMP7) serum concentration, or secon

92 hip between the expression of FXR and matrix metalloproteinase-7 (MMP7), a collagenase and signaling

93 opoietin-2 (related to angiogenesis), matrix metalloproteinase-7 (related to extracellular matrix tur

94 similar CCL expression and suggested matrix metalloproteinase-7 and MMP9 as possible extracellular m

95 ession of Kaiso target genes, such as matrix metalloproteinase-7.

96 Because CGPQG IWGQC can be cleaved by matrix metalloproteinase 8 (MMP-8), minocycline hydrochloride,

97 s all analyses was MMP8, encoding the matrix metalloproteinase 8, which is a regulator of innate immu

98 a point-of-care (PoC) test of active matrix metalloproteinase-8 (aMMP-8) predicts levels of inflamma

99 y evaluated two protein coding genes, matrix metalloproteinase-8 (MMP-8) and transcription factor T-B

100 ptidylarginine deiminase 2 (PAD2) and matrix metalloproteinase-8 (MMP-8) in gingival crevicular fluid

101 ve glutathione ratio [GSH/GSSG]), and matrix metalloproteinase-8 (MMP-8) levels; and histopathologica

102 ototype biosensor to measure salivary matrix metalloproteinase-8 (MMP-8) using specific antibodies an

103 livary periodontal biomarkers (active matrix metalloproteinase-8 [aMMP-8], polymorphonuclear leukocyt

104 ntrol group 3 and 6 months after SRP, matrix metalloproteinase-8 level decreased in the test group 3

105 s and platelet markers such as MMP-8 (matrix metalloproteinase-8) and TIMP-1 (tissue inhibitor of met

106 interleukin-1beta, and downregulated matrix metalloproteinase-8, whereas periodontal bone level and

107 Matrix metalloproteinase 9 (MMP-9) antisense oligonucleotides (

108 ammatory cytokine TNFalpha stimulates matrix metalloproteinase 9 (MMP9) at the ocular surface through

109 e expression of the metalloproteinase matrix metalloproteinase 9 (MMP9) in human breast cancer sample

110 Further, mutation of matrix metalloproteinase 9 (mmp9) results in delayed growth pla

111 roglia activation and redox-sensitive matrix metalloproteinase 9 (MMP9) stimulation, leading to the r

112 Matrix metalloproteinase 9 (MMP9), which degrades NGF, was over

113 bretastatin A4 nanodrug (CA4-NPs) and matrix metalloproteinase 9 (MMP9)-activated doxorubicin prodrug

114 ty and differentiation, in particular matrix metalloproteinase 9 (MMP9).

115 Additionally, levels of matrix metalloproteinase 9 and the chemokines C-C motif chemoki

116 e haploinsufficiency results in lower matrix metalloproteinase 9 expression, and reduced migration an

117 inal region, via the action of MMP-9 (matrix metalloproteinase 9).

118 ing as well as expression of IL-8 and matrix metalloproteinase 9, ankle loading decreased them.

119 ermore, we showed an increased expression of metalloproteinase 9, at both gene and protein levels, in

120 s, likely via proteolytic cleavage of matrix metalloproteinase 9.

121 eceptor gamma, and reducing Snail and matrix metalloproteinase 9.

122 y modulating the activity of secreted matrix metalloproteinases 9 (MMP-9).

123 beta induces activities of A disintegrin and metalloproteinases 9, 10, and 17 by specific prodomain c

124 The dysregulation of matrix metalloproteinase-9 (MMP-9) has been implicated in multi

125 ELISA demonstrates reduced levels of matrix metalloproteinase-9 (MMP-9) in the plasma and brains at

126 Matrix metalloproteinase-9 (MMP-9) is required for structural s

127 xide dismutase (SOD), catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTn

128 zation, and (iv) TNF-alpha-stimulated matrix metalloproteinase-9 (MMP9) expression and activity.

129 Remarkably, proteinases including matrix metalloproteinase-9 (Mmp9) released from endothelial cel

130 of tumor-secreted factors, including matrix metalloproteinase-9 (MMP9), fibronectin (FN), and solubl

131 tory factor 3, which directly induced matrix metalloproteinase-9 expression.

132 drug clearance.SIGNIFICANCE STATEMENT Matrix metalloproteinase-9 inhibition appears to attenuate memo

133 ty of the BBB-degrading cyclophilin A-matrix metalloproteinase-9 pathway(19) in cerebrospinal fluid.

134 of EC and NS (myeloperoxidase [MPO], matrix metalloproteinase-9) as well as between DS and EC for bi

135 ors in tumors, including IL-1beta and matrix metalloproteinase-9, and we found upregulation of these

136 n-6, tumor necrosis factor-alpha, and matrix metalloproteinase-9, suggesting that KC may have an infl

137 Downstream of integrin ligation, the metalloproteinase A disintegrin and metalloproteinase 17

138 ation and activity of membrane type 1-matrix metalloproteinase, a key factor for extracellular matrix

139 evels to that of controls and reduced matrix metalloproteinase activation in the sub-acute stages fol

140 through a pathway involving increased matrix metalloproteinase activation.

141 decreased histologic lung injury and matrix metalloproteinase activity, and prevented the expression

142 ocessing, inclusive of cysteine, serine, and metalloproteinase activity, generates cationic amphipath

143 ere was poor EVT invasion and reduced matrix metalloproteinase activity, reinforcing their critical r

144 isplayed significantly decreased MMP (matrix metalloproteinases) activity in the aorta (mean differen

145 for proteolyticlly active A Disintegrin And Metalloproteinase (ADAM) family members.

146 A disintegrin and metalloproteinase (ADAM)10 and ADAM17 are physiologic re

147 been liberated from the cell surface by the metalloproteinase, ADAM-10, in combination with heparan

148 The metalloproteinase ADAM17 plays a pivotal role in initiat

149 MPs) and the related families of disintegrin metalloproteinases (ADAMs) and ADAMs with thrombospondin

150 d cleaving enzyme (Bace1), A disintegrin and metalloproteinases (Adams), and presenilins (Psen).

151 nes, including inactivating mutations of the metalloproteinase ADAMTS12 in lung adenocarcinoma.

152 GM6001, an inhibitor of matrix metalloproteinase, alleviated UA-induced glycocalyx shed

153 nalling-and therefore the activity of matrix metalloproteinases and basement membrane perforations-to

154 ed cellular bioenergetics, suppressed matrix metalloproteinases and chemokine receptors, and the indu

155 ere marked by increased expression of matrix metalloproteinases and degradation of the basement membr

156 tracellular matrix because of the release of metalloproteinases and degrading enzymes, and subsequent

157 roinflammatory (with higher levels of matrix metalloproteinases and inflammatory cytokines).

158 f apoptosis, suppressed expression of matrix metalloproteinases and reduction in MDSCs infiltration,

159 resulting in proteolytic cleavage by matrix metalloproteinases, and reduced activity of VEGFR2 and i

160 inhibitors of metalloproteinases, decreased metalloproteinases, and Wnt family member WNT2/beta-cate

161 ay be a general mechanism by which inhibited metalloproteinases are removed from the extracellular en

162 TIMPs from invertebrates also inhibit metalloproteinases, bind to pro-MMPs, and contribute to

163 ed analyses, we found that the extracellular metalloproteinase bone morphogenetic protein 1 (BMP-1) i

164 We identified the secreted zinc metalloproteinase, bone morphogenetic protein 1 (BMP1),

165 3 can facilitate the clearance of its target metalloproteinases by bridging their binding to LRP-1.

166 This suggests that LRP-1 scavenging of TIMP/metalloproteinase complexes may be a general mechanism b

167 nes including increased tissue inhibitors of metalloproteinases, decreased metalloproteinases, and Wn

168 ADAMTS (A Disintegrin-like and Metalloproteinase domain with Thrombospondin type 1 Moti

169 al agonist Yoda1 activated a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10),

170 signaling and increased expression of matrix metalloproteinases driving the induction of c-Jun/activa

171 r findings underscore the key role of matrix metalloproteinases during the progression of aortic aneu

172 corporating S16 revealed a potential role of metalloproteinase dysregulation in proliferative, premal

173 , we examined the IgAN expression profile of metalloproteinases, enzymes involved in the remodelling

174 hase of wound healing, with increased matrix metalloproteinase expression and reduced collagen produc

175 entiation and cell death in SMCs, and matrix metalloproteinase expression in macrophages.

176 ement membrane degradation, decreased matrix metalloproteinase expression, as well as clonogenic surv

177 ctivation of focal adhesion kinase (FAK) and metalloproteinase expression.

178 , decreasing NF-kB activation, cytokines and metalloproteinases expression, and macrophages migration

179 ins belonging to the ADAM (a disintegrin and metalloproteinase) family, known to process extracellula

180 lso found to increase the affinity of target metalloproteinases for LRP-1, albeit to a lesser extent.

181 a are dynamic protrusions that harbor matrix metalloproteinases for pericellular matrix degradation.

182 bits the proteolytic activity of snake venom metalloproteinases from five clinically relevant species

183 gle, deeply conserved adam28 disintegrin and metalloproteinase gene, to as many as 31 tandem genes in

184 Matrix metalloproteinases have a broad spectrum of substrates r

185 and specifically cleaved by tumor-associated metalloproteinases in the Hi-Myc model.

186 enitor cell recruitment, but systemic matrix metalloproteinase inhibition might prevent efflux of pro

187 re, treatment with the broad-spectrum matrix metalloproteinase inhibitor batimastat (BB94) or inhibit

188 Here, we identify the metalloproteinase inhibitor TIMP1 as a molecular switch

189 at functions as an effective, broad-spectrum metalloproteinase inhibitor.

190 Doxycycline, a nonselective matrix metalloproteinases inhibitor, was reported to improve th

191 ectodomain, mimicking the effects of matrix metalloproteinase inhibitors.

192 The proteolytic activity of metalloproteinases is post-translationally regulated by

193 eness, we investigated the expression of the metalloproteinase matrix metalloproteinase 9 (MMP9) in h

194 simulate 1-y clinical function, or a matrix metalloproteinase-mediated aging process.

195 is regulated by catalytic activity of matrix metalloproteinases MMP-2,9.

196 protein (FABP) 2, fas ligand (FASLG), matrix metalloproteinase (MMP) 1, MMP7, soluble CD14 (sCD14), a

197 tion of interleukin 1 beta (IL1B) and matrix metalloproteinase (MMP) 3 in the cecum.

198 einase with thrombospondin motifs 4-, matrix metalloproteinase (MMP) 9-, and MMP13-positive cells and

199 d quantitative RT-PCR with subsequent matrix metalloproteinase (MMP) activity.

200 otein that functions as an inducer of matrix metalloproteinase (MMP) expression in fibroblasts.

201 that all inhibit members of the large matrix metalloproteinase (MMP) family but differ in their other

202 phosphorylated NF-kappaB, as well as matrix metalloproteinase (MMP) family members including MMP-1,

203 Since their discovery, the matrix metalloproteinase (MMP) family proteases have been consi

204 Certain matrix metalloproteinase (MMP) family proteins have been associ

205 We further show that the matrix metalloproteinase (MMP) mmp14a is required in pioneer ax

206 phiphiles (RBA) capable of exposing a matrix metalloproteinase (MMP) substrate on the surface of thei

207 cued with collagen IV overexpression, matrix metalloproteinase (MMP), and Furin inhibitors in Antimyc

208 down-regulation of the expression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

209 Macrophage elastase [matrix metalloproteinase (MMP)-12] is the most upregulated MMP

210 ollagen 1 and increased expression of matrix metalloproteinase (MMP)-2 and -9.

211 of matrix metalloproteinase (TIMP)-1, matrix metalloproteinase (MMP)-2, MMP-9, Galectin-3 (Gal-3), N-

212 , via transcriptional upregulation of matrix metalloproteinase (MMP)-2.

213 ciation between the concentrations of matrix metalloproteinase (MMP)-8 and -9 in gingival crevicular

214 Matrix metalloproteinase (MMP)-8 and -9 released by degranulati

215 presence of proinflammatory mediators matrix metalloproteinase (MMP)-8 and interleukin (IL)-1beta and

216 g on salivary periodontal biomarkers, matrix metalloproteinase (MMP)-8, MMP-9, tissue inhibitor of me

217 , bone morphogenetic protein (BMP)-2, matrix metalloproteinase (MMP)-8, tissue inhibitor of MMP (TIMP

218 thase (iNOS), cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9 and tissue inhibitor of metall

219 cancer yet may increase the level of matrix metalloproteinases (MMP) -2 and -9, which increase the r

220 d by extracellular proteases, such as matrix metalloproteinases (MMP) that are overexpressed in the t

221 % level) were interleukin (IL)-1beta, matrix metalloproteinases (MMP)-1, MMP-3, MMP-8, MMP-9, from ba

222 and occludin; increased expression of matrix-metalloproteinases (MMP)-3 and -9 and enhanced lipid per

223 5 targets of 4 main protease classes: matrix metalloproteinases (MMP-14, a predominant target in meta

224 sociated with higher plasma levels of matrix metalloproteinases ([MMP]-1, -2, -7, -8, and -9) in PTB

225 [TNF]-alpha, interleukin [IL]-1beta, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels

226 mor necrosis factor alpha [TNFalpha], matrix metalloproteinase [MMP]-9, macrophage migration inhibito

227 feedback mechanisms between CAV1, the matrix metalloproteinase MMP14 and oestrogen receptors.

228 X1), which relieved repression of the matrix metalloproteinase MMP14.

229 e-2), and ECM turnover genes/enzymes (matrix metalloproteinases-MMP2,14 and their inhibitors-TIMP2).

230 tory cytokine interleukin-10 (IL-10) and the metalloproteinase MMP9.

231 fibrocartilage matrix via E2-induced matrix metalloproteinases MMP9 and MMP13.

232 of G protein signalling 2 (RGS2), and matrix metalloproteinases (MMPs) 1, 8, and 10 were also strongl

233 esence of elevated proteases, such as matrix metalloproteinases (MMPs) and a disintegrin and metallop

234 The induction of matrix metalloproteinases (MMPs) and reduction in tissue inhibi

235 Matrix metalloproteinases (MMPs) and the related families of di

236 but also ECM-degrading enzymes called matrix metalloproteinases (MMPs) and their inhibitors (TIMPs).

237 y known as an endogenous inhibitor of matrix metalloproteinases (MMPs) and thus associated with tumor

238 Matrix metalloproteinases (MMPs) are associated with decreased

239 Matrix metalloproteinases (MMPs) are extracellular enzymes invo

240 lators of ECM structure and function, matrix metalloproteinases (MMPs) are highly expressed in cancer

241 Although matrix metalloproteinases (MMPs) are implicated in the regulati

242 Matrix metalloproteinases (MMPs) are inducible endopeptidases t

243 Matrix metalloproteinases (MMPs) are involved in a spectrum of

244 A few matrix metalloproteinases (MMPs) are known to support this key

245 We assessed host matrix metalloproteinases (MMPs) as the BV-associated secreted

246 pe plasminogen activator (uPA) and/or matrix metalloproteinases (MMPs) as well as some of the EMT mar

247 Matrix metalloproteinases (MMPs) can proteolytically cleave VEG

248 Matrix metalloproteinases (MMPs) degrade extracellular matrix a

249 Matrix metalloproteinases (MMPs) degrade several ECM components

250 Certain matrix metalloproteinases (MMPs) have the ability to degrade co

251 reported doxycycline, a nonselective matrix metalloproteinases (MMPs) inhibitor, to attenuate aortic

252 Increased activity of matrix metalloproteinases (MMPs) is associated with worse progn

253 these processes is the production of matrix metalloproteinases (MMPs) that modify the microenvironme

254 to bind or inhibit the activities of matrix metalloproteinases (MMPs), a family of zinc-dependent en

255 ctivation revealed the requirement of matrix metalloproteinases (MMPs), EGFR ligands and calcium.

256 ses (TIMPs) are natural inhibitors of matrix metalloproteinases (MMPs), enzymes that contribute to ca

257 Matrix metalloproteinases (MMPs), especially MMP-13, are key en

258 rived M exposed to NE releases active matrix metalloproteinases (MMPs), increase expression of pro-in

259 cells must exocytose proteases, like matrix metalloproteinases (MMPs), that are key in extracellular

260 P-1), the endogenous inhibitor of the matrix metalloproteinases (MMPs), to be translocated to the cel

261 JNK pathway and induces expression of matrix metalloproteinases (MMPs), which are necessary for the i

262 and is involved in the activation of matrix metalloproteinases (MMPs).

263 scular smooth muscle cells (VSMC) and matrix metalloproteinases (MMPs).

264 several downstream targets, including matrix metalloproteinases (MMPs).

265 ent tumor cells through activation of matrix metalloproteinases (MMPs).

266 mplified with the tumor-overexpressed matrix metalloproteinase MT1-MMP as a target.

267 The directed recruitment of the metalloproteinase MT1-MMP to invadopodia plays a critica

268 owth and the targeted delivery of the matrix metalloproteinase MT1-MMP via endosomal transport by mec

269 Membrane type 1-matrix metalloproteinase (MT1-MMP) and tumor necrosis factor al

270 C-terminal propeptides from procollagens by metalloproteinases of the ADAMTS (a disintegrin and meta

271 Blocking of matrix metalloproteinases or tyrosine kinases are novel modes o

272 and roles of proteases in vivo In addition, metalloproteinases, particularly meprins of the astacin

273 signaling changes inhibit cofilin and matrix metalloproteinases reducing in vitro and in vivo NB cell

274 o increased invadopodia formation and matrix metalloproteinase secretion.

275 ded for cell protrusion formation and matrix metalloproteinases secretion during cell invasion.

276 s TIMPs lost inhibitory activity toward some metalloproteinases, specialized in effects on different

277 ion of one prominent family, the snake venom metalloproteinases (SVMPs) that play key roles in subdui

278 IL-1beta increases the expression of matrix metalloproteinases, tenascin-C and Sox9 and decreases th

279 nzyme (TACE) are prominent membrane-anchored metalloproteinases that regulate the turnover of extrace

280 in-paired cues increased tissue inhibitor of metalloproteinases TIMP-1,2, which caused transient inhi

281 oteinase (MMP)-8, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and myeloperoxidase (MPO).

282 loproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 were obtained through reverse

283 luble ST2 (sST2), tissue inhibitor of matrix metalloproteinase (TIMP)-1, matrix metalloproteinase (MM

284 n a catalytically active tissue inhibitor of metalloproteinases (TIMP)-resistant forms.

285 a number of MMPs, ADAMs, ADAMTSs, TIMPs and metalloproteinase/TIMP complexes.

286 vity is inhibited by the tissue inhibitor of metalloproteinase (TIMP1-4) family of proteins, suggesti

287 Tissue inhibitors of metalloproteinases (TIMPs) are natural inhibitors of mat

288 s (Gnathostomes) have 4 tissue inhibitors of metalloproteinases (TIMPs), multifunctional proteins tha

289 us inhibitors, known as tissue inhibitors of metalloproteinases (TIMPs).

290 MTS9 is known to be a secreted extracellular metalloproteinase, we found that ADAMTS9 localized near

291 an inherited deficiency of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, me

292 alloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs).

293 catenin, pSMAD2-, pSMAD3-, a disintegrin and metalloproteinase with thrombospondin motifs 4-, matrix

294 proteinases of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and BMP1 (

295 Adamts16 encodes a disintegrin-like and metalloproteinase with thrombospondin motifs, 16, a memb

296 rally cleaved by ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type-1 motif-13).

297 ADAMTS (a disintegrin-like and metalloproteinase with thrombospondin) are a family of p

298 and function of ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin-1 repeats, member

299 structurally similar to the family of matrix metalloproteinases with critical roles in damage and rep

300 Inactivation of ADAM17, a disintegrin and metalloproteinase, with a specific inhibitor TMI-1 or by