ライフサイエンスコーパス: MMP-1

1 ) heterotrimers with fibroblast collagenase (MMP-1).

2 educed levels of matrix metalloproteinase 1 (MMP-1).

3 pregulates MMP-3 and MT1-MMP, in addition to MMP-1.

4 ion of MMP-1 and MMP-3 and the activation of MMP-1.

5 n tissue formation, and blunted induction of MMP-1.

6 ared with the X-ray "closed" conformation of MMP-1.

7 the epithelial-mesenchymal transition marker MMP-1.

8 h was associated with induction of Ets-1 and MMP-1.

9 icantly increased k(cat)/K(m) and k(cat) for MMP-1.

10 alloproteinase-1, and vascular reactivity to MMP-1.

11 IRAK1 prevented cigarette smoke induction of MMP-1.

12 (10 MPa) down-regulates CITED2 and increases MMP-1.

13 ust induction of high levels of HO-1 but not MMP-1.

14 antly attenuated this enhanced production of MMP-1.

15 beta3 or alphaV integrin subunits increased MMP-1/10 secretion in M. tuberculosis-stimulated monocyt

16 -10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8, -9, -12, and -14 enable this comp

17 s) are able to cleave ephrinA1, most notably MMP-1, -2, -9, and -13.

18 We studied total MMP-1,-2,-3,-7,-8,-9,-12,-13 levels, their activity stat

19 carriers of the matrix metalloproteinase-1 (MMP-1) 2G (rs1799750) or the MMP-3 6A (rs3025058) allele

20 gly, HA polymers may normalize the levels of MMP-1, -3 and -13.

21 on of TCF4, but not of TCF3 or LEF1, induced MMP-1, -3, and -13 expression and generic MMP activity i

22 At MOI 50, the protein levels of pro-MMP-1, -3, and -9 also decreased while PAI-1 and TIMP-1

23 d human monocytes (CoMTb) stimulated greater MMP-1, -3, and -9 gene expression in human microglial ce

24 by a fair selectivity for MMP-2/9/12/13 over MMP-1/3/14.

25 ally unopposed, network-dependent microglial MMP-1/-3 gene expression and secretion regulated by NF-k

26 Dexamethasone suppression of MMP-1/-3 gene expression provides a novel mechanism expl

27 In patients with CNS TB, MMP-1/-3 immunoreactivity was demonstrated in the center

28 MMP-1/-3 secretion was significantly inhibited by dexame

29 Jun/FosB heterodimers regulate CoMTb-induced MMP-1/-3 secretion.

30 et MMPs but not shallow-pocketed MMPs (e.g., MMP-1, ~850 to >50,000 nM; MMP-7, ~4000 to >25,000 nM).

31 emonstrated using matrix metallopeptidase 1 (MMP-1), a protease of the same family.

32 IMP-2 that are selective inhibitors of human MMP-1, a collagenase whose unregulated action is linked

33 ated with bronchial hyperresponsiveness, and MMP-1 activation are associated with exacerbation severi

34 1.5-fold (P < 0.05), which was dependent on MMP-1 activation.

35 Active MMP-1, active MMP-2, and MMP-14 in the ECM fraction of t

36 During exacerbations, MMP-1 activity increased and was associated with fall in

37 OX-containing eluates promoted inhibition of MMP-1 activity when compared to the control.

38 inhibitor, suppressed M. tuberculosis-driven MMP-1 activity.

39 script levels but inhibited type I collagen, MMP 1 and TIMP 1 mRNA levels.

40 on monocytes, which upregulates secretion of MMP-1 and -10 on adhesion to the ECM.

41 e (iNOS), matrix metalloproteinases 1 and 8 (MMP-1 and -8), bone morphogenetic protein-2 (BMP-2), rec

42 Simvastatin reduced expression of iNOS, MMP-1 and -8, RANK, and RANKL and increased BMP-2 and OP

43 ensed MMP inhibitor, suppressed TB-dependent MMP-1 and -9 secretion from primary human macrophages an

44 Vessel expression of MMP-1 and circulating MMP-1 levels were increased in pre

45 contrast, thrombin-induced up-regulation of MMP-1 and COX-2 was mediated through Toll-like receptor-

46 In vivo, MMP-1 and GVSK degraded collagen I when perfused in Zuck

47 hain reaction, and the protein expression of MMP-1 and IL-6 was examined by enzyme-linked immunosorbe

48 IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.

49 A positive correlation between IL-6/MMP-1 and IL-6/MMP-9 was detected in PDSG and PDCimG.

50 11d plus UVA also decreased MMP-1 and increased TIMP-1 protein levels.

51 le chains, is more favorable for cleavage by MMP-1 and may be the determining factor for collagen rec

52 Moreover, the secreted collagenases MMP-1 and MMP-13 and the glycosylphosphatidylinositol-an

53 Unexpectedly, MMP-1 and MMP-13 cleave the N-terminal exodomain of PAR1

54 with manufacturer specifications except for MMP-1 and MMP-2 which were significantly higher than rep

55 nction by counteracting the transcription of MMP-1 and MMP-3 and the activation of MMP-1.

56 (SBEs) within the proximal promoters of the MMP-1 and MMP-3 genes, which in association with AP-1 co

57 Human Cad-11-Fc up-regulated MMP-1 and MMP-3 protein production by RA synovial fibrob

58 n metalloproteinases and prostanoids whereby MMP-1 and MMP-3, commonly found in inflammatory and neop

59 and MMP-9, whereas rapamycin decreased both MMP-1 and MMP-3.

60 o activate transcription of its target genes MMP-1 and MMP-7, which regulate extracellular matrix in

61 oximal catalytic PI3K p110 subunit augmented MMP-1 and MMP-9 in a dose-dependent manner (all P<0.001)

62 s with fFN resulted in dramatic increases in MMP-1 and MMP-9 mRNA and enzymatic activity as well as C

63 l, cells with thrombin resulted in increased MMP-1 and MMP-9 mRNA and enzymatic activity.

64 he proximal PI3K catalytic subunit increases MMP-1 and MMP-9, whereas rapamycin decreased both MMP-1

65 serum MMP-9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly hi

66 as well as reduction of tissue inhibitor of MMP-1 and tissue inhibitor of MMP-4 in P2Y4-null mice.

67 Although MMP-1 and VEGFR2 co-exist in many normal and pathophysio

68 Presently, matrix metalloproteinase 1 (MMP-1) and collagen triple-helical peptide models have b

69 uman collagenase matrix metalloproteinase-1 (MMP-1) and collagenase from Clostridium histolyticum.

70 RATIONALE: Matrix metalloproteinase-1 (MMP-1) and mast cells are present in the airways of peop

71 -8, CCL5/RANTES, matrix metalloproteinase 1 (MMP-1), and MMP-3 after TNFalpha stimulation was sustain

72 ally upregulates matrix metalloproteinase-1 (MMP-1), and using rescue approaches we demonstrate that

73 nslocation and the production of IL-6, IL-8, MMP-1, and MMP-13 in human RA SFs.

74 he use of ELISA and the expression of TSG-6, MMP-1, and MMP-3 transcripts and proteins with the use o

75 esize that this antiulcer drug reduces IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with induce

76 oclast number and induces reduction of IL-6, MMP-1, and MMP-9 immunoexpression, reinforcing the idea

77 alveolar process surface and number of IL-6, MMP-1, and MMP-9-immunolabeled cells in the gingival muc

78 umber of TRAP-positive osteoclasts and IL-6, MMP-1, and MMP-9-immunolabeled cells was significantly l

79 rations of matrix metalloproteinase (MMP)-7, MMP-1, and surfactant protein D were assessed by ELISA.

80 We found that MMP-1- and MMP-3-dependent release of TNF-alpha induced

81 mmatory markers (matrix metalloproteinase 1 [MMP-1] and heme oxygenase 1 [HO-1]), and proinflammatory

82 or through electrostatic effects of a unique MMP-1 arginine.

83 ly, these findings disclose a novel role for MMP-1 as a mediator of vasoconstriction and vascular dys

84 rk identifies Draper-dependent activation of MMP-1 as a novel cascade required for proper glial clear

85 this library, showed a similar affinity for MMP-1 as wild-type TIMP-2 but reduced affinity for MMP-3

86 We used matrix metalloproteinase-1 (MMP-1) as a model protease and found peptide aggregation

87 tly, we identify matrix metalloproteinase-1 (MMP-1) as a novel downstream target of TWIST1.

88 High levels of IL-6 and MMP-1 at baseline demonstrated the strongest ability to

89 In addition, CITP:MMP-1-based categorization yielded significant integrate

90 heterotrimer cleavage kinetics revealed that MMP-1 binding promotes stochastic helix unwinding, resol

91 Similar MMP-1 binding to the two isoforms and similar cleavage e

92 ld increase in collagen proteolysis rates by MMP-1 but does not affect cleavage rates by Clostridium

93 selective having a nanomolar K(i) value for MMP-1 but no detectable inhibitory activity toward MMP-3

94 CXCR3 blockade reduced levels of MMP-1 by 65%, inhibited receptor signaling (64-100% redu

95 The triple-helix is then presented to the MMP-1 catalytic (CAT) domain in a distinct orientation.

96 MMP-1 caused activation of the nuclear factor-kappaB (NF

97 with M. tuberculosis to investigate whether MMP-1 caused lung immunopathology.

98 in cultured vascular smooth muscle cells and MMP-1 cells.

99 e known collagen cross-linking sites and the MMP-1 cleavage site in collagens I and II.

100 However, MMP-1 collagen preferences were not recapitulated by the

101 evaluated for gene and protein expression of MMP-1, collagen type 1alpha, tissue inhibitor of metallo

102 ginal bacterial CL domain was not cleaved by MMP-1 (collagenase 1) or MMP-13 (collagenase 3).

103 he expression of matrix metalloproteinase 1 (MMP-1; collagenase-1) by leading-edge basal keratinocyte

104 Plasma PIIINP correlated with induced sputum MMP-1 concentrations and radiological scores, demonstrat

105 MMP-1 concentrations were significantly increased in bot

106 The MMP-1 conformations with large MO values (up to 47%) are

107 to calculate the maximum occurrence (MO) of MMP-1 conformations.

108 To investigate whether MMP-1 could be activated by mast cells and increase asth

109 be mediated by neutrophils, and (3) whether MMP-1 could be responsible for vascular dysfunction.

110 rating characteristic curves rendered a CITP:MMP-1 cutoff </=1.968 (80% sensitivity and 76% specifici

111 Our data support a model in which MMP-1 cuts a transient, stretched conformation of its re

112 Concomitantly, MMP-1 deficiency led to decreased levels of intratumoral

113 naturally acquired or experimentally induced MMP-1 deficiency substantially suppressed HEp3-hi/diss i

114 ting noncollagenolytic mechanisms underlying MMP-1-dependent cell intravasation.

115 s have also indicated that the mechanisms of MMP-1-dependent vascular permeability in tumors involve

116 In MMP-1 depleted flies, glia do not properly infiltrate ne

117 ons of the 115-A-long triple helix with both MMP-1 domains.

118 The crystal structure of MMP-1(E200A) bound to a triple-helical collagen peptide

119 cally underscore the contribution of a tumor MMP-1/endothelial PAR1 axis to actual intravasation even

120 omoter and leads to hypersecretion of active MMP-1 enzyme and degradation of collagen type I in the E

121 ter not reaching statistical significance]), MMP-1 (expressed predominantly in DA rats), MMP-3 (79-fo

122 ic pressure (IHP) treatment suppresses basal MMP-1 expression and up-regulates CITED2 in human chondr

123 on assays demonstrate that CITED2 suppresses MMP-1 expression by competing with MMP transactivator, E

124 TSG-6 siRNA led to extracellular MMP-1 expression by normal fibroblasts such as CCh fibro

125 Paralleling these findings, attenuation of MMP-1 expression by shRNA in A549 (human) AECs markedly

126 tuberculosis-induced HO-1 activity, inhibits MMP-1 expression by suppressing c-Jun/AP-1 activation.

127 f Rho GTPases revealed that Cdc42 attenuates MMP-1 expression by suppressing ERK activity.

128 ing pathway by which cigarette smoke induces MMP-1 expression has been undefined.

129 The critical role of COX-2 in regulating MMP-1 expression in articular cartilage in vivo was demo

130 ntally induced DNA hypomethylation increased MMP-1 expression in cultured vascular smooth muscle cell

131 Finally, induction of MMP-1 expression in dermal fibroblasts by CCN1 N-termina

132 ibition markedly blocked collagen-stimulated MMP-1 expression in keratinocytes.

133 ere, we evaluated the mechanisms controlling MMP-1 expression in primary human keratinocytes from neo

134 MMP-1 expression is also associated with active TB.

135 MMP-1 expression is detected in fluid shear stress (20 d

136 a indicate that injured keratinocytes induce MMP-1 expression through ERK activation, and this proces

137 in dermal fibroblasts in vivo and stimulates MMP-1 expression through functional interaction with alp

138 KT and p38 signaling pathways, it stimulated MMP-1 expression via activating heme oxygenase 1 (HO-1).

139 y demonstrates that cigarette smoke mediates MMP-1 expression via activation of the TLR4 signaling ca

140 ic mice, M. tuberculosis infection increased MMP-1 expression, resulting in alveolar destruction in l

141 ibitory activity against IL-8 production and MMP-1 expression, showing the most potent inhibitory act

142 ibitory activity against IL-8 production and MMP-1 expression, with compounds 1, 3, and 4 having the

143 T domain, are required for CCN1 to stimulate MMP-1 expression.

144 adjacent IGFBP and TSP1 domains to stimulate MMP-1 expression.

145 ut also reversed miR-199a-5p-induced loss of MMP-1 expression.

146 have elevated TLR4 signaling and subsequent MMP-1 expression.

147 2 (FGF-2), which led to a marked increase in MMP-1 expression.

148 nd inhibition of matrix metalloproteinase-1 (MMP-1) expression before and after treatment with cigare

149 he inhibition of matrix metalloproteinase-1 (MMP-1) expression, an inflammatory marker for chronic ob

150 The preference of MMP-1 for type III collagen appears to be primarily base

151 tuberculosis-stimulated monocytes increased MMP-1 gene expression by 2.6-fold and 4.3-fold respectiv

152 The SNPs of the PTGFR and MMP-1 genes may determine the latanoprost response in a

153 As compared with MMP-1, GVSK degraded soluble collagen I at the high but

154 that endothelial cells incubated with active MMP-1 had higher mRNA and protein levels of VEGFR2.

155 MMP-1 has been shown to be highly expressed in AECs from

156 MMP-1 has been shown to cleave and activate the protease

157 n degradation by matrix metalloproteinase 1 (MMP-1) has been proposed to critically rely on flexibili

158 nism of action for the collagenolytic enzyme MMP-1 have been defined experimentally, and insights int

159 The triple-helix is bound initially by the MMP-1 hemopexin-like (HPX) domain via a four amino acid

160 o model for the functional analysis of human MMP-1 in both physiological and pathological conditions.

161 and mechanistic studies on the relevance of MMP-1 in cancer have been hampered by the absence of an

162 DNA methylation increases the expression of MMP-1 in cultured vascular smooth muscle cells and a neu

163 ould attenuate Pg LPS-enhanced production of MMP-1 in HGFs, whereas this attenuation might be due to

164 level, we studied the expression of HO-1 and MMP-1 in M. tuberculosis-infected human and murine macro

165 blunted angiogenic response and induction of MMP-1 in miR-199a-5p-deprived HMECs.

166 ety of tumor-derived proteins, TGF-beta1 and MMP-1 in particular, which regulate bone formation.

167 In this study, we explored the role of MMP-1 in several AECs functions.

168 the highest MO conformations indicated that MMP-1 in solution was poised to interact with collagen a

169 ed expression of matrix metalloproteinase-1 (MMP-1) in endothelial cells, vascular smooth muscle, and

170 eases thrombin and matrix metalloprotease-1 (MMP-1) in triggering PAR1-mediated arterial restenosis.

171 in vivo role of the collagenolytic protease, MMP-1, in cancer cell intravasation and metastasis was a

172 Application of exogenous MMP-1, in vitro, stimulates PAR1 dependent increases in

173 Overexpression of MMP-1, in vivo, increases dendritic complexity and induc

174 s that stimulation of endothelial cells with MMP-1 increases their levels of VEGFR2.

175 Furthermore, MMP-1 induced vasoconstriction via protease-activated re

176 We show that MMP-1 induces cellular and behavioral phenotypes consist

177 MyD88 and IRAK1, plays a predominant role in MMP-1 induction by cigarette smoke.

178 fter daily treatment with the small molecule MMP-1 inhibitor, an effect that was lost in PAR1-deficie

179 dings indicate that epithelial expression of MMP-1 inhibits mitochondrial function, increases HIF-1al

180 Human MMP-1 is a matrix metalloproteinase repeatedly associate

181 MMP-1 is activated by mast cell tryptase resulting in a

182 brillar type I collagen, and the activity of MMP-1 is required for human keratinocytes to migrate on

183 Matrix metalloproteinase-1 (MMP-1) is a collagenase that is highly active in extrace

184 ing: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in systemic vessels of preeclamptic

185 One factor, matrix metalloproteinase-1 (MMP-1), is induced in Drosophila ensheathing glia respon

186 e concentration over a range from endogenous MMP-1 level in human serum ( approximately 3 ng/mL) to 1

187 associated with airway smooth muscle growth, MMP-1 levels are associated with bronchial hyperresponsi

188 reover, TB patients with either high HO-1 or MMP-1 levels displayed distinct clinical presentations,

189 Vessel expression of MMP-1 and circulating MMP-1 levels were increased in preeclamptic women, where

190 ngs from smokers exhibited elevated TLR4 and MMP-1 levels.

191 In summary, MMP-1 may drive tissue destruction in TB and represents

192 These results suggest a mechanism by which MMP-1 may prime or sensitize endothelial cell functions.

193 ontribute to human skin aging by stimulating MMP-1-mediated collagen fibril fragmentation.

194 r RNA (mRNA) for matrix metalloproteinase 1 (MMP-1), MMP-13, and ADAMTS-4 also increased, while type

195 sion of the matrix metalloproteinase 1 gene (MMP-1), MMP-13, and several other genes involved in the

196 lecule 3 matrix metalloproteinase protein 1 (MMP-1), MMP-3, MMP-9, P-selectin, thrombomodulin, and va

197 ilage-degrading enzyme production, including MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5.

198 The IC(50) of ONO-4817 and galardin for MMP-1, MMP-2 and MMP-7 determined by the proposed colori

199 membrane extracts, as well as mRNA levels of MMP-1, MMP-2, and MMP-14.

200 gradation, protein levels of active forms of MMP-1, MMP-2, MMP-3, and MMP-14 in conditioned media, an

201 librated gingival fluid meter, and levels of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 we

202 JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity

203 age site mediate substrate selectivity among MMP-1, MMP-2, MMP-8, MMP-13, and MMP-14/membrane-type 1

204 e I and type IV are resistant to cleavage by MMP-1, MMP-2, MMP-9, and MMP-13, whereas non-cross-linke

205 regression model, the relationships between MMP-1, MMP-2, MMP-9, tissue inhibitor of matrix metallop

206 Matriptase also induced MMP-1, MMP-3, and MMP-13 gene expression.

207 age-derived TNF-alpha augments expression of MMP-1, MMP-3, and MMP-9 in decidual cells to interfere w

208 tor-alpha (TNF-alpha) significantly enhanced MMP-1, MMP-3, and MMP-9 mRNA and protein levels and acti

209 Unlike highly regulated MMP-1, MMP-3, and MMP-9, MMP-2 mRNA and protein expressi

210 signaling mediated TNF-alpha enhancement of MMP-1, MMP-3, and MMP-9, whereas IFN-gamma inhibited p38

211 MMP-1, MMP-8, MMP-9, MMP-12, and MMP-13 levels were redu

212 centrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly higher in Gg compa

213 ependent binding of a catalytically inactive MMP-1 mutant (E200A) to collagen through the cooperative

214 data suggest that the activity of the human MMP-1 mutant GVSK can be regulated by Ca(2+) both in vit

215 Induction of MMP-1 occurs by signaling from the alpha2beta1 integrin

216 meras indicated that the rate of cleavage by MMP-1 of the chimera containing six triplets (P7-P11') o

217 pathophysiological conditions, the effect of MMP-1 on cellular VEGFR2 that can promote the above proc

218 h areas of increased and functionally active MMP-1 on infected monocytes, and alphaVbeta3 blockade ma

219 Matrix metalloproteinase 1 (MMP-1), one of the Ets-1 downstream mediators, was negat

220 r 21 days with a small molecule inhibitor of MMP-1 or a direct thrombin inhibitor and compared with v

221 was not achieved by the catalytic domain of MMP-1 or MMP-13, nor by full-length MMP-3.

222 r very high levels of HO-1 and low levels of MMP-1 or the converse.

223 Since the mouse MMP-1 ortholog is not expressed in the lung and mice inf

224 d rapamycin, a p70(S6K) inhibitor, inhibited MMP-1 (P<0.001) and MMP-3 (P<0.01) but not MMP-9.

225 uppress restenosis by targeting noncanonical MMP-1-PAR1 signaling in vascular SMCs.

226 Noncanonical MMP-1-PAR1 signaling resulted in the opposite effect and

227 MMP-1-PAR1 significantly stimulated hyperplasia and migr

228 c-Abl promotes invasion through a STAT3 --> MMP-1 pathway.

229 Moreover, MMP-1 plays a key role in the metastatic behavior of mel

230 MMP-1, principally derived from dermal fibroblasts, is t

231 Surprisingly, abrogation of MMP-1 production and activity did not significantly affe

232 Pg LPS significantly increased MMP-1 production in HGFs, whereas adding EGCG significan

233 urthermore, the role of IL-6 on LPS-enhanced MMP-1 production is evaluated using human gingival fibro

234 tion of IL-6 significantly enhanced cellular MMP-1 production, whereas anti-IL-6 antibody inhibited L

235 as anti-IL-6 antibody inhibited LPS-enhanced MMP-1 production.

236 ibiting p38 or JNK pathways had no effect on MMP-1 production.

237 Also, MMP-1 promoted MLE12 cell migration through collagen I,

238 is studies with cultured cells revealed that MMP-1 promoted recruitment of neutrophils via vascular s

239 g mediated by retinoic acid receptors on the MMP-1 promoter and leads to hypersecretion of active MMP

240 We conclude that MMP-1 promotes VEGFR2 expression and proliferation of en

241 MMP-1 protein and activity were assessed.

242 with airway smooth muscle proliferation and MMP-1 protein associated with bronchial hyperresponsiven

243 In this population, the serum CITP:MMP-1 ratio identifies patients with increased CCL and h

244 Patients were categorized according to CITP:MMP-1 ratio values as normal ratio (>1.968) or low ratio

245 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio.

246 consistent with studies suggesting that the MMP-1 recognition site in heterotrimeric collagen I is p

247 t, activation of which by carcinoma-produced MMP-1 regulates endothelial permeability and transendoth

248 The enriched phages selectively bound MMP-1 relative to MMP-3 and contained mutations only in

249 Interestingly, glial induction of MMP-1 requires the highly conserved engulfment receptor

250 sing 5-fold increase in TB network-dependent MMP-1 secretion to 4900 +/- 1100 pg/ml.

251 Thus, MMP-1 serves a critical role in the repair of damaged hu

252 MLE12 cells expressing human MMP-1 showed a significant repression of oxygen consumpt

253 thelial cells (MLE12) transfected with human Mmp-1 showed significantly increased cell growth and pro

254 study was to determine whether noncanonical MMP-1 signaling through PAR1 would contribute to aberran

255 ion, supplementation of recombinant MMP-1 to MMP-1-silenced primary tumors restored their impaired va

256 upport of such noncollagenolytic mechanisms, MMP-1 silencing in HEp3-hi/diss cells modulated the micr

257 Elevation in VEGFR2 after MMP-1 stimulation was inhibited by PAR-1 knockdown and N

258 ode is readily modeled, without altering the MMP-1 structure or the exosite interactions, by axial ro

259 igh MO values differ largely from the closed MMP-1 structures obtained by x-ray crystallography.

260 precise mechanisms underlying shear-induced MMP-1 synthesis remain unknown.

261 pathways, which were in turn responsible for MMP-1 synthesis via NF-kappaB- and c-Jun-transactivating

262 Knockdown by TSG-6 siRNA upregulated more MMP-1 than MMP-3 transcripts in normal and CCh fibroblas

263 gnized interplay between ERK1/2, TWIST1, and MMP-1 that is likely significant in the progression of m

264 verexpression of matrix metalloproteinase 1 (MMP-1), the gene encoding the metalloproteinase that deg

265 the induction of matrix metalloproteinase-1 (MMP-1) through the activation of ERK1/2, which is critic

266 elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patients with polycystic ovary s

267 loproteinase (MMP)-8 and tissue inhibitor of MMP-1 (TIMP-1) gene polymorphisms in generalized aggress

268 ent trichiasis was associated with a reduced MMP-1/TIMP-1 ratio (P = 0.029).

269 t by promoting a synergistic decrease in the MMP-1/TIMP-1 ratio.

270 of IL-1beta and CsA showed a decrease in the MMP-1/TIMP-1 ratio.

271 loproteinase (MMP)-1 and tissue inhibitor of MMP-1 (TIMP1).

272 In addition, during SIBO, MMP-1, tissue inhibitor of metalloproteinase (TIMP)-1, a

273 ntravasation, supplementation of recombinant MMP-1 to MMP-1-silenced primary tumors restored their im

274 peractive ERK1/2 signaling and regulation of MMP-1 transcription.

275 MMP-1 transcriptional up-regulation in TTD is caused by

276 er activation of this factor was detected in MMP-1-transfected cells under normoxia and hypoxia.

277 rial reactive oxygen species was observed in MMP-1-transfected cells.

278 In the MMP-1 transgenic mice, M. tuberculosis infection increas

279 ndothelial proliferation were elevated after MMP-1 treatment.

280 isolated after five rounds of selection with MMP-1, using MMP-3 as a competitor.

281 In asthma, airway pro-MMP-1 was 5.4-fold higher than control subjects (P = 0.0

282 Active MMP-1 was found in CCh fibroblasts intracellularly and e

283 This activation of MMP-1 was further enhanced by IL-1beta.

284 CITP:MMP-1 was inversely associated with CCL (r = -0.460; p =

285 CITP:MMP-1 was not associated with the risk of cardiovascular

286 inversely correlated expression of HO-1 and MMP-1 was not observed in patients with other nontubercu

287 es demonstrated that cigarette smoke-induced MMP-1 was regulated by TLR4 via MyD88/IRAK1.

288 (CITP) and matrix metalloproteinase-1 (CITP:MMP-1) was determined in blood samples.

289 ssociated genes, matrix metalloproteinase-1 (MMP-1), was decreased, while elastin, procollagen I type

290 in the catalytic and linker domains of human MMP-1, we generated a protein library amenable to physio

291 Multiple testing found 2 genes, PTGFR and MMP-1, were related to refractoriness to latanoprost.

292 hat M. tuberculosis drives the expression of MMP-1, which in turn promotes the collagen breakdown tha

293 ted assessment of MMP-2 and MMP-9 to include MMP-1, which preferentially degrades fibrillar collagens

294 Airway smooth muscle cells generated pro-MMP-1, which was proteolytically activated by mast cell

295 C in high Ca(2+) (10 mm) was comparable with MMP-1 (wild type), but in low Ca(2+) (1 mm), there was a

296 we infected transgenic mice expressing human MMP-1 with M. tuberculosis to investigate whether MMP-1

297 All were effective inhibitors of MMP-1 with nanomolar K(i) values, but TM8, containing Se

298 interactions of the catalytic domain (cd) of MMP-1 with the inhibitory domains of TIMP-1 and TIMP-2 (

299 nhibitors of MMP's-2, -9, and -13 that spare MMP-1, with oral efficacy in inhibiting tumor growth in

300 Pro-antibody activation in vitro by MMP-1 yielded a 200-fold increase in binding affinity an