ライフサイエンスコーパス: MMP-1

1 antly attenuated this enhanced production of MMP-1.

2 myofibroblasts and decreased expressions of 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 h was associated with induction of Ets-1 and MMP-1.

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

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

10 IRAK1 prevented cigarette smoke induction of MMP-1.

11 the epithelial-mesenchymal transition marker MMP-1.

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

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

14 MMP-1, -2 -7, -9, tissue inhibitor of MMP (TIMP) -1, and

15 -10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8, -9, -12, and -14 enable this comp

16 ted an MMP profile characterized by elevated MMP-1, -2, -3, -7, and -8 and tissue inhibitor of metall

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 lloproteinase (MMP) family members including MMP-1, -3, -9, and -13 in tenocytes upon OX-50 treatment

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

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

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

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

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

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

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

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

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

31 1.5-fold (P < 0.05), which was dependent on MMP-1 activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 11d plus UVA also decreased MMP-1 and increased TIMP-1 protein levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 -8, CCL5/RANTES, matrix metalloproteinase 1 (MMP-1), and MMP-3 after TNFalpha stimulation was sustain

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

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

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

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

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

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

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

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

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

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

77 MMP-1 appears to blend selected fit with induced fit mec

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

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

80 This identified MMP-1 as a new LRP-1 ligand.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 MMP-1 concentrations were significantly increased in bot

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

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

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

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

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

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

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

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

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

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

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

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

113 interactions between a collagen peptide and MMP-1(E200A) - an active-site mutant of an archetypal ve

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

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

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

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

118 stically, CD34(+) cells reduced the level of MMP-1 expression by inhibiting recruitment of NF-kappaB

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 2 (FGF-2), which led to a marked increase in MMP-1 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Human MMP-1 is a matrix metalloproteinase repeatedly associate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 13B (TNFSF13B), matrix metalloproteinase 1 (MMP-1), MMP-2, and MMP-3.

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

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

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

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

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

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

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

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

199 MMP-1, MMP-3 and MMP-10 concentrations decreased with ti

200 CSF concentrations of MMP-1, MMP-3 and MMP-10 were increased in TBI patients (

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

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

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

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

205 ed to analyze expression changes in secreted MMP-1, MMP-3, and TGFbeta.

206 d DNA breaks, and increase the expression of MMP-1, MMP-3, and TGFbeta.

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

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

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

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

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

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

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

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

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

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

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

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

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

220 l activity (p = 0.002) and elevated neuronal MMP-1 (p < 0.001), suggesting microscale collagen degrad

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

222 sed in the periphery (substance P, pERK, and MMP-1; p <= 0.039) and spinal cord (substance P and MMP-

223 p <= 0.039) and spinal cord (substance P and MMP-1; p <= 0.041).

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

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

226 MMP-1-PAR1 significantly stimulated hyperplasia and migr

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

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

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

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

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

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

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

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

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

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

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

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

239 y inhibiting recruitment of NF-kappaB to the MMP-1 promoter site in dermal fibroblasts.

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

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

270 have a K(D) of 34.6 nM for LRP-1, while the MMP-1/TIMP-3 complex had a sevenfold higher affinity (K(

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 For example, the free form of MMP-1 was found to have a K(D) of 34.6 nM for LRP-1, whi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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