ライフサイエンスコーパス: MMP-3

1 -/-)) with mice possessing functional MMP-3 (mmp-3(+/+)).

2 ed branching morphogen, metalloproteinase-3 (MMP-3).

3 IL-6, and matrix metalloproteinases such as MMP-3.

4 omain of MMP-1 or MMP-13, nor by full-length MMP-3.

5 as wild-type TIMP-2 but reduced affinity for MMP-3.

6 interactions and improve complementarity to MMP-3.

7 site sides of the interaction interface with MMP-3.

8 ase, matrix metalloproteinase 1 (MMP-1), and MMP-3.

9 and the matrix metalloproteinases MMP-1 and MMP-3.

10 trix metalloproteinase 1 (MMP-1), MMP-2, and MMP-3.

11 ase in aqueous concentration and activity of MMP-3.

12 , whereas rapamycin decreased both MMP-1 and MMP-3.

13 f matrix degrading MMP, such as MMP-2 (67%), MMP-3 (63%), MMP-7 (62%), and MMP-9 (60%) in hairless mo

14 loproteinase-1 (MMP-1) 2G (rs1799750) or the MMP-3 6A (rs3025058) allele but not in homozygous carrie

15 ADAMTS-4 and -5; cathepsins K, B, and L; and MMP-3, -7, -12, and -13 were incapable of cleavage of ch

16 In non-MFS samples, MMP-1 (70+/-16%), MMP-3 (77+/-18%), MMP-8 (75+/-11%), MMP-9 (69+/-14%), an

17 MMP-1 (expressed predominantly in DA rats), MMP-3 (79-fold and 8-fold, respectively), and MMP-14 (21

18 of MMPs: Human arteries were incubated with MMP-3 (a member of stromelysins), MMP-9 (considered a ge

19 ed stromelysin-1/matrix metalloproteinase-3 (MMP-3), a stromal enzyme upregulated in many breast tumo

20 MMP-3 activation was induced by FN-45 and did not show a

21 We observed decreased MMP-3 activity in human glaucomatous AH compared to age-

22 MMP-3 activity was not detected on zymography.

23 in stressed DA cells, and the active form of MMP-3 (actMMP-3) was released into the medium.

24 ct of IL-1beta on catabolic genes, including MMP-3, ADAMTS-5, syndecan 4, and prolyl hydroxylase 3.

25 TES, matrix metalloproteinase 1 (MMP-1), and MMP-3 after TNFalpha stimulation was sustained for sever

26 MMP-3 also has enhanced subnanosecond fluctuations in he

27 The transcription of the genes for MMP-3 and -17 is increased by latanoprost treatment.

28 ream targets, integrin-alpha3 and -beta6 and MMP-3 and -9.

29 4 > MMP-24 > MMP-1, -11, -15, -16, and -19 > MMP-3 and 17, > MMP-12.

30 The expression of catabolic genes (MMP-3 and ADAMTS-4) in AF cells derived from nondegenera

31 Among these genes, MMP-3 and ANGPT1 were significantly upregulated in sFRP3

32 ry plaques were significantly larger in apoE/MMP-3 and apoE/MMP-9 double knockouts than in controls.

33 rix-basolateral membrane interactions, CD63, MMP-3 and Cdc42, and that PYY/NPY regulation of expressi

34 d phages selectively bound MMP-1 relative to MMP-3 and contained mutations only in L1.

35 Multivariate models that include MMP-3 and CTX-II perform better than existing traditiona

36 By multivariate analysis, a model including MMP-3 and CTX-II was identified as providing the best pr

37 n the anterior surface of the condyle, while MMP-3 and CXCL16 presented statistically significant ass

38 MMP-3 and M-CSF are potentially useful markers of AS dis

39 n and migration, and decreased production of mmp-3 and mmp-10 by human conjunctival fibroblasts.

40 MMP-1, MMP-3 and MMP-10 concentrations decreased with time afte

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

42 evels of MMPs in both fibroblast monolayers (MMP-3 and MMP-10) and 3D cultures (MMP-9 and MMP-10).

43 a, produced intense synergistic increases in MMP-3 and MMP-12 but not in MMP-9.

44 n of MMP-9 also suppressed the expression of MMP-3 and MMP-12 in the heart of mdx mice.

45 Immunosuppression increased both MMP-3 and MMP-12 mRNA levels in CNS resident cells, sugg

46 iated with increased levels of mRNA encoding MMP-3 and MMP-12.

47 APO866 blockade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in

48 uated release of NO and blunted induction of MMP-3 and MMP-13 release.

49 in part, by activating the zymogen forms of MMP-3 and MMP-13, which are constitutively present in ar

50 tion (P < 0.01), and attenuated induction of MMP-3 and MMP-13.

51 grecanolysis were prevented by inhibitors of MMP-3 and MMP-13.

52 but no detectable inhibitory activity toward MMP-3 and MMP-14 up to 10 muM.

53 By overexpressing HPSE, we have identified MMP-3 and MMP-7 as important sheddases of syndecan-1 she

54 monstrate that the shedding of syndecan-1 by MMP-3 and MMP-7 supports viral egress.

55 MMP-3 and MMP-7 were also naturally upregulated during H

56 Hence, MMP-3 and MMP-9 appear normally to play protective roles

57 K activity is necessary for the induction of MMP-3 and MMP-9 by TNFalpha, IL-1alpha, or IL-1beta in T

58 IL-6 induced MMP-3 and MMP-9 expression and activity in mouse brain a

59 a role for this pathway in the induction of MMP-3 and MMP-9 in the TM in response to these cytokines

60 Changes in MMP-3 and MMP-9 protein levels in the media were then de

61 lpha, IL-1alpha, and IL-1beta increase media MMP-3 and MMP-9 protein levels, and JNK inhibitor 2 bloc

62 When both MMP-3 and MMP-9 were inhibited, both early- and late-pha

63 ion by decreasing the levels and activity of MMP-3 and MMP-9.

64 a STAT3-independent manner, and upregulates MMP-3 and MT1-MMP, in addition to MMP-1.

65 8 inhibitor effect on IL-1alpha induction of MMP-3 and phosphorylation of p38 delta/gamma suggests co

66 ryptase-beta was able to activate latent pro-MMP-3 and pro-MMP-13 in vitro.

67 nfiltrate, adhesion molecule expression, and MMP-3 and proinflammatory cytokine gene expression, part

68 counteracting the transcription of MMP-1 and MMP-3 and the activation of MMP-1.

69 ) expression and matrix metalloproteinase 3 (MMP-3) and ADAMTS-4 messenger RNA expression in human in

70 he expression of matrix metalloproteinase 3 (MMP-3) and MMP-13, degraded type II collagen, and the di

71 Matrix metalloproteinase 3 (MMP-3) and tissue inhibitor of metalloproteinases 1 (TIM

72 leukin-6 (IL-6), matrix metalloproteinase 3 (MMP-3), and MMP-13 in joint tissue as compared to ASIC-3

73 lease of HMGB-1, matrix metalloproteinase 3 (MMP-3), and MMP-13, and protein expression of type X col

74 at -110 for MMP-13, -36 for MMP-9, -635 for MMP-3, and -753 for ADAMTS-4.

75 81% versus 47% for MMP-9, 57% versus 30% for MMP-3, and 48% versus 0% for ADAMTS-4.

76 while osteopontin binds proMMP-3 and active MMP-3, and dentin matrix protein-1 binds proMMP-9 and ac

77 ment, in concert with TGFalpha by activating MMP-3, and increasing invasion into the fat pad during b

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

79 ial growth factor, and enzymes MMP-1, MMP-2, MMP-3, and MMP-13 in RA synovial membrane cell cultures.

80 Gene expression of synovial IL-6, MMP-3, and MMP-13 was significantly inhibited in MKK-6-d

81 tein levels of active forms of MMP-1, MMP-2, MMP-3, and MMP-14 in conditioned media, and the low-mole

82 CLU inhibited enzymatic activities of MMP-2, MMP-3, and MMP-7.

83 In biochemical system, MMP-2, MMP-3, and MMP-9 bind with high affinity to, and are act

84 plasmic reticulum, ERK activation, and IL-6, MMP-3, and MMP-9 expression were all blocked in FAK knoc

85 ived TNF-alpha augments expression of MMP-1, MMP-3, and MMP-9 in decidual cells to interfere with nor

86 ha (TNF-alpha) significantly enhanced MMP-1, MMP-3, and MMP-9 mRNA and protein levels and activity me

87 Interestingly, whereas MMP-2, MMP-3, and MMP-9 were exclusively expressed by stromal c

88 Unlike highly regulated MMP-1, MMP-3, and MMP-9, MMP-2 mRNA and protein expression was

89 ing mediated TNF-alpha enhancement of MMP-1, MMP-3, and MMP-9, whereas IFN-gamma inhibited p38 mitoge

90 MMP-1, MMP-3, and MT1-MMP/MMP-14 were not inhibited effectively

91 nalyze expression changes in secreted MMP-1, MMP-3, and TGFbeta.

92 reaks, and increase the expression of MMP-1, MMP-3, and TGFbeta.

93 ability, we compared apolipoprotein E (apoE)/MMP-3, apoE/MMP-7, apoE/MMP-9, and apoE/MMP-12 double kn

94 The beta-sheet of MMP-3 appears to be stabilized still more.

95 e active AAV and decline with treatment, but MMP-3 appears to distinguish active AAV from remission b

96 r five rounds of selection with MMP-1, using MMP-3 as a competitor.

97 ene expression of collagen type I, MMP-1 and MMP-3, as well as the protein secretion of these gene pr

98 cantly increased the expression of MMP-1 and MMP-3 at both mRNA and protein levels.

99 otentiated the IL-1alpha-induced increase in MMP-3 at later times.

100 Induction of MMPs, such as MMP-1 and MMP-3 at the mRNA level, was also observed after stimula

101 We identified a Notch3-MMP-3 axis in human prostate cancer bone metastases that

102 nt with hyaluronidase occluded the effect of MMP-3 blockade on LTP, further confirming a critical rol

103 strands A and B of TIMP-1 makes contact with MMP-3 but not with MMP-1, and there are marked differenc

104 There was also a significant reduction in MMP-3, but not TIMP-1, expression.

105 mma, RANTES, and matrix metalloproteinase 3 (MMP-3) by NK cell and FLS coculture was greatest in SpA

106 lated in many breast tumours, and found that MMP-3 can cause epithelial-mesenchymal transition (EMT)

107 nability to cleave triple-helical collagens, MMP-3 can still bind to them, but the mechanism, locatio

108 the induction of matrix metalloproteinase 3 (MMP-3), causing the cleavage of E-cadherin and increased

109 ed expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an effect inhibited by APO866.

110 In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production

111 and SDM and catalytic domain of recombinant MMP-3 (cMMP-3) activated microglia in primary microglia

112 as well as catalytically active recombinant MMP-3 (cMMP-3) led to microglial activation and superoxi

113 roteinases and prostanoids whereby MMP-1 and MMP-3, commonly found in inflammatory and neoplastic foc

114 asis samples had higher levels of Notch3 and MMP-3 compared with patient matched visceral metastases

115 that were up to 10-fold improved in binding MMP-3 compared with WT TIMP-1, with inhibition constants

116 orted structure of the TIMP-1/stromelysin-1 (MMP-3) complex shows that the mechanisms of inhibition o

117 Crystal structures of MMP-3 complexes with TIMP-1 variants revealed conformati

118 observed binding pattern casts light on how MMP-3 could regulate collagen turnover and compete with

119 interval 0.66-0.85]), while a combination of MMP-3, CTX-II, and swollen joint count formed the best l

120 s of a variety of biochemical markers, i.e., MMP-3, CTX-II, COMP, TIMP-1, Pyr, and Glc-Gal-Pyr, corre

121 . enterocolitica infection in stromelysin-1 (MMP-3)-deficient mice (mmp-3(-/-)) with mice possessing

122 ere was little difference in the survival of MMP-3-deficient mice infected with Y. enterocolitica whe

123 In addition, MMP-3-deficient mice injected with pathogenic IgG develo

124 truct on TNFalpha and IL-1alpha induction of MMP-3 demonstrate an essential role for p38 in this sign

125 xtracellular matrix component, disrupted the MMP-3-dependent component of LTP.

126 We found that MMP-1- and MMP-3-dependent release of TNF-alpha induced rapid and t

127 MMP-3 dose-dependently induced the neutrophil (up to 5-f

128 e we explain the molecular pathways by which MMP-3 exerts these effects: exposure of mouse mammary ep

129 induction was associated with an increase in MMP-3 expression and activity in CA1 stratum radiatum.

130 on of LTP was associated with an increase in MMP-3 expression and activity.

131 th failed to block MSU-induced NO release or MMP-3 expression in parallel experiments.

132 terized as the central modulator for altered MMP-3 expression in prostate cancer cells and CAFs, but

133 enuated matrix metalloproteinase (MMP)-2 and MMP-3 expression in the peri-infarct area, suggesting de

134 with the control group showing the abundant MMP-3 expression localized at healing junction.

135 MMP-3 expression was described for the first time in the

136 MMP-3 expression was determined by enzyme-linked immunos

137 As determined by immunohistochemistry, MMP-3 expression was increased only in chondrocytes near

138 Whereas virus-induced MMP-3 expression was restricted to CNS resident astrocyt

139 y in the TNFalpha and IL-1alpha induction of MMP-3 expression was then evaluated.

140 ominant-negative p38 MAP kinase construct on MMP-3 expression were evaluated.

141 ent of TMJ chondrocytes resulted in enhanced MMP-3 expression, whereas wash-out of the HA(oligos) in

142 ases transduce MSU-induced NO production and MMP-3 expression.

143 in transducing MSU-induced NO production and MMP-3 expression.

144 regulatory pathways for FN-45 on MMP-13 and MMP-3 expression.

145 nd IL-1 increase matrix metalloproteinase-3 (MMP-3) expression in the trabecular meshwork (TM).

146 he expression of matrix metalloproteinase-3 (MMP-3) following treatment with hyaluronan oligosacchari

147 Therefore, the release of MMP-3 from apoptotic neurons may play a major role in de

148 oculation of AAV-2/9 containing a CMV-driven MMP-3 gene (AAV-MMP-3) into wild type mice resulted in e

149 n people homozygous for the 5A allele of the MMP-3 gene (odds ratio [OR], 3.1; 95% confidence interva

150 he MMP-1 gene, the 5A/6A polymorphism in the MMP-3 gene and the Arg-->Gln polymorphism in exon 6 of t

151 thin the proximal promoters of the MMP-1 and MMP-3 genes, which in association with AP-1 components (

152 n of RANKL, tumor necrosis factor alpha, and MMP-3 genes.

153 disease, induces the production of MMP-1 and MMP-3 have not been elucidated.

154 ophage colony-stimulating factor, CXCL8, and MMP-3 in both synovial and skin fibroblasts.

155 athway for the transcriptional repression of MMP-3 in CAFs.

156 RK1/2 completely inhibited the expression of MMP-3 in human chondrocytes following B. burgdorferi inf

157 xygen species in the switching expression of MMP-3 in stromal fibroblasts and prostate cancer cells d

158 LTP, further confirming a critical role for MMP-3 in this form of LTP.

159 ukin (IL)-1alpha are efficacious inducers of MMP-3 in TM.

160 ngside increased expression of progelatinase MMP-3 in WT mice.

161 increased MMP-1 (in four of five cultures), MMP-3 (in four of five cultures), MMP-17 (in three of fi

162 Latanoprost increased MMP-3 (in three of five cultures), MMP-17 (in four of fi

163 by the activity of matrix metalloprotease 3 (MMP-3), in contrast to NMDAR-dependent LTP regulated by

164 This MMP-3 increase appears to play a key role in the efficac

165 The cytokines TNF and IL-1 mediate the MMP-3 increase that occurs in response to trabecular mes

166 ression after injurious compression, whereas MMP-3 increased approximately 250-fold, ADAMTS-5 increas

167 Most importantly, AAV-mediated expression of MMP-3 increased outflow facility and decreased IOP, and

168 ssential signaling components in transducing MMP-3 increases produced by treatment of TM cells with t

169 pha or IL-1beta, produces highly synergistic MMP-3 increases.

170 mossy fiber-CA3 projection did not depend on MMP-3, indicating the pathway specificity of the actions

171 xposure of mouse mammary epithelial cells to MMP-3 induces the expression of an alternatively spliced

172 MMP-3 induction by both cytokines was blocked by dominan

173 p38 MAP kinase inhibitor SB202190 diminished MMP-3 induction by TNFalpha at all times and at 24 hours

174 A(6) treatment resulted in abrogation of the MMP-3 induction.

175 MMP-3 inhibition and knock-out prevented the induction o

176 We found that MMP-3 inhibition or knock-out impaired late-phase LTP in

177 e totally abolished by preincubation with an MMP-3 inhibitor, NNGH [N-isobutyl-N-(4-methoxyphenylsulf

178 talytic (Cat) and hemopexin (Hpx) domains of MMP-3 interact with the peptides, revealing cooperative

179 ical domains of collagens II and III, to map MMP-3 interaction sites.

180 the N-terminal domain of TIMP-1 and proximal MMP-3 interface and by changes in secondary structure wi

181 n [LTF], matrix metalloproteinase-1 [MMP-1], MMP-3, interferon induced-15 [IFI-15], and Homo sapiens

182 of an eye drop, of AAV-mediated secretion of MMP-3 into AH could have therapeutic potential for those

183 -2/9 containing a CMV-driven MMP-3 gene (AAV-MMP-3) into wild type mice resulted in efficient transdu

184 AH, or supplemented treatment with exogenous MMP-3.Intracameral inoculation of AAV-2/9 containing a C

185 We propose that MMP-3 is expressed as a protective response and plays an

186 We hypothesize that MMP-3 is involved in initiating an early and lethal cyto

187 Further study of MMP-3 is warranted to determine its clinical utility in

188 MMP-3 levels correlated weakly with ESR and CRP levels.

189 adiographic progression in RA and that serum MMP-3 levels decrease significantly with MTX therapy.

190 TX) during the followup period, median serum MMP-3 levels decreased after the initiation of MTX thera

191 MMP-3 levels were also higher among the 23 patients with

192 ha, and IL-1beta each individually increased MMP-3 levels, whereas TNF-alpha in combination with IL-1

193 Both cytokines increased MMP-3 levels.

194 Although MMP-10 is closely related to MMP-3, little is known about the role of MMP-10 in carti

195 erturbations of the NMR spectra of MMP-1 and MMP-3 map to similar locations across MMP-12 and encompa

196 lar changes in SS and suggest that targeting MMP-3 may be effective in protecting vascular wall integ

197 MMP-3-mediated microglial activation mostly depended on

198 um in the mmp-3(-/-) mice in comparison with mmp-3(+/+) mice.

199 n a delayed fashion, to equivalent levels as mmp-3(+/+) mice.

200 es were detected in tissues and serum in the mmp-3(-/-) mice in comparison with mmp-3(+/+) mice.

201 Surprisingly though, mmp-3(-/-) mice were markedly more resistant to S. typhi

202 S. typhimurium was able to colonize mmp-3(-/-) mice, albeit in a delayed fashion, to equival

203 roxide generation were largely attenuated in MMP-3-/- mice.

204 (mmp-3(-/-)) with mice possessing functional MMP-3 (mmp-3(+/+)).

205 tor-alpha, IL-8, matrix metalloproteinase-3 (MMP-3), MMP-9, and MMP-12.

206 s, such as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the develop

207 ression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

208 MMP-3, MMP-12, and MMP-13 levels also correlated with me

209 ion and increased levels of beta interferon, MMP-3, MMP-12, and TIMP-1 mRNA.

210 ycans and aggrecan expression, and decreased MMP-3, MMP-13 and RANKL expressions in cartilage, increa

211 epresses aggrecans expression but stimulates MMP-3, MMP-13 and RANKL production by chondrocytes throu

212 MMP-3, MMP-13, MMP-14, and tumor necrosis factor-alpha (

213 ty of the matrix metalloproteinases (MMP)-2, MMP-3, MMP-7, and MMP-9, and basic fibroblast growth fac

214 ients and were analyzed for levels of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP-1 usin

215 The matrix metalloproteinases MMP-2, MMP-3, MMP-7, MMP-9, and MMP-13 are highly expressed in

216 sion markedly increased expression of MMP-2, MMP-3, MMP-7, MMP-9, MT3-MMP, and ADAMTS5.

217 in vivo by the secreted MMPs, MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, or MMP-13.

218 disequilibrium was seen in all of the MMP-1, MMP-3, MMP-8, and MMP-12 SNPs and in four of five MMP-9

219 lite polymorphism in MMP genes MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, and MMP-12 with bladder cancer risk

220 trated elevated baseline levels of IL-1beta, MMP-3, MMP-8, MMP-9, and NGAL compared with the other st

221 L)-1beta, matrix metalloproteinases (MMP)-1, MMP-3, MMP-8, MMP-9, from baseline to week 2; regulated

222 icant correlations were noted between MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 levels and perce

223 val fluid meter, and levels of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 were assessed us

224 se of microgram and nanogram levels of IL-6, MMP-3, MMP-9, and MCP-1, whereas only picogram levels we

225 Western immunoblots were used to evaluate MMP-3, MMP-9, MMP-12, TNF-alpha, IL-1alpha, IL-1beta, IL

226 tabolic markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA

227 aled an increase in the expression of MMP-2, MMP-3, MMP-9, MMP-13, and MT1-MMP (MMP-14) in hyperplast

228 JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not i

229 matrix metalloproteinase protein 1 (MMP-1), MMP-3, MMP-9, P-selectin, thrombomodulin, and vascular e

230 ere stained for metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloproteinases 1 (

231 micro results in the inhibition of MMP-1 and MMP-3 mRNA and protein expression as a result of p44/42

232 MMP-3 mRNA levels and transcription rates also demonstra

233 tion to promote the translation of Snail and Mmp-3 mRNAs, and the induction of epithelial-to-mesenchy

234 was concomitant with a higher percentage of MMP-3 null mice evidencing surface lung metastases.

235 Tumors from MMP-3 null mice had a prevalence of undifferentiated spi

236 Tumor progression in MMP-3 null mice was inversely associated with leukocyte

237 lly to nanomolar concentrations of activated MMP-3 or cocultured with interleukin-1beta-stimulated, M

238 oplasmic MMP-2 over time, but no significant MMP-3 or MMP-8 production was observed.

239 einase (MMP)-1 (p = 0.03), MMP-2 (p = 0.06), MMP-3 (p = 0.02), and tissue inhibitor of metalloprotein

240 6K) inhibitor, inhibited MMP-1 (P<0.001) and MMP-3 (P<0.01) but not MMP-9.

241 ependent manner (all P<0.001) but suppressed MMP-3 (P<0.01).

242 .000), and MMP-1 (P=0.000), MMP-2 (P=0.004), MMP-3 (P=0.000), and MMP-9 (P=0.006) production.

243 ix metalloproteinase-1 (MMP-1; P=0.002), and MMP-3 (P=0.000), as well as nuclear factor-kappaB activa

244 Matrix metalloproteinase-3 (MMP-3) participates in normal extracellular matrix turno

245 ator inhibitor-1 (PAI-1), and stromelysin-1 (MMP-3) polymorphisms as risk factors for MI, but the pre

246 e protection in the EX2 regime suggests that MMP-3 possesses 2.8 kcal/mol higher folding stability th

247 Maximum MMP-3 production for individual cytokines, even at high

248 Finally, MMP-3 production only required MKK-7, and there was no e

249 ls with hydrogen peroxide directly inhibited mmp-3 promoter activity with concomitant nuclear translo

250 A 2.3-kb MMP-3 promoter fragment was cloned into a secreted alkal

251 minant-negative JNK dramatically reduces the MMP-3 promoter-driven reporter activity induced by these

252 f known transcription factors binding to the MMP-3 promoter.

253 as assessed by transfecting TM cells with an MMP-3 promoter/reporter construct.

254 nes and p38 MAP kinase pathway inhibitors on MMP-3 protein levels, p38 MAP kinase isoforms, and phosp

255 Human Cad-11-Fc up-regulated MMP-1 and MMP-3 protein production by RA synovial fibroblasts, bot

256 The higher stability of MMP-3 relative to MMP-12 coincides with the former's con

257 y NICD3-expressing tumors, and inhibition of MMP-3 rescued the NICD3-induced osteoblastic phenotypes.

258 ines showed that the increased expression of MMP-3 resulted directly from claudin-7 depletion, wherea

259 1 secretion and act synergistically to drive MMP-3 secretion.

260 ld weaker than the inhibition of the similar MMP-3 (stromelysin-1) catalytic domain (MMP-3cd) by TIMP

261 netic effectors, matrix metalloproteinase-3 (MMP-3/stromelysin-1), and fibronectin.

262 fects on TNFalpha and IL-1alpha induction of MMP-3 suggest divergent p38 isoform use, as do the morph

263 The more extensive line broadening in MMP-3 suggests greater sampling of conformational substa

264 ndicates that the activation of perisynaptic MMP-3 supports L-type channel-dependent LTP in the CA1 r

265 drogen peroxide reduced thrombospondin 2 (an MMP-3 suppressor) expression in prostate cancer cells by

266 ution of full-length human TIMP-1 to develop MMP-3-targeting ultrabinders.

267 l apoptosis is the release of active form of MMP-3 that activates microglia and subsequently exacerba

268 -gamma), chemokines (CXCL-10 and CCL-5), and MMP-3, that are stimulated by dry eye.

269 acilitate understanding of the regulation of MMP-3, the authors investigated the involvement of p38 M

270 ences in the levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 between patients on prostagland

271 Levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 were quantified by protein assa

272 asure the levels of mRNA for MT1-MMP, MMP-2, MMP-3, TIMP-1, TIMP-2, and TIMP-3 in the scleras of tree

273 The MMP-2 + MMP-3/TIMP-1 + TIMP-2 ratio was higher in PACG (0.83 +/-

274 rix metalloproteinase 1 [MMP-1], MMP-13, and MMP-3), tissue inhibitor of metalloproteinases 1 (TIMP-1

275 ed expression of matrix metalloproteinase-3 (MMP-3) to a level sufficient to induce cell migration by

276 The greater activity of MMP-12 than MMP-3 toward substrates from protein fibrils has been qu

277 creased TNFalpha expression and ADAMTS-4 and MMP-3 transcription by fibrochondrocytes.

278 MMP-3 transcription rate was assessed by transfecting TM

279 LISA and the expression of TSG-6, MMP-1, and MMP-3 transcripts and proteins with the use of qRT-PCR a

280 n by TSG-6 siRNA upregulated more MMP-1 than MMP-3 transcripts in normal and CCh fibroblasts.

281 Ultrastructural analysis of MMP-3 treated matrices by transmission electron microsco

282 e expressions of matrix metalloproteinase 3 (MMP-3), type II collagen, and cartilage oligomeric matri

283 nalysis showed that the expression levels of MMP-3, type II collagen, and COMP messenger RNA, which a

284 ated with the higher activity of MMP-12 than MMP-3, using nuclear magnetic resonance to monitor backb

285 Logistic regression analysis showed that MMP-3 values were high in those with severely active dis

286 Levels of the salivary biomarkers MMP-3, VE-cadherin, 6Ckine, and PAI-1 were correlated to

287 MMP-3 was significantly higher in POAG compared to contr

288 MMP-3 was specifically elevated and secreted by NICD3-ex

289 e cancer growth, matrix metalloproteinase-3 (MMP-3) was lower in CAFs but elevated in prostate cancer

290 report here that matrix metalloproteinase-3 (MMP-3) was newly induced and activated in stressed DA ce

291 e active form of matrix metalloproteinase-3 (MMP-3) was released into the serum-deprived media (SDM)

292 trix metalloproteinases (MMPs), particularly MMP-3, was significantly up-regulated.

293 cts for TNF-alpha, IL-1alpha and IL-1beta on MMP-3 were evaluated.

294 deduce the putative collagen-binding mode of MMP-3, where all three collagen chains make contacts wit

295 erentially degrades fibrillar collagens, and MMP-3, which can initiate a local proteolytic cascade.

296 MMP-3, which contains the RXXR furin consensus sequence,

297 The mRNAs of myocilin, SPARC, and MMP-3, which do not have AREs, were more stable after ac

298 ng/mL) stimulated the secretion of MMP-1 and MMP-3, which were blocked by TSA (100 nM).

299 ion in stromelysin-1 (MMP-3)-deficient mice (mmp-3(-/-)) with mice possessing functional MMP-3 (mmp-3

300 Neither MMP-3 zymogen (proMMP-3) nor the individual catalytic (C