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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

19 MMP-3 activity was not detected on zymography.

20 Increased MMP-3 activity, which enhanced cell migration, also indu

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

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

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

24 MMP-3 also has enhanced subnanosecond fluctuations in he

25 Array analysis demonstrated increases of MMP-3 and -10 mRNA after exposure to 100 nM latanoprost

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

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

28 4 > MMP-24 > MMP-1, -11, -15, -16, and -19 > MMP-3 and 17, > MMP-12.

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

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

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

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

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

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

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

36 MSU induced MMP-3 and iNOS expression and NO release in chondrocytes

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

38 Serum levels of MMP-3 and M-CSF were measured in AS patients who did and

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

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

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

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

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

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

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

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

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

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

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

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

51 cted with B. burgdorferi showed induction of MMP-3 and MMP-19 but no other MMP or tissue inhibitor of

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

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

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

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

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

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

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

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

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

61 8 inhibitor effect on IL-1alpha induction of MMP-3 and phosphorylation of p38 delta/gamma suggests co

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

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

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

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

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

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

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

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

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

71 81% versus 47% for MMP-9, 57% versus 30% for MMP-3, and 48% versus 0% for ADAMTS-4.

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

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

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

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

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

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

78 nase (MMP)-deficient mice showed that MMP-9, MMP-3, and MMP-7 but not MMP-2 or MMP-12 are needed for

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

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

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

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

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

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

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

86 different matrix metalloproteinases (MMP-2, MMP-3, and MMP-9, respectively) in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

99 he values of the BASDAI as well as the serum MMP-3, but no change in the serum M-CSF values.

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

101 cytes to suppress IL-1-induced expression of MMP-3, but this has not been shown in human gingival fib

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

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

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

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

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

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

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

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

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

111 s not treated with biologics, both M-CSF and MMP-3 correlated with the Bath Ankylosing Spondylitis Di

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

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

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

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

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

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

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

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

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

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

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

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

124 F-alpha) significantly reduced MMP-1 but not MMP-3 expression from B. burgdorferi-infected cells; inh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 tly reduced B. burgdorferi-induced MMP-1 and MMP-3 expression.

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

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

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

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

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

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

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

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

148 ns in matrix metalloproteinase 1 (MMP-1) and MMP-3 have been found in patients with Lyme arthritis an

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

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

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

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

153 IL-4 inhibits the IL-1 induction of MMP-3 in human gingival fibroblasts isolated from patien

154 ts of IL-4 on the IL-1-induced expression of MMP-3 in human gingival fibroblasts isolated from patien

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 -2/9 containing a CMV-driven MMP-3 gene (AAV-MMP-3) into wild type mice resulted in efficient transdu

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

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

181 an and murine squamous cell carcinoma (SCC), MMP-3 is expressed in the stromal compartment at all of

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

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

184 ctivities of the metalloproteases, MMP-9 and MMP-3, leading to enhanced cell migration.

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

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

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

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

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

190 Both cytokines increased MMP-3 levels.

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

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

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

194 MMP-3-mediated microglial activation mostly depended on

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 nd IL-1 transcripts in human chondrocytes or Mmp-3, Mmp-8, Adamts-4, Adamts-5, and Il-1 in mouse chon

215 since we did not observe induction of MMP-1, MMP-3, MMP-8, ADAMTS-4, ADAMTS-5, and IL-1 transcripts i

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

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

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

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

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

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

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

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

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

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

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

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

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

229 MMP-3 mRNA levels and transcription rates also demonstra

230 d IL-4 resulted in a significant decrease in MMP-3 mRNA levels compared to IL-1 alone, with a concomi

231 the effects of IL-4 on the IL-1 induction of MMP-3 mRNA.

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

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

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

235 with our expectations, tumors originating on MMP-3 null mice had enhanced initial tumor growth rates

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

237 lays a causal role during SCC, wild-type and MMP-3 null mice were subjected to chemical carcinogenesi

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

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

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

241 6K) inhibitor, inhibited MMP-1 (P<0.001) and MMP-3 (P<0.01) but not MMP-9.

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

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

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

245 To elucidate whether MMP-3 plays a causal role during SCC, wild-type and MMP-

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

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

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

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

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

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

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

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

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

255 MMP-3 protein levels were determined by enzyme-linked im

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

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

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

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

260 1 secretion and act synergistically to drive MMP-3 secretion.

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

262 n periodontitis, matrix metalloproteinase-3 (MMP-3, stromelysin 1) is present at increased levels in

263 ed expression of matrix metalloproteinase-3 (MMP-3/stromelysin-1) is associated with a variety of tum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 MMP-3 transcription rate was assessed by transfecting TM

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

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

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

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

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

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

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

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

289 Expression of MMP-1 and MMP-3 was significantly inhibited by inhibition of JAK3

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

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

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

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

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

295 thase (iNOS) and matrix metalloproteinase 3 (MMP-3) were assessed in cultured chondrocytes treated wi

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

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

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

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

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