ライフサイエンスコーパス: MMP-2

1 , NF-kappaB, and matrix metalloproteinase-2 (MMP-2).

2 he production of matrix metalloproteinase-2 (MMP-2).

3 ivator (uPA) and matrix metalloproteinase-2 (MMP-2).

4 ve metabolism (PGC-1alpha) and adipogenesis (MMP-2).

5 activator (uPA)/matrix metalloproteinase-2 (MMP-2).

6 ng matrix metalloproteinase (MMP)-9, but not MMP-2.

7 a stable complex that prevents activation of MMP-2.

8 f TGF-beta1 in upregulation of MMP-9 but not MMP-2.

9 ants were selective and potent inhibitors of MMP-2.

10 igestion of alpha5beta1 and alpha2beta1 with MMP-2.

11 olon cancer cells transfected with pCMV6-XL5-MMP-2.

12 he beta1 integrin subunit is associated with MMP-2.

13 mation in the retina are mediated by p53 and MMP-2.

14 and MMP-9 while zymography could only detect MMP-2.

15 l MMPs in the low nanomolar range, including MMP-2 (~2 to 50 nM), MMP-13 (~2 to 50 nM), and MMP-14 (~

16 to Gtn-HPA/SDF-1alpha-PCN hydrogels involved MMP-2, 3, and 9, respectively, demonstrating the hydroge

17 feature-selection methods for prediction of MMP-2, -3, -7, -8, -9 and -12 substrate-cleavage sites o

18 The BAL levels of TIMP-1 and -2 and MMP-2, -3, -7, -8, and -9 were significantly increased i

19 increased levels of TIMP-1 and -2 and total MMP-2, -3, -7, -8, and -9.

20 entally verified cleavage sites, such as for MMP-2, -3, -7, and -8.

21 we studied the spatial expression pattern of MMP-2, -3, -9 and MT1-MMP in the healthy mouse retina.

22 The spatial expression pattern of MMP-2, -3, -9 and MT1-MMP was studied in the healthy mou

23 Basal expression of MMP-2,-3, -9 and MT1-MMP was found in the retina of heal

24 raded by the metalloproteinase (MMP) enzymes MMP-2, -7, and -9 produced by infiltrating inflammatory

25 y our group, are highly potent inhibitors of MMP-2, -8, -9, and -13.

26 suggested that anacardic acid binds into the MMP-2/9 active site, with the carboxylate group of anaca

27 Inhibition of MMP-2/9 activity increased PEDF and decreased VEGF level

28 Both series inhibited recombinant human MMP-2/9 activity with nanomolar potency.

29 However, expression of MMP-2/9 and their protease activity was elevated.

30 tting, ELISA, and real-time PCR; activity of MMP-2/9 by gelatin zymography.

31 broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increased amyloid formation and the re

32 s on both vimentin cytoskeletal function and MMP-2/9 matrix remodeling, because inhibiting either of

33 MMP-2/9, vascular endothelial growth factor (VEGF) and p

34 anomolar range and by a fair selectivity for MMP-2/9/12/13 over MMP-1/3/14.

35 ible response to matrix metalloproteinase-2 (MMP-2), a protease which may interfere with MMP-9 detect

36 In the present study, the regulation of MMP-2 activation by alpha1(IV)NC1 was evaluated.

37 role in cellular invasion and inhibition of MMP-2 activation by alpha1(IV)NC1.

38 In vitro MMP-2 activation of the multistage nanoparticles reveale

39 ng sites, which in turn led to inhibition of MMP-2 activation.

40 3, which respectively facilitate and prevent MMP-2 activation.

41 within the tumor periphery colocalized with MMP-2 activity (evaluated by in situ zimography).

42 tant hormones associated with HTN, increases MMP-2 activity and its key regulator, MMP-14, in RPE, in

43 ular modulator of Ang II-induced increase in MMP-2 activity and MMP-14 and BSG protein expression.

44 of ERK or p38 MAPK abrogated the increase in MMP-2 activity and MMP-14 and BSG proteins in ARPE-19 ce

45 We found enduring increases in MMP-2 activity in rats after withdrawal from self-admini

46 h no effect on levels of major regulators of MMP-2 activity such as the tissue inhibitors of metallop

47 Increased MMP-2 activity was further associated with cleavage of C

48 1 integrin can be abolished by inhibition of MMP-2 activity; it can be induced by up-regulation of MM

49 MMP-2/alpha5beta1 binding is enhanced in human recombina

50 nifies the therapeutic potential of blocking MMP-2/alpha5beta1 interaction in glioma treatment.

51 Our data indicate the possible role of MMP-2/alpha5beta1 interaction in the regulation of alpha

52 ncing high expression and co-localization of MMP-2/alpha5beta1, which is decreased upon pM treatment

53 These results identify the MMP-2-alphaIIbbeta3-PAR1 interaction as a potential targ

54 Altogether, our data demonstrate that MMP-2 amplifies the motility of colon cancer cells, not

55 Mmp-2 and -13a were increasingly present in RGC somata d

56 Moreover, Mmp-2 and -9 became upregulated in regrowing RGC axons a

57 In situ, MMP-2 and -9 generate a collagen Ialpha1 C-1158/59 fragm

58 beta3 integrins), matrix metalloproteinases (MMP-2 and -9), and vascular endothelial cell growth fact

59 ases-3 and -9, and down-regulation of Bcl-2, MMP-2 and -9, NF-kappaB and IkappaBalpha.

60 zes in the release of inflammatory mediators MMP-2 and -9, suggesting a cross-talk between these rece

61 but it is unclear whether MMPs--particularly MMP-2 and -9, the major MMPs operative in brain--contrib

62 hRs expressed on HRMECs upregulate levels of MMP-2 and -9, which stimulate retinal angiogenesis.

63 ntiation markers, as well as the activity of MMP-2 and -9.

64 ression of matrix metalloproteinase-2 and 9 (MMP-2 and 9), tissue inhibitor of metalloproteinase-1 (T

65 eased secretion of pro-MMP-9, as well as pro-MMP-2 and active MMP-2 from elastase-treated male rat ao

66 ences with disease, in particular, decreased MMP-2 and ADAM-9 activities.

67 We found that alpha1(IV)NC1 binds the CBD of MMP-2 and forming a stable complex that prevents activat

68 ciated in multivariable analysis with higher MMP-2 and lower superoxide dismutase 3 gene expression,

69 e IC(50) of ONO-4817 and galardin for MMP-1, MMP-2 and MMP-7 determined by the proposed colorimetric

70 ckout mice for MMP-2 and MMP-9, we show that MMP-2 and MMP-9 act synergistically mainly at the initia

71 phil entry into the peritoneal cavity, where MMP-2 and MMP-9 act synergistically to potentiate the ac

72 MMP-2 and MMP-9 are detected using label free porous sil

73 Gly-Asp-Lys clusters may diminish potential MMP-2 and MMP-9 collagenolytic activity.

74 and gel contraction alongside suppression of MMP-2 and MMP-9 expression.

75 Matrix metalloproteases (MMPs) MMP-2 and MMP-9 have been implicated in the physiologica

76 MMP-2 and MMP-9 immunolocalized to punctate structures w

77 investigate the activity of the gelatinases MMP-2 and MMP-9 in both cell lines.

78 F-beta1 (0.1-10ng/mL for 24h), the levels of MMP-2 and MMP-9 in culture media were significantly incr

79 characterize expression and localization of MMP-2 and MMP-9 in early postnatal and adult rat hippoca

80 atory mediators, TNF-alpha, IL-1 beta, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyperosmotic medium.

81 nd increases in activity of metalloproteases MMP-2 and MMP-9 in the spinal cord were evident in the m

82 The current study used MMP-2 and MMP-9 knockout (KO) mice to further determine

83 ritical for the maintenance of physiological MMP-2 and MMP-9 levels during the FBR and contributes to

84 nflammation, airspace enlargement, increased MMP-2 and MMP-9 levels, and altered expression of 2332 p

85 Of the MMPs tested, MMP-2 and MMP-9 most greatly favored the presence of cha

86 MMP-2 and MMP-9 mRNA were present in mouse islets but on

87 nteraction between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologically or genetically is suff

88 We therefore investigated whether MMP-2 and MMP-9 play a role in reducing islet amyloid de

89 , this is the first in vivo demonstration of MMP-2 and MMP-9 processing of a chemokine that has been

90 In both diabetic and nondiabetic patients, MMP-2 and MMP-9 protein levels were significantly increa

91 The MMP-2 and MMP-9 quantification correlated well with the

92 denosine receptors (A(1)ARs) increased total MMP-2 and MMP-9 release.

93 The ability to detect picogram amounts of MMP-2 and MMP-9 released by primary retinal pigment epit

94 imeric mice revealed the cellular sources of MMP-2 and MMP-9 to be distinct, with resident cells bein

95 extend our previous PE-related assessment of MMP-2 and MMP-9 to include MMP-1, which preferentially d

96 A THPI selective for MMP-2 and MMP-9 was redesigned to incorporate non-native

97 stand this dichotomy, recombinant human (rh) MMP-2 and MMP-9 were incubated with Abeta40 and Abeta42,

98 i microsensors detected the presence of both MMP-2 and MMP-9 while zymography could only detect MMP-2

99 lerenol Gd@C82(OH)22 can effectively inhibit MMP-2 and MMP-9 with high antitumoral efficacy.

100 l highly selective inhibitor of gelatinases (MMP-2 and MMP-9) and MMP-14, accelerates diabetic wound

101 icantly increased matrix metalloproteinases (MMP-2 and MMP-9) messenger RNA as well as miR-181b expre

102 (CD44 and RHAMM), matrix-degrading enzymes (MMP-2 and MMP-9), interleukin-8, and chemokine receptors

103 hen acted upon by matrix metalloproteinases (MMP-2 and MMP-9), which are up-regulated in heart tissue

104 cathepsin L, and matrix metalloproteinases (MMP-2 and MMP-9).

105 MMP-2 and MMP-9, and TIMP-1 protein levels were assessed

106 , and abrogated gains in secreted proteases, MMP-2 and MMP-9, following radiation.

107 The activity of MMP-2 and MMP-9, predicted to be decreased in DN, was in

108 Using single and double knockout mice for MMP-2 and MMP-9, we show that MMP-2 and MMP-9 act synerg

109 ion of two matrix metalloproteinases (MMPs): MMP-2 and MMP-9.

110 reased the TGF-beta1-induced upregulation of MMP-2 and MMP-9.

111 f migration/invasion-associated genes, CD24, MMP-2 and MMP-9.

112 y inhibited the catalytic activities of both MMP-2 and MMP-9.

113 In addition, MMP-2 and MMP-9/TIMP-1 protein ratios were significantly

114 he cell surface, subsequently activating pro-MMP-2 and promoting TGF-beta1 signaling.

115 The platelet surface target of MMP-2 and the mechanism through which it primes platelet

116 MMP-2 and the uPA/uPAR/plasminogen cascade provide thera

117 -induced MT1-MMP-dependent activation of pro-MMP-2 and up-regulation of MT1-MMP at the gene and prote

118 Matrix metalloprotease 2 (MMP-2) and cathepsin S were present at baseline and were

119 , which stimulates matrix metalloprotease-2 (MMP-2) and MMP-9 activity in the extracellular space.

120 egulation of the matrix metalloproteinase 2 (MMP-2) and MMP-9 expression.

121 ia activation of matrix metalloproteinase-2 (MMP-2) and MMP-9.

122 sion of one major metalloproteinase protein (MMP-2) and unchanged expression of lysyl oxidase and a s

123 iferation, production of VEGF, IL-8, and pro-MMP-2, and migration and invasion of RA-FLS.

124 We hypothesized that MAFB, MMP-2, and MMP-14 have integral roles in carpal/tarsal a

125 MafB, Mmp-2, and Mmp-14 were expressed widely, and tartrate-re

126 y significant improvement in hsCRP, d-8-iso, MMP-2, and MMP-9 levels.

127 ycated hemoglobin A1c (A1c), hsCRP, d-8-iso, MMP-2, and MMP-9.

128 es the initial adsorption of Gd@C82(OH)22 on MMP-2, and then its further location of the most favorab

129 , IL-6, IL-10, MCP-1, MIP-1alpha, MIP-1beta, MMP-2, and TNF-alpha.

130 x metalloproteinases (MMPs), i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors of metallop

131 ive association between Ang-2 and AVP index, MMP-2, Ang-1, and VEGF in SRA.

132 NA and protein expressions of MMP-9, but not MMP-2, are significantly higher in AVM tissues compared

133 gulation of MMP-2 in retinal NV and identify MMP-2 as a target for the treatment of PDR.

134 Secretion and activation of MMP-2 as well as susceptibility of the Abeta peptides to

135 nd the subsequent cleavage of PAR1 by active MMP-2 at a noncanonical site, exposing a previously unde

136 remodeling of the RMS through recruitment of MMP-2 by a previously unrecognized neuronal constituent.

137 ependent manner, associated with blockade of MMP-2 by AEP.

138 is a necessary cofactor for PAR1 cleavage by MMP-2 by binding the MMP-2 hemopexin domain, thus favori

139 hese studies demonstrated that inhibition of MMP-2 by doxycycline delayed the manifestations of MFS,

140 mes for corneal expression of testican-1 and MMP-2, by PCR array, real-time RT-PCR, ELISA, activity a

141 luorescence-based studies on the recombinant MMP-2 catalytic core domain demonstrated that anacardic

142 also abolished the degradation of gelatin by MMP-2, confirming that PEX9 is not an MMP-9 antagonist.

143 explore the role of MMP-2 in MFS, we created MMP-2-deficient Fbn1(mgR/mgR) mice.

144 doxorubicin (DOX) to HPMA copolymer, and an MMP-2-degradable linker (PLGLAG) connected tumor-homing

145 l as susceptibility of the Abeta peptides to MMP-2 degradation were dependent on the peptide conforma

146 MMP-2 deletion inhibited activation of TGF-beta and phos

147 d urea 6b show potential for intervention of MMP-2-dependent diseases such as brain metastasis.

148 (alpha6B), couples beta1-integrin to mediate MMP-2-dependent pericellular proteolysis of BM collagen

149 ormation with alpha5 and beta1 integrins and MMP-2 downregulation inhibited alpha5beta1 integrin-medi

150 We show that active MMP-2 enhances platelet activation induced by weak stimu

151 Among these, active MMP-2 enhances platelet aggregation by favoring the acti

152 of testican-1 and its temporal regulation of MMP-2 expression and activation after induction of bacte

153 MMP-2 expression and activation was also disparate betwe

154 of VEGF, which, in turn, promotes increased MMP-2 expression and activity in neighboring endothelial

155 n MUC18-silenced cells resulted in increased MMP-2 expression and activity.

156 ect p-ERK1/2 and given chronically activated MMP-2 expression and inhibited TGF-beta1-induced Smad2 a

157 ecipitation showed that further induction of Mmp-2 expression by transforming growth factor-beta I wa

158 These data may indicate that CD147 regulates MMP-2 expression in uveal melanoma cells.

159 MMP-2 expression was detected in ECs in retinal NV tissu

160 MMP-2 expression was seen in Muller glia, predominantly

161 rmed to analyse the association of CD147 and MMP-2 expression with known prognostic factors, vasculog

162 y, we evaluated the correlation of CD147 and MMP-2 expression with major prognostic factors for uveal

163 Testican-1 was shown to influence MMP-2 expression, activation, and regulation, as well.

164 ivity; it can be induced by up-regulation of MMP-2 expression, as exemplified by HT29 colon cancer ce

165 data showed that only doxycycline inhibited MMP-2 expression, whereas both drugs decreased Erk1/2 ph

166 n was significantly correlated with a higher MMP-2 expression.

167 actor (VEGF) and matrix metalloproteinase 2 (MMP-2) expression in brain cortex.

168 robing in vivo and in vitro demonstrate that MMP-2 externalization occurs on demand and that its loss

169 externalization of matrix metalloprotease-2 (MMP-2) for reconfiguring the extracellular matrix locall

170 f pro-MMP-9, as well as pro-MMP-2 and active MMP-2 from elastase-treated male rat aortic smooth muscl

171 Toward MMP-2, Gd@C82(OH)22 could block either the Zn(2+)-cataly

172 act (CNSE) on two matrix metalloproteinases, MMP-2/gelatinase A and MMP-9/gelatinase B, which are kno

173 In BAVnon-dil patients, TGF-beta1 and MMP-2 gene expression increased significantly, whereas M

174 of the MMP-2 promoter with p53 and decreased MMP-2 gene expression.

175 cell invasion could be via the regulation of MMP-2 gene transcription.

176 Matrix metalloproteinase-2 (MMP-2) has pivotal role in the degradation of extracellu

177 or for PAR1 cleavage by MMP-2 by binding the MMP-2 hemopexin domain, thus favoring the interaction of

178 and Ang-1, Ang-2, VEGF, TGF-beta1, Cys-LTs, MMP-2, IL-13, ECP, and IL-8 measurement in supernatants.

179 udy investigates the expression of MMP-9 and MMP-2 in aggressive extracranial AVMs.

180 t that relaxin crosses the BBB and activates MMP-2 in brain cortex, which may interact with PAs to in

181 peptide-MPA probes, we successfully examined MMP-2 in live cells and tumor on nude mouse, respectivel

182 that MMP-9 expression is more critical than MMP-2 in mediating TGF-beta-induced ASC formation.

183 We investigated the role of MMP-2 in MFS and compared the effects of losartan and do

184 However, the role of MMP-2 in MFS and effect of losartan on the lifespan of M

185 To further explore the role of MMP-2 in MFS, we created MMP-2-deficient Fbn1(mgR/mgR) m

186 egarded as tooth specific, participates with MMP-2 in processing dentin sialophosphoprotein (DSPP) in

187 rs, and neighboring ECs in the regulation of MMP-2 in retinal NV and identify MMP-2 as a target for t

188 Inhibitors were characterized by Ki for MMP-2 in the nanomolar range and by a fair selectivity f

189 eability, elevated albumin index and reduced MMP-2 index (factor 2; AUC=0.78).

190 sverse aortic constriction prevented cardiac MMP-2 induction, leading to decreased cardiac fibrosis a

191 terfering RNA to matrix metalloproteinase-2 (MMP-2) inhibited endothelium activation, and this effect

192 In contrast, a specific MMP-2 inhibitor had no effect on either amyloid depositi

193 oinjection of an MMP-9 inhibitor, but not an MMP-2 inhibitor, reduced pericyte-associated FITC-gelati

194 positive magnitude and significant for CRP, MMP-2, insulin, adiponectin, GM-CSF and IL-5.

195 Mechanistically, MMP-2 is involved in complex formation with alpha5 and b

196 Herein we show that MMP-2 is up-regulated in resected colorectal tumors and

197 Matrix metalloproteinase-2 (MMP-2) is a protease related to tumor invasion and metas

198 The serum level of MMP-9, but not MMP-2, is also elevated in AVM patients compared to heal

199 lar endothelial growth factor and PDGF-BB in MMP-2 knockdown cells.

200 to the anterior chamber of all wild-type and MMP-2 KO mice led to the formation of distinct ASC plaqu

201 lens epithelial explants from wild-type and MMP-2 KO mice that were treated with TGF-beta exhibited

202 MMP-2 levels remained unchanged after periodontal treatm

203 mounts in situ, indicated that MMP-9 and not MMP-2 mediated the gelatinase activity observed in infil

204 The MMP-2-mediated shedding of the I-like domain from beta1

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

206 e growth factor, matrix metalloproteinase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase

207 iduals were stained for metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloprotein

208 as well as on the protein and mRNA levels of MMP-2, MMP-14, and TIMP-2.

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

210 In biochemical system, MMP-2, MMP-3, and MMP-9 bind with high affinity to, and

211 all patients and were analyzed for levels of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP

212 Significant correlations were noted between MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 levels an

213 d gingival fluid meter, and levels of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 were asse

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

215 differences in the levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 between patients on pros

216 Levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 were quantified by prote

217 MMP-2, MMP-7, and MMP-9 activities increased concurrentl

218 e mediate substrate selectivity among MMP-1, MMP-2, MMP-8, MMP-13, and MMP-14/membrane-type 1 (MT1)-M

219 s and excellent MMP inhibition potencies for MMP-2, MMP-8, MMP-9, and MMP-13 (IC(50) = 0.006-107 nM).

220 MP-driven wall destruction by downregulating MMP-2, MMP-9 expression and upregulating TIMP-1.

221 orrelated positively with the expressions of MMP-2, MMP-9, and EMMPRIN in gingiva.

222 ium through inhibiting integrin alphavbeta6, MMP-2, MMP-9, and ERK phosphorylation by HT29.

223 Levels of MMP-2, MMP-9, and miR-181b were also up-regulated in rat

224 VEGF induced the expression of MMP-2, MMP-9, and MMP-13 and hence regulated the metasta

225 type IV are resistant to cleavage by MMP-1, MMP-2, MMP-9, and MMP-13, whereas non-cross-linked colla

226 In particular, MMP-2, MMP-9, and MMP-14 have been reported to be crucia

227 A nanomolar MMP-2, MMP-9, and MMP-14 inhibitor was identified, compo

228 tes with improved inhibitory activity toward MMP-2, MMP-9, and MMP-14 with respect to the previously

229 ollagenolytic MMPs, including MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, we identify the membrane-ancho

230 sion model, the relationships between MMP-1, MMP-2, MMP-9, tissue inhibitor of matrix metalloproteina

231 genin also down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cel

232 Administration of MMP-2/MMP-9 II, a dual active-site inhibitor, reduced th

233 s present in anacardic acid, are much weaker MMP-2/MMP-9 inhibitors.

234 sis factors, including HIF1alpha, VEGFR, and MMP-2/MMP-9.

235 ke highly regulated MMP-1, MMP-3, and MMP-9, MMP-2 mRNA and protein expression was constitutive in de

236 ation of TFPI-2 contributed to inhibition of MMP-2 mRNA expression, which could be reversed after the

237 We observed comparable MMP-2 mRNA expressions in control and transplanted group

238 Blocking MMP-2 or MMP-9 reverses EphB1-Fc treatment-induced downr

239 Further degradation of Abeta(1-16) by either MMP-2 or MMP-9 was not observed even after prolonged inc

240 ted MMP-9 and an accumulation of cytoplasmic MMP-2 over time, but no significant MMP-3 or MMP-8 produ

241 idual experiments, IL-6 or siRNA-insensitive MMP-2 overexpression by pM-FL-A141G counteracted and res

242 matrix metalloproteinase (MMP)-1 (p = 0.03), MMP-2 (p = 0.06), MMP-3 (p = 0.02), and tissue inhibitor

243 m activation and provide clear evidence that MMP-2 plays a pivotal role in the autocrine regulation o

244 Matrix metalloproteinase-2 (MMP-2) plays important roles in invasion and vasculariza

245 analyse the exact localisation of CD147 and MMP-2 positivity.

246 critical role for Meg3 in the regulation of MMP-2 production by CFs in vitro and in vivo, identifyin

247 MMP-2 promoter activity was also regulated by Nox1 knock

248 In cultured cells, CTGF/CCN2 activated the MMP-2 promoter through increased expression and tetherin

249 that culminated in reduced enrichment of the MMP-2 promoter with p53 and decreased MMP-2 gene express

250 a attenuated the binding of AP-2alpha to the MMP-2 promoter, therefore reducing the transcriptional a

251 ly conserved p53-binding sequence within the MMP-2 promoter.

252 through the inhibition of P53 binding on the Mmp-2 promoter.

253 retinal NV tissue from PDR patients, whereas MMP-2 protein levels were elevated in the aqueous of PDR

254 Further experiments showed that active MMP-2 regulates VEGF-A in melanoma cells on a transcript

255 elease, and CCD increased the active form of MMP-2 release.

256 y for pro-MMP-9 than for active MMP-9 or pro-MMP-2, requiring the N-terminal propeptide domain of pro

257 al properties of matrix metalloproteinase 2 (MMP-2)-responsive N-(2-hydroxypropyl)methacrylamide (HPM

258 wed elevated metalloproteinase-9 (MMP-9) and MMP-2 secretion, increased invasiveness, increased colon

259 2000-paclitaxel conjugate (as a prodrug and MMP 2-sensitive moiety), transactivating transcriptional

260 dicate that covalent conjugation of iRGD via MMP-2-sensitive bonds enhances accumulation and penetrat

261 Knockdown of MMP-2 using MMP-2 small interfering RNA (pM) in human glioma xenogra

262 tection of matrix metalloproteinases-2 via a MMP-2-specific peptide substrate (GPLGVRGKGG).

263 The novel PAR1-tethered ligand exposed by MMP-2 stimulates PAR1-dependent Gq and G12/13 pathway ac

264 y correlated with preterm birth (PICP, ICTP, MMP-2, TGF-beta1, desmosine, CTGF, TIMP-1).

265 at both cell types secrete higher amounts of MMP-2 than MMP-9 in their stimulated state, with RPE cel

266 swapped MT1-MMP chimeras in which the PEX of MMP-2 (that forms a complex with TIMP-2) and of MMP-9 (t

267 For MMP-2, the C-terminal residues enhanced K(m) and dramati

268 When these probes were exposed to MMP-2, the selective cleavage of the peptide resulted in

269 Similarly, the MMP-2/TIMP-1 ratio was highest in PACG (1.50 +/- 1.69),

270 y concentrations of IL-1beta, TNF-alpha, and MMP-2/TIMP-2 complex were assessed using enzyme-linked i

271 nificant association among the production of MMP-2/TIMP-2 complex with the presence of CP (P = 0.008)

272 rachial artery and higher salivary levels of MMP-2/TIMP-2 complex.

273 ot statistically significant (p > 0.05), the MMP-2/TIMP-2 ratio was highest in PACG (2.83 +/- 7.40),

274 n VI, desmosine, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 1 (TIMP-1

275 Supplementing MMP-2 to culture media did not induce EMT, suggesting th

276 elet activation that involves the binding of MMP-2 to integrin alphaIIbbeta3 and the subsequent cleav

277 eg3 in CFs resulted in the downregulation of Mmp-2 transcription, which, in turn, was dependent on P5

278 ta1 binding is enhanced in human recombinant MMP-2 treatments, resulting in elevated Stat3 DNA-bindin

279 tivity of matrix metalloprotease (MMP)-9 and MMP-2, two pro-angiogenic proteases.

280 Cord CRP, NT-proBNP, MMP-2, uPA, uPAR, and plasminogen levels were higher in

281 MMP-2, uPA, uPAR, and plasminogen were evaluated using E

282 ines examined, and enhanced cell invasion by MMP-2 upregulation and EMT induction.

283 g that EMT induction by Nox1 was not through MMP-2 upregulation.

284 o formation of channels displaying Tie-1 and MMP-2 upregulation.

285 Knockdown of MMP-2 using MMP-2 small interfering RNA (pM) in human gl

286 expand our study toward another gelatinase, MMP-2, using molecular dynamics simulations.

287 The expression of CD147 and MMP-2 was analyzed in 49 samples of uveal melanomas.

288 matrix metalloproteinase activity involving MMP-2 was necessary for fibronectin matrix disruption an

289 MMP-2 was significantly higher in PACG (p = 0.032) and P

290 We also observed that MMP-2 was transiently increased in BAL following AFSC tr

291 Matrix metalloproteinase-2 (MMP-2) was increased by Nox1 overexpression at the mRNA,

292 CD147 and MMP-2 were expressed in 47 (96.0 %) of the uveal melanom

293 Basal VEGF and MMP-2 were increased by 31% and 22%, respectively, compa

294 facturer specifications except for MMP-1 and MMP-2 which were significantly higher than reported.

295 ctor (VEGF), and matrix metalloproteinase-2 (MMP-2), which are upregulated, and adiponectin, which is

296 ressed in the tumor microenvironment such as MMP-2, which degrade the cores of 100-nm gelatin nanopar

297 hrough the peptide for in vitro detection of MMP-2, while 720 nm-emitting CdTeS QDs was linked to nea

298 reased levels of matrix metalloproteinase-2 (MMP-2), with no effect on levels of major regulators of

299 endent inhibition of tumor growth and active-MMP-2, without affecting MMP-9, MMP-7 and angiostatin.

300 not inhibit activation of the highly related MMP-2 zymogen.