ライフサイエンスコーパス: MMP-2

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

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

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

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

5 and MMP-9 while zymography could only detect 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 ) - an acute phase reactant - inhibits human MMP-2.

14 domains D and E of FBG in the inhibition of MMP-2.

15 assays, and IgG L13 inhibited MMP-9 but not MMP-2/-12/-14 and significantly relieved neuropathic pai

16 yes (IL-6: 11.90 vs. 4.38 pg/mL, p < 0.0001; MMP-2: 13.10 vs. 8.82 ng/mL, p = 0.0003) while adjusting

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

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

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

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

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

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

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

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

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

26 Y27632 also promoted the gene expression of MMP-2/-3 (matrix remodeling) and Notch-1 (Notch signalin

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

28 subtypes on distinct cell populations poses MMP-2,9 activity as an important mediator and contributo

29 ansduced D1- and D2-MSNs and astrocytes, and MMP-2,9 gelatinase activity adjacent to cell surfaces wa

30 alytic activity of matrix metalloproteinases MMP-2,9.

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

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

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

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

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

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

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

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

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

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

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

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

43 n training induced long-lasting increases in MMP-2 activity adjacent to D2-MSN synapses.

44 MP-1,2, which caused transient inhibition of MMP-2 activity around D2-MSNs during cue-induced heroin

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 o understand the exercise-induced changes in MMP-2 and -9 in women undergoing anthracycline chemother

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

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

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

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

63 arkers associated with collagen degradation, MMP-2 and -9, were lower than published referent control

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

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

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

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

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

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

70 Increased concentrations of MMP-2 and MMP-10 in CSF at baseline were associated with

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

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

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

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

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

76 MMP-2 and MMP-9 expression was reduced in the skin of do

77 disorganization accompanied by a decrease in MMP-2 and MMP-9 expression within the aortic wall in dox

78 l viability, migration and invasion, reduced MMP-2 and MMP-9 expression, and reduced N-cadherin expre

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

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

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

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

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

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

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

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

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

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

89 iability, migration, and invasion, increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 vities of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).

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

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

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

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

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

113 ated with parallel cell-specific activity of MMP-2 and MMP-9.

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

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

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

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

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

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 FSF13B), matrix metalloproteinase 1 (MMP-1), MMP-2, and MMP-3.

127 ments and Main Results: Neutrophil elastase, MMP-2, and MMP-9 activities and protein levels were equa

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

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

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

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

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

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

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

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

136 es (IL-6, beta = 0.065, p < 0.0001, n = 134; MMP-2, beta = 0.097, p < 0.0001, n = 131).

137 leavage of fluorescein-conjugated gelatin by MMP-2, but not MMP-9.

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

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

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

141 Significant selectivity of MMP 13 versus MMP-2 can be achieved by subtle chain contraction in a B

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

143 478 +/- 50 nM, P < 0.05) for the reaction of MMP-2 cleavage of fluorescein-conjugated gelatin.

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

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

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

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 MMP-2 enzyme activities in HGFs were also significantly

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

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

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

156 Administration of exogenous CD147 enhanced MMP-2 expression in HGFs, whereas treatment with cyclosp

157 its functional effect on the enhancement of MMP-2 expression in HGFs.

158 lasts might play a role in monocyte-enhanced MMP-2 expression in HGFs.

159 ited CD147 expression, reduced U937-enhanced MMP-2 expression in HGFs.

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

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

162 Synergistically enhanced MMP-2 expression was recently observed in the coculture

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 itive association between levels of IL-6 and MMP-2 in aqueous humor and the axial lengths of the eye

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

184 med to evaluate the mRNA levels of CD147 and MMP-2 in HGFs and U937 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

198 In conclusion, FBG is a natural selective MMP-2 inhibitor, whose pathological elevation could lead

199 by pathological overexpression of endogenous MMP-2 inhibitors such as TIMPs and/or the acute phase re

200 , whose pathological elevation could lead to MMP-2 insufficiency in humans.

201 Non-genetic MMP-2 insufficiency is a relatively unexplored condition

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

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

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

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

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

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

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

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

210 MMP-2 levels remained unchanged after periodontal treatm

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

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

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

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

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

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

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

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

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

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

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

222 pared with the iNPH group (p < 0.001), while MMP-2, MMP-9 and MMP-12 did not differ between the group

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 n of c-Jun mediated the increasing levels of MMP-2 mRNA transcription.

241 -to-mesenchymal transition and expression of MMP-2 occurred via activation of the PI3K/AKT signaling

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

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

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

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

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

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

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

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

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

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

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 The enzyme activities of MMP-2 released from cells were examined by zymography.

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

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

258 2000-paclitaxel conjugate (as a prodrug and MMP 2-sensitive moiety), transactivating transcriptional

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

260 MMP-2 significantly increased in both the HIIT group [76

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

267 Upon addition of MMP-2, these filaments rapidly break into fragments prio

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

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

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

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

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

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

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

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

276 n of JNK2 expression, c-Jun phosphorylation, MMP-2 transcription and, ultimately, BC invasion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 IL-6 and MMP-2 were significantly higher in the highly myopic eye

294 in 6 (IL-6), and matrix metalloproteinase-2 (MMP-2) were measured using an enzyme-linked immunosorben

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

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

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.