ライフサイエンスコーパス: TIMP-2

1 nd tissue inhibitor of metalloproteinases-2 (TIMP-2).

2 hibitor of metalloproteinases 1 [TIMP-1] and TIMP-2).

3 r, tissue inhibitor of metalloproteinases-2 (TIMP-2).

4 0.08 for untreated cells; 0.71 +/- 0.09 with TIMP-2).

5 nd tissue inhibitor of metalloproteinases-2 (TIMP-2).

6 rotein and mRNA levels of MMP-2, MMP-14, and TIMP-2.

7 MT6-MMP partially exists in its complex with TIMP-2.

8 s regulated by their physiological inhibitor TIMP-2.

9 ecrease in the levels of secreted TIMP-1 and TIMP-2.

10 P-2 (2-fold), while not affecting TIMP-1 and TIMP-2.

11 xpressed higher levels of MMP-2, TIMP-1, and TIMP-2.

12 nverting enzyme (TACE), but not by TIMP-1 or TIMP-2.

13 nd -2 and MMP1, -2, -9, and -10 and inducing TIMP-2.

14 s caused by the downregulation of MMP-14 and TIMP-2.

15 reduced neurite length, which is rescued by TIMP-2.

16 n effector of the antiangiogenic function of TIMP-2.

17 IMP-3, but was insensitive to treatment with TIMP-2.

18 nhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2.

19 ype 1-matrix metalloproteinase (MT1-MMP) and TIMP-2.

20 ientation of crystalline MT1-MMP(DeltaC) and TIMP-2.

21 nhibitors of metalloproteinase (TIMP) -1 and TIMP-2.

22 ough paracrine mechanisms involving bFGF and TIMP-2.

23 meras were then inhibited by both TIMP-1 and TIMP-2.

24 these mechanisms to the antitumor effects of TIMP-2.

25 generated containing 2 x 10(10) variants of TIMP-2.

26 TIMP-2, -3, and -4 are also upregulated.

27 ve cultures), MMP-24 (in all five cultures), TIMP-2, -3, and -4 expression (in three of five cultures

28 In A549 cells expressing increased levels of TIMP-2, a significant decrease in SP was observed, and t

29 In vivo, both TIMP-2 and Ala+TIMP-2 A549 xenografts exhibited reduced growth rate, CD

30 We demonstrate here that TIMP-2 abrogates angiogenic factor-induced endothelial c

31 ds tissue inhibitor of metalloproteinases-2 (TIMP-2), activates matrix metalloproteinase-2 (MMP-2), a

32 ry resulted in a decrease of both MMP-14 and TIMP-2 activity and protein.

33 mogenates were collected to assess MMP-2 and TIMP-2 activity by zymography and reverse zymography, pr

34 collected for analysis of MMP-2, MMP-14, and TIMP-2 activity, mRNA and protein expression.

35 Neither TIMP-1 or TIMP-2 affected the onset of rejection pathology.

36 invasion assays showed that re-expression of TIMP-2 after a combined treatment with 5-aza and trichos

37 Overexpression of either MMP-14 or TIMP-2 alone before oxidant injury is not enough to prev

38 d identical behavior to those overexpressing TIMP-2 alone.

39 anifested by the selective downregulation of TIMP-2 along with upregulation of MMP-2 and CVF-I in the

40 TIMP-2 and Ala+TIMP-2 also suppress basal hMVEC migration via a time-de

41 G, EGFL6, EGFR, angiopn-1, angiopn-2, ICAM2, TIMP-2, among others.

42 ative expressions of TIMP mRNA were TIMP-1 > TIMP-2 and -3 > TIMP-4.

43 all, these data reveal a novel role for both TIMP-2 and -3 in the pericyte-induced stabilization of n

44 and invasion) is primarily controlled by the TIMP-2 and -3 target membrane type (MT) 1 MMP.

45 reased MMPs-2, -3 & -9, ADAMTS-4 and -5, and TIMP-2 and -3 transcript levels but inhibited type I col

46 omain cleavage of ICAM-1 that was blocked by TIMP-2 and -3.

47 In vivo, both TIMP-2 and Ala+TIMP-2 A549 xenografts exhibited reduced

48 TIMP-2 and Ala+TIMP-2 also suppress basal hMVEC migratio

49 In vitro, growth assays suggested that TIMP-2 and Ala+TIMP-2 did not alter basal cell prolifera

50 (Ser473) showed decreased activation in both TIMP-2 and Ala+TIMP-2 tumor cells.

51 ibitor of matrix metalloproteinase (TIMP)-1, TIMP-2 and C-terminal propeptide of collagen type-I with

52 or-1 receptor as a binding partner of Loop 6/TIMP-2 and characterize this interaction on the endothel

53 Invasion was blocked by TIMP-2 and GM6001 but not by TIMP-1.

54 Urinary TIMP-2 and IGFBP7 were measured using a clinical immunoa

55 TIMP-2 and IGFBP7 were measured with ELISA on postoperat

56 However, the association of urinary TIMP-2 and IGFBP7 with long-term outcomes is unknown.

57 Cell cycle arrest biomarkers, TIMP-2 and IGFBP7, improve risk stratification for sever

58 ral delivery system, we stably overexpressed TIMP-2 and its mutant Ala+TIMP-2 (devoid of MMP inhibito

59 In contrast, TIMP-2 and mutant Ala+TIMP-2, which is devoid of MMP inh

60 plasmin activity and decreased expression of TIMP-2 and PAI-1 in tubular cells, and upregulation of r

61 eolytic activity, and elevated expression of TIMP-2 and PAI-1 in tubular cells.

62 fering RNA technology, the suppression of EC TIMP-2 and pericyte TIMP-3 expression leads to capillary

63 l system appears to occur through EC-derived TIMP-2 and pericyte-derived TIMP-3 to block both the cap

64 deoxycytidine and trichostatin A reactivated TIMP-2 and restored its expression in TIMP-2-silenced me

65 mino acid peptide corresponding to Loop 6 of TIMP-2 and show that Loop 6 is a potent inhibitor of bot

66 4, but not by TIMP-1 and less efficiently by TIMP-2 and TIMP-3.

67 TIMP-2 and TIMP-4 also inhibited the activation of pro-M

68 eviously shown that the C-terminal domain of TIMP-2 and, in particular, Loop 6 inhibit capillary endo

69 Tissue inhibitor metalloproteinase-2 (TIMP-2) and IGF-binding protein-7 (IGFBP7) have been val

70 ry tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor binding protein-7

71 the PEX of MMP-2 (that forms a complex with TIMP-2) and of MMP-9 (that forms a complex with TIMP-1)

72 ved tissue inhibitor of metalloproteinase-2 (TIMP-2) and pericyte-derived TIMP-3 are shown to coregul

73 tic tissue inhibitor of metalloproteinase-2 (TIMP-2) and plasminogen activator inhibitor-1 (PAI-1).

74 inhibitor of metalloproteinases (TIMP-1 and TIMP-2), and activation of p38 mitogen-activated protein

75 itor of matrix metalloproteinase 1 (TIMP-1), TIMP-2, and hypoxanthine phosphoribosyl transferase-1 (H

76 nhibitor of metalloproteinase (TIMP) -1, and TIMP-2, and IL-13 level increased markedly in both CD73K

77 s of mRNA for MT1-MMP, MMP-2, MMP-3, TIMP-1, TIMP-2, and TIMP-3 in the scleras of tree shrews that ha

78 The observed changes in MT1-MMP, MMP-2, TIMP-2, and TIMP-3 mRNA are consistent with visually mod

79 aled that MMP-26 was colocalized with MMP-9, TIMP-2, and TIMP-4 in DCIS cells.

80 The expression levels of MMP-26, MMP-9, TIMP-2, and TIMP-4 proteins in DCIS were significantly h

81 issue inhibitor of matrix metalloproteinase [TIMP-2] and epidermal growth factor [EGF]) and/or bacter

82 n tissue inhibitor of metalloproteinases-2 ([TIMP-2]) and insulin growth factor binding protein 7 ([I

83 Here, we examine the hypothesis that the TIMP-2 antitumor activity may involve regulation of the

84 However, the mechanisms underlying TIMP-2 antitumor effects are not fully characterized.

85 Both TIMP-1 and TIMP-2 are capable of inhibiting the proteolytic activit

86 recently reported that forced expression of TIMP-2, as well as the modified form Ala+TIMP-2 (that la

87 the balanced regulation of the MT1-MMP/MMP-2/TIMP-2 axis and the invasive behavior in cancer cells.

88 An MT1-MMP/MMP-2/TIMP-2 axis plays a key role in the invasive behavior of

89 dependently of plasminogen, the gelatinase A/TIMP-2 axis, gelatinase B, collagenase-3, collagenase-2,

90 -9, MMP-2, tissue inhibitor of MMP (TIMP)-1, TIMP-2, Bax, and BCl-2 proteins in retinal extracts were

91 sue inhibitor of matrix metalloproteinase-2 (TIMP-2) belongs to a small family of endogenous proteins

92 s of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 between patients on prostaglandin analogues and t

93 TIMP-2 binding to MT1-MMP induces activation of ERK1/2 b

94 by TIMP-3 and TIMP-4 and weakly inhibited by TIMP-2 but not by TIMP-1, a profile distinct from other

95 Overexpression of TIMP-2 but not TIMP-1 inhibits atherosclerotic plaque de

96 ed a similar affinity for MMP-1 as wild-type TIMP-2 but reduced affinity for MMP-3.

97 d only after co-overexpression of MMP-14 and TIMP-2, but activity further decreased after HQ for 18 h

98 Urinary TIMP-2, but not IGFBP7, is a promising biomarker to pred

99 In addition, up-regulation of TIMP-2 by alpha1(IV)NC1 led to saturation of MT1-MMP bin

100 Secondly, TIMP-2 can disrupt VEGF signaling required for initiatio

101 Third, TIMP-2 can enhance expression of RECK via Rap1 signaling

102 First, TIMP-2 can inhibit cell migration after VEGF stimulation

103 These results suggest that TIMP-2 can inhibit cell migration via several distinct m

104 inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, CD68, and caspase 3.

105 sue inhibitor of matrix metalloproteinase-2 (TIMP-2), characterized for its ability to inhibit matrix

106 entrations of IL-1beta, TNF-alpha, and MMP-2/TIMP-2 complex were assessed using enzyme-linked immunos

107 nt association among the production of MMP-2/TIMP-2 complex with the presence of CP (P = 0.008) and p

108 l artery and higher salivary levels of MMP-2/TIMP-2 complex.

109 Transfection with MMP-14 and/or TIMP-2 contributed to the return of type IV collagen lev

110 on to extracellular proteolysis, MT1-MMP and TIMP-2 control cell proliferation and migration through

111 TIMP-2 decreases cyclins B and D expression and increase

112 TIMP-2 deletion causes a delay in neuronal differentiati

113 ably overexpressed TIMP-2 and its mutant Ala+TIMP-2 (devoid of MMP inhibitory activity) in human aden

114 growth assays suggested that TIMP-2 and Ala+TIMP-2 did not alter basal cell proliferation rates, how

115 ely inhibits KL cleavage, whereas Timp-1 and Timp-2 do not, a profile that indicates the involvement

116 inhibition, as A549 cells overexpressing Ala+TIMP-2 exhibited identical behavior to those overexpress

117 sorbent assay (ELISA), we confirmed enhanced TIMP-2 expression and its MMP inhibitory activity by rev

118 involved concurrent reciprocal modulation of TIMP-2 expression by ERK1/2 and p38 MAPKs, such that inh

119 nduces a specific pattern of furin, MMP, and TIMP-2 expression in corneal myofibroblasts.

120 ted by peroxynitrite, as the latter reversed TIMP-2 expression in iNOS(-/-) lung smooth muscle cells

121 re, we investigated the mechanism underlying TIMP-2 expression in prostate cancer cell lines and prim

122 putative physiological inhibitors TIMP-1 and TIMP-2 for the active catalytic domain of human MMP-10 (

123 ed amounts of IL-8, hBD-1, VEGF, TIMP-1, and TIMP-2 from corresponding EVPOMEs.

124 our data provide strong evidence that these TIMP-2 functions occur independent of MMP inhibition, as

125 sults suggest that the downregulation of the TIMP-2 gene is associated with promoter methylation and

126 igenetic analysis of the MT1-MMP, MMP-2, and TIMP-2 gene promoters in highly migratory glioblastoma c

127 oter hypermethylation and lost expression of TIMP-2 gene, which was supported by other results demons

128 n (ANT), PDGF-BB, VEGF, FGF-2, IL-8, TIMP-1, TIMP-2, GM-CSF, and IP-10.

129 The relative expression of TIMP mRNA was TIMP-2 > TIMP-1 > TIMP-3 > TIMP-4.

130 TIMP-1 and TIMP-2 had differential effects on delayed type hypersen

131 MP-1 and TIMP-2 (N-TIMPs) and MMP-3cd with N-TIMP-2 have been characterized by isothermal titration c

132 ed for the protein detection of EGF, TIMP-1, TIMP-2, HGF, angiopn-1, angiopn-2, VEGF-A, IP-10, PDGF,

133 en HCV cirrhosis and HCV-HCC groups (TIMP-1, TIMP-2, HGF, angiopn-1, angiopn-2, VEGF-A, IP-10, PDGF,

134 CI 0.62-0.73) and improved with addition of [TIMP-2]*[IGFBP7] (0.72, 95%CI 0.66-0.77 p=0.03).

135 In patients with negative [TIMP-2]*[IGFBP7] at baseline, those who became positive

136 We measured [TIMP-2]*[IGFBP7] before and after a 6-hour resuscitation

137 Changes in urinary [TIMP-2]*[IGFBP7] following initial fluid resuscitation i

138 A positive [TIMP-2]*[IGFBP7] following resuscitation was associated

139 demonstrate that the associated risks of a [TIMP-2]*[IGFBP7] greater than 2.0 is equivalent to acute

140 presence of acute kidney injury (stage 1), [TIMP-2]*[IGFBP7] greater than 2.0 leads to an increased

141 urine output, serum creatinine, and urinary [TIMP-2]*[IGFBP7] greater than 2.0 were all predictive of

142 We now validate a clinical test for urinary [TIMP-2].[IGFBP7] at a high-sensitivity cutoff greater th

143 Urinary [TIMP-2].[IGFBP7] greater than 0.3 (ng/ml)(2)/1,000 ident

144 Critically ill patients with urinary [TIMP-2].[IGFBP7] greater than 0.3 had seven times the ri

145 del including clinical information, urinary [TIMP-2].[IGFBP7] remained statistically significant and

146 For a single urinary [TIMP-2].[IGFBP7] test, sensitivity at the prespecified h

147 primary analysis was the ability of urinary [TIMP-2].[IGFBP7] to predict moderate to severe AKI withi

148 % CI, 0.80-0.90 for clinical variables plus [TIMP-2].[IGFBP7]).

149 Two predefined [TIMP-2][IGFBP7] cutoffs (0.3 for high sensitivity and 2.

150 e analysis adjusted for the clinical model, [TIMP-2][IGFBP7] levels>0.3 were associated with death or

151 In conclusion, [TIMP-2][IGFBP7] measured early in the setting of critica

152 Baseline [TIMP-2][IGFBP7] values were available for 692 subjects,

153 Univariate analysis showed that [TIMP-2][IGFBP7]>2.0 was associated with increased risk o

154 ent samples revealed aberrant methylation of TIMP-2 in 33/90 (36.7%) cases of non-Hodgkin's lymphoma

155 expression by pericytes, whereas ECs produce TIMP-2 in EC-pericyte cocultures.

156 est expression in the epithelial tissues and TIMP-2 in the fibers.

157 macrophage-derived foam cells with exogenous TIMP-2 in vitro.

158 rge tissue inhibitor of metalloproteinase-2 (TIMP-2) increase detected in wild-type mice was absent i

159 nhibitor of metalloproteinase 1 (TIMP-1) and TIMP-2 increased after CCl(4) only in the gp91(phox(-/-)

160 ng RNA-mediated down-regulation of MMP-2 and TIMP-2 increased intravasation of HT-lo/diss cells.

161 ontrol at day 1 after MI (P < 0.05), whereas TIMP-2 increased only at later time points.

162 TIMP-2 induced collagen contraction, but the effect was

163 TIMP-2-induced RECK decreases cell-associated MMP activi

164 Here, we report that TIMP-2 induces pheochromocytoma PC12 cell-cycle arrest v

165 of a dominant negative Shp-1 mutant ablates TIMP-2 induction of p27Kip1.

166 embrane interactions beside the active site, TIMP-2-inhibited MMP-12 binds vesicles and cells, sugges

167 an unexpected, MMP-independent mechanism for TIMP-2 inhibition of endothelial cell proliferation in v

168 iable" Shp-1-deficient mice are resistant to TIMP-2 inhibition, demonstrating that Shp-1 is an import

169 TIMP-2 inhibits endothelial cell proliferation and migra

170 TIMP-2 inhibits the MMP-10cd with a K(i) of 5.8 x 10(-9)

171 ors of metalloproteinase 1 and 2 (TIMP-1 and TIMP-2), insulinlike growth factor-binding protein 2 (IG

172 findings illustrate a novel role for MT1-MMP-TIMP-2 interaction, which controls cell functions by a m

173 In contrast, TIMP-2 is a better inhibitor of MT1-MMP.

174 e conclude that promoter hypermethylation of TIMP-2 is a novel epigenetic event in the pathogenesis o

175 Tissue inhibitor of metalloproteinases-2 (TIMP-2) is a broad spectrum inhibitor of the matrix meta

176 Tissue inhibitor of metalloproteinase 2 (TIMP-2) is an angiogenesis inhibitor initially character

177 he tissue inhibitor of metalloproteinases-2 (TIMP-2) is known to antagonize matrix metalloproteinase

178 rresponding in vivo differences in levels of TIMP-2, JAM-C, and TF were demonstrated in primary tumor

179 referentially by TIMP-1 (K(i) = 0.2 nm) over TIMP-2 (K(i) = 2.0 nm), because of a slower association

180 with the PC12 cell data, primary cultures of TIMP-2 knock-out cerebral cortical neurons exhibit signi

181 mice and mice expressing a mutant truncated TIMP-2 (knock-down) show deficits in fear-potentiated st

182 at neither male nor female mice deficient in TIMP-2 (knockout) exhibit prepulse inhibition of the sta

183 inase phosphatase 1 in tumors overexpressing TIMP-2 leads to dephosphorylation of p38 mitogen-activat

184 inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 levels increased across all participant groups.

185 ls and fibroblasts, suggesting that the iNOS-TIMP-2 link may explain the protective effect of iNOS-kn

186 SP phenotype and function, and suggests that TIMP-2 may act as an endogenous suppressor of the SP in

187 The regulatory effect of iNOS on TIMP-2 may be mediated by peroxynitrite, as the latter r

188 e for the TIMP-2(-/-) mice and suggests that TIMP-2 may play a role in the synaptic plasticity underl

189 ta suggest that the antiangiogenic action of TIMP-2 may rely on matrix metalloproteinase-independent

190 urine embryo fibroblasts fail to demonstrate TIMP-2-mediated decrease in cell migration despite activ

191 TIMP-2-mediated inhibition of Cdk4 and Cdk2 activity is

192 We conclude that TIMP-2-mediated inhibition of tumor growth occurs, at le

193 Expression of dominant-negative Rap1 blocks TIMP-2-mediated neurite outgrowth.

194 body increases MMP activity and reverses the TIMP-2-mediated reduction in cell migration.

195 Here, we show that TIMP-2 mediates G1 growth arrest in human endothelial ce

196 The frequency of TIMP-2 methylation was slightly higher in aggressive NHL

197 s is the first report of a phenotype for the TIMP-2(-/-) mice and suggests that TIMP-2 may play a rol

198 gen degradation, and increased the levels of TIMP-2, MMP-14, and the active MMP-2 in the membrane ext

199 r findings provide the first indication that TIMP-2 modulates SP phenotype and function, and suggests

200 ied 24-hour urinary creatinine excretion and TIMP-2/mOsm as significant predictors of fDGF (AUC, 0.90

201 tive TIMP-2/mOsm values showed a decrease in TIMP-2/mOsm before an increase in estimated glomerular f

202 TIMP-2/mOsm on day-1 and day-10 adequately identified pa

203 Consecutive TIMP-2/mOsm values showed a decrease in TIMP-2/mOsm befo

204 0 were 24-hour urinary creatinine excretion, TIMP-2/mOsm, and total warm ischemia time with an AUC of

205 icantly increased MT1-MMP, MMP-2, MMP-9, and TIMP-2 mRNA expression, followed by increased active MT1

206 ptase-PCR analysis, we found that endogenous TIMP-2 mRNA levels showed a significant inverse correlat

207 Variants of the N-terminal domain of TIMP-2 (N-TIMP-2) with the sequences of the most selecti

208 -1 with the inhibitory domains of TIMP-1 and TIMP-2 (N-TIMPs) and MMP-3cd with N-TIMP-2 have been cha

209 From these candidates, four targets (i.e. TIMP-2, NCAM-1, JAM-C, and tissue factor (TF)) were sele

210 Neither TIMP-2 nor a synthetic MMP inhibitor protects breast epi

211 olecular pathways involved in the effects of TIMP-2 on processes dependent on tumor-host interactions

212 The effects of TIMP-2 on RECK expression and cell migration were confir

213 d is a consequence of both direct effects of TIMP-2 on tumor cells and modulation of the tumor microe

214 pro-MMP-9) even in the presence of exogenous TIMP-2 or TIMP-1.

215 lexes with a catalytic domain of MT3-MMP and TIMP-2 or TIMP-3 suggesting that pro-MMP-2 activation by

216 inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, or GM6001.

217 ssue inhibitor of metalloproteases (TIMP)-1, TIMP-2, or the N-terminal inhibitory domain of TIMP-3 (N

218 degrees rotation toward the MT1-MMP(DeltaC)/TIMP-2 orientation.

219 r more in the arc toward the MT1-MMP(DeltaC)/TIMP-2 orientation.

220 The SP isolated from TIMP-2-overexpressing A549 cells also demonstrated impai

221 MMP-14 or TIMP-2 overexpression alone contributed as much as the c

222 unctional analysis of A549 cells showed that TIMP-2 overexpression increased chemosensitivity to cyto

223 th first-generation adenoviruses, but murine TIMP-2 overexpression mediated by helper-dependent adeno

224 rine tumor model, we compared the effects of TIMP-2 overexpression on gene expression profiles in vit

225 Levels of MMP-2 (p<0.0005) and TIMP-2 (p<0.01), were elevated in ischemic samples.

226 These findings demonstrate that TIMP-2 possesses two distinct types of anti-angiogenic a

227 P-14 together with the addition of exogenous TIMP-2 prevented the reduction of MMP-2 activation.

228 hibition of ERK1/2 phosphorylation decreased TIMP-2 production, and down-regulation of p38 MAPK activ

229 ulting in defective formation of the MT1-MMP/TIMP-2/proMMP-2 trimeric activation complex.

230 TIMP-2 promoter hypermethylation in the lymphoma cell li

231 methylation status of the CpG island in the TIMP-2 promoter region by methylation-specific polymeras

232 Furthermore, CpG methylation of TIMP-2 promoter was also shown in primary prostate tumor

233 Furthermore, TIMP-2 promotes cell differentiation via activation of t

234 ntegrin in the cerebral cortex suggests that TIMP-2 promotes neuronal differentiation and maintains m

235 -MMP protein expression at 12 hours, whereas TIMP-2 protein increased at 24 hours.

236 ary prostate tumors that expressed decreased TIMP-2 protein levels.

237 ic array data, demonstrating that, in vitro, TIMP-2 protein was increased in the HT-lo/diss variant,

238 iological effects were the result of a known TIMP-2 protein-protein interaction or of a receptor-medi

239 ing the gene for human TIMP-1 (RAdTIMP-1) or TIMP-2 (RAdTIMP-2) or a control adenovirus (RAd66) and w

240 The MMP-2 + MMP-3/TIMP-1 + TIMP-2 ratio was higher in PACG (0.83 +/- 0.80) and POAG

241 tistically significant (p > 0.05), the MMP-2/TIMP-2 ratio was highest in PACG (2.83 +/- 7.40), follow

242 n baseline and 8 weeks of therapy were TSP4, TIMP-2, SEPR, MRC-2, Antithrombin III, SAA, CRP, NPS-PLA

243 TIMP-2 significantly inhibited migration and apoptosis o

244 T-hi/diss tumors with recombinant TIMP-1 and TIMP-2 significantly reduced HT-hi/diss cell intravasati

245 ivated TIMP-2 and restored its expression in TIMP-2-silenced metastatic prostate cell lines.

246 binding of MeCP2 to methylated CpG island in TIMP-2-silenced metastatic prostate cell lines.

247 ning alone (P = .001) or coexistent with low TIMP-2 staining was associated with dolichoectasia only

248 own-regulation of p38 MAPK activity enhanced TIMP-2 synthesis.

249 demonstrate that the COOH-terminal domain of TIMP-2 (T2C) inhibits the proliferation of capillary EC

250 splay was used to identify variants of human TIMP-2 that are selective inhibitors of human MMP-1, a c

251 of TIMP-2, as well as the modified form Ala+TIMP-2 (that lacks MMP inhibitory activity) significantl

252 characterize the anti-angiogenic domains of TIMP-2, the endogenous MMP inhibitor that uniquely inhib

253 in complex with TIMP-1 or in a mixture with TIMP-2, the protease failed to rescue the inhibitory eff

254 r association constant and, in contrast with TIMP-2, TIMP-1 is inefficient against MT1-MMP.

255 her of the general MMP inhibitors, GM6001 or TIMP-2 (tissue inhibitor of MMP), or with the specific g

256 MT3-MMP requires TIMP-2 to accomplish full pro-MMP-2 activation and this

257 alpha 3 beta 1 integrin-mediated binding of TIMP-2 to endothelial cells.

258 While binding of TIMP-2 to MMP-12 hinders membrane interactions beside th

259 gnificantly correlated with LA dimension and TIMP-2 to MMP-2 ratio.

260 in vitro, and addition of the MMP inhibitor TIMP-2 to TSP-2-null cells restored tTG activity (0.3 +/

261 of tissue inhibitor of metalloproteinases-2 (TIMP-2) to the cell surface, resulting in defective form

262 and 3) binding of exogenous Timp-1 (but not Timp-2) to Timp-1(-/-) murine PMNs reconstitutes the bin

263 TIMP-2 treatment also results in a concomitant increase

264 TIMP-2 treatment of hMVECs increases the association of

265 decreased activation in both TIMP-2 and Ala+TIMP-2 tumor cells.

266 ing agent 5-aza-2'-deoxycytidine resulted in TIMP-2 upregulation in both cell lines.

267 ery and tested for MMP-2, MMP-9, TIMP-1, and TIMP-2 using substrate gel electrophoresis (zymography)

268 p16, p21ras, p21WAF1, p27kip1, p53, TIMP-1, TIMP-2, vascular endothelial growth factor (VEGF), and b

269 d by NR4A2 and TNFalpha, while expression of TIMP-2 was antagonized.

270 The pattern of epigenetic regulation of TIMP-2 was clearly distinct from that of MMPs and includ

271 ed compared with control values (P<0.05) and TIMP-2 was elevated (128+/-31%) compared with non-MFS (7

272 TIMP-2 was expressed in the cell lines HL60, U266 and XG

273 ycle arrest and neurite outgrowth induced by TIMP-2 was independent of MMP inhibitory activity.

274 In contrast, TIMP-2 was not hypermethylated in any of the 40 cases of

275 tudies, overexpression with either MMP-14 or TIMP-2 was performed to revert the cells to a preinjury

276 TIMP-2 was significantly higher in POAG (p = 0.004) comp

277 TIMP-2 was unchanged by bimatoprost and latanoprost, but

278 TIMP-1 and TIMP-2 were also found to increase the affinity of targe

279 inogen activator, MMP-2, MMP-9, MT1-MMP, and TIMP-2 were determined by real-time PCR.

280 MMP-1, -3, and -9 and TIMP-2 were either not detected or their secretion was n

281 The mRNA levels of MMP-2, MMP-14, and TIMP-2 were measured by reverse transcription-polymerase

282 s of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 were quantified by protein assay and enzyme immun

283 nificantly higher levels of IL-8, hBD-1, and TIMP-2 were secreted from controls than from thermally s

284 , and tissue inhibitor of metalloproteinase (TIMP-2) were consistently and progressively up-regulated

285 inhibitors of metalloproteinases (TIMP-1 and TIMP-2) were overexpressed by gene therapy in F344 rat l

286 The MMP inhibitors, TIMP-1 and TIMP-2, were significantly reduced in the urine of mice

287 higher levels of HIF-1alpha, TGF-beta3, and TIMP-2 when compared with those from normal pregnant wom

288 up-regulation of HIF-1alpha, TGF-beta3, and TIMP-2 when compared with wild-type mice; normal levels

289 In contrast, TIMP-2 and mutant Ala+TIMP-2, which is devoid of MMP inhibitory activity, bloc

290 le with those previously reported for intact TIMP-2, while the NH2-terminal domain (T2N), which inhib

291 The interaction of TIMP-2 with alpha3beta1 integrin in the cerebral cortex

292 riants of the N-terminal domain of TIMP-2 (N-TIMP-2) with the sequences of the most selective clones

293 e inhibitor of metalloproteinase (TIMP)-1 or TIMP-2 would attenuate atherosclerotic plaque developmen

294 gate whether overexpression of MMP-14 and/or TIMP-2 would overcome the effect of nonlethal oxidant in

295 Cystatin C in combination with [TIMP-2] x [IGFBP7] 24 hours outperformed all standard re

296 [TIMP-2] x [IGFBP7] and soluble urokinase-type plasminoge

297 he primary outcome measure was achieved for [TIMP-2] x [IGFBP7] at 24 hours after inclusion by applyi

298 Diagnostic performance of urinary [TIMP-2] x [IGFBP7] improved over time with the highest a

299 Urinary [TIMP-2] x [IGFBP7] levels over time and serum soluble ur

300 sulin-like growth factor-binding protein 7 ([TIMP-2] x [IGFBP7]), and the soluble urokinase-type plas