ライフサイエンスコーパス: TIMP-1

1 ene tissue inhibitor of metalloproteinase-1 (TIMP-1).

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

3 CP, ICTP, MMP-2, TGF-beta1, desmosine, CTGF, TIMP-1).

4 of tissue inhibitor of metalloproteinase-1 (TIMP-1).

5 of tissue inhibitor of metalloproteinases-1 (TIMP-1).

6 n activity and osteogenic differentiation by TIMP-1.

7 ial binding of stromelysin family members to TIMP-1.

8 stromelysin-1) catalytic domain (MMP-3cd) by TIMP-1.

9 tion of MMP-9 and prevented the reduction of TIMP-1.

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

11 even in the presence of exogenous TIMP-2 or TIMP-1.

12 ntial when stoichiometrically complexed with TIMP-1.

13 and SDHD, were decreased in the presence of TIMP-1.

14 ity and suppressing the endogenous inhibitor TIMP-1.

15 suggesting a metastasis-stimulating role of TIMP-1.

16 on serum neutrophilic enzyme levels, except TIMP-1.

17 ing MMP-2, MMP-9 expression and upregulating TIMP-1.

18 ession and produced proMMP-9 unencumbered by TIMP-1.

19 ormal DNA methylation and restored the MMP-9/TIMP-1, -2 balance.

20 tivity-based extraction and their binding to TIMP-1, -2, -3, and -4 in bronchoalveolar lavage (BAL) o

21 hanges in pro-MMP-1, -2, -3, -9, and -24 and TIMP-1, -2, -3, and -4 levels were evaluated by Western

22 -8, -9, -10, -13, and -14) and three TIMPs (TIMP-1, -2, and -3) in cultured cells in vitro and in pr

23 TIMP-1 372 T/C and *429 T/G genotypes in males were also

24 it can be suggested that MMP-8 -799 C/T and TIMP-1 372 T/C, *429 T/G gene polymorphisms in males may

25 MMP-8 +17 C/G, -799 C/T, -381 A/G and TIMP-1 372 T/C, *429 T/G polymorphisms were determined b

26 ytes is a pathogenic mechanism for impairing TIMP-1 activity during inflammation.

27 TIMP-1 also inhibited matrilysin-mediated cell migration

28 binant human proMMP-9, operationally free of TIMP-1, also induced angiogenesis at subnanomolar levels

29 sue inhibitor of matrix metalloproteinase-1 (TIMP-1), amino-terminal peptide of type III procollagen

30 The BAL levels of TIMP-1 and -2 and MMP-2, -3, -7, -8, and -9 were signifi

31 f BOS is associated with increased levels of TIMP-1 and -2 and total MMP-2, -3, -7, -8, and -9.

32 the activity of MMP-2 and the expression of TIMP-1 and -2 in hONAs.

33 The expression of TIMP-1 and -2 induced by ET-1 was abolished by applicati

34 thylation and an imbalance between MMP-9 and TIMP-1 and -2 lead to ECM remodeling and renal fibrosis.

35 ssue inhibitor of metalloproteinase 1 and 2 (TIMP-1 and -2) into the spent medium, which was collecte

36 sed the expression and activity of MMP-2 and TIMP-1 and -2.

37 f MMP-2 but also decreased the expression of TIMP-1 and -2.

38 in the regulation of expression of MMP-2 and TIMP-1 and -2.

39 1, -3, and -9 also decreased while PAI-1 and TIMP-1 and -3 increased.

40 Decreased MMP-2 with concurrent increases of TIMP-1 and -4 by unoprostone may explain the lower clini

41 n the MI region, MMP-2 levels were lower and TIMP-1 and collagen levels were higher with LHFS than in

42 ntly attenuated albumin-induced increases in TIMP-1 and collagen-I levels.

43 Moreover, UDCA regulates the expression of TIMP-1 and gelatinases activity in PMA stimulated cells.

44 the increased permeability were reversed by TIMP-1 and GM6001.

45 Blockade of TIMP-1 and HER-2/neu activity may be beneficial in a sub

46 Combined analysis of both serum TIMP-1 and HER-2/neu conferred additional ability to pre

47 Furthermore, TIMP-1 and matrilysin co-localized in airway epithelial

48 We found that TIMP-1 and matrilysin co-localized in the epithelium of

49 n the present community-based sample, higher TIMP-1 and MMP-9 concentrations were associated with BP

50 The MMP-8-to-TIMP-1 and MMP-9-to-TIMP-1 ratios were markedly elevated

51 he kinetic inhibitors of metalloproteinases, TIMP-1 and PAI-1 protein levels, increased at MOI 25.

52 noma development modulates the expression of TIMP-1 and sTNFR1, which in turn affect tumor cell proli

53 We identified TIMP-1 and sTNFRI as the two relevant factors expressed

54 MPs and fibrosis by suppressing elevation of TIMP-1 and TGF-beta.

55 (cd) of MMP-1 with the inhibitory domains of TIMP-1 and TIMP-2 (N-TIMPs) and MMP-3cd with N-TIMP-2 ha

56 Both TIMP-1 and TIMP-2 are capable of inhibiting the proteoly

57 n the levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 between patients on prostaglandin anal

58 -3 effectively inhibits KL cleavage, whereas Timp-1 and Timp-2 do not, a profile that indicates the i

59 (K(i)) of putative physiological inhibitors TIMP-1 and TIMP-2 for the active catalytic domain of hum

60 TIMP-1 and TIMP-2 had differential effects on delayed ty

61 Levels of total protein, MMP-2, MMP-3, TIMP-1 and TIMP-2 were quantified by protein assay and e

62 on, tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2) were overexpressed by gene therapy in

63 s of tissue inhibitor of metalloproteinases (TIMP-1 and TIMP-2), and activation of p38 mitogen-activa

64 sue inhibitors of metalloproteinase 1 and 2 (TIMP-1 and TIMP-2), insulinlike growth factor-binding pr

65 ped-PEX chimeras were then inhibited by both TIMP-1 and TIMP-2.

66 nt with a decrease in the levels of secreted TIMP-1 and TIMP-2.

67 aphy) of MMP-2 (2-fold), while not affecting TIMP-1 and TIMP-2.

68 did not affect production of the inhibitors TIMP-1 and TIMP-3 when IL-1alpha was present.

69 of tissue inhibitor of metalloproteinases-1 (TIMP-1) and collagen type Ialpha 1 is either reduced or

70 4.) Tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIMP-2 increased after CCl(4) only in the gp

71 ing tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIMP-3/4 as assessed by zymography and rever

72 ), tissue inhibitor of metalloproteinases 1 (TIMP-1), and cartilage oligomeric matrix protein (COMP)

73 sue inhibitor of matrix metalloproteinase-1 (TIMP-1), and macrophage galactose-type C-type lectin-1.

74 ), tissue inhibitor of metalloproteinases 1 (TIMP-1), and TIMP-4.

75 optosis; that TGF-beta(1) stimulates MMP-12, TIMP-1, and cathepsins and inhibits MMP-9 and p21 via Ba

76 The inhibitor of MMP-9 is TIMP-1, and high levels of this enzyme have been associa

77 A 3-variable model consisting of serum HA, TIMP-1, and platelet count was better than other publish

78 analysis identified a 3-variable model (HA, TIMP-1, and platelet count) that had an area under the r

79 ng to secreted amounts of IL-8, hBD-1, VEGF, TIMP-1, and TIMP-2 from corresponding EVPOMEs.

80 nsistently expressed higher levels of MMP-2, TIMP-1, and TIMP-2.

81 s (tissue inhibitor of metalloproteinases 1 [TIMP-1] and TIMP-2).

82 Specifically, IL-6 and Timp-1 are released in the thymus in response to DNA dam

83 Our results identify TIMP-1 as an essential promoter of hepatic premetastatic

84 yl-cyclase-dependent modulation of the MMP-9/TIMP-1 balance, or proteolytically through regulation of

85 erminal portion of the enzyme containing the TIMP-1 binding site.

86 The benefits of TIMP-1 blockade in treating viral myocarditis were confi

87 We solved the x-ray crystal structure of TIMP-1 bound to the MMP-10cd at 1.9 A resolution; the st

88 matrix metalloproteinase 1 (MMP1) inhibitor TIMP-1, broad-spectrum MMP inhibitor GM 6001, heparin-bo

89 by the MPO-H2O2-chloride system inactivates TIMP-1 by oxidizing its N-terminal cysteine.

90 on of MMP-9 and stimulated the expression of TIMP-1 by preventing the binding of transcription factor

91 of tissue inhibitor of metalloproteinases-1 (TIMP-1) by UDCA was studied using zymography and qRT-PCR

92 ssue inhibitor of matrix metalloproteinases (TIMP-1) cDNA transfection or GM6001 was used to inhibit

93 P-9/ tissue inhibitor of metalloproteases-1 (TIMP-1) complex presents as a major form detected in nor

94 Similar proMMP-9/TIMP-1 complexes, but naturally produced by human monocy

95 However, elevated systemic levels of TIMP-1 correlate with poor prognosis in cancer patients,

96 only oxidation of the N-terminal cysteine of TIMP-1 correlated well with loss of inhibitory activity.

97 levels of p57, p21, and p53, suggesting that TIMP-1 could be intrinsically involved in the regulation

98 In vivo, TIMP-1 deficiency enhanced airway re-epithelialization a

99 Notably, TIMP-1 deficiency led to lethal liver IRI, as over 60% o

100 Inhibition of the cell cycle progression by TIMP-1 deficiency was linked to depressed levels of cycl

101 TIMP-1-deficient cultures migrated faster, and epithelia

102 and nuclear localization of beta-catenin in TIMP-1-deficient hMSCs.

103 ion into S phase and mitosis was impaired in TIMP-1-deficient livers after IRI.

104 del of OB, airway obliteration is reduced in TIMP-1-deficient mice.

105 Let-7f was up-regulated in TIMP-1-depleted hMSCs and demonstrably reduced axin 2, a

106 That neutrophil proMMP-9, unencumbered by TIMP-1, directly mediates FGF-2-dependent angiogenesis w

107 of tissue inhibitor of metalloproteinases 1 (TIMP-1), downregulated expression of proinflammatory cyt

108 accompanied by induction of low-angiogenic, TIMP-1-encumbered proMMP-9.

109 -derived M2 macrophages also shut down their TIMP-1 expression and produced proMMP-9 unencumbered by

110 unexpected findings indicate that increased TIMP-1 expression exacerbates, rather than ameliorates,

111 investigated the functional significance of TIMP-1 expression in a well-established mouse model of p

112 We show herein that TIMP-1 expression is induced in the myocardium by CVB3 i

113 on of Akt, emphasizing an important role for TIMP-1 expression on hepatocyte survival.

114 s support a critical protective function for TIMP-1 expression on promoting survival and proliferatio

115 TIMP-1 expression rose from 21-fold more than controls a

116 Lack of TIMP-1 expression was accompanied by markedly high level

117 signaling pathway to critically up-regulate TIMP-1 expression, as a consecutive secondary cellular r

118 We observed a linear relationship between TIMP-1 expression, liver metastatic burden, and infiltra

119 type, caused a substantial downregulation of TIMP-1 expression, resulting in production of angiogenic

120 MMP-9 and MMP-1 induction, while augmenting TIMP-1 expression.

121 iometric complex of neutrophil proMMP-9 with TIMP-1 failed to induce angiogenesis.

122 sulfide structure are crucial for preventing TIMP-1 from inhibiting MMPs.

123 Adenoviruses carrying the human TIMP-1 gene had no effect on tumor growth or the immune

124 inase (MMP)-8 and tissue inhibitor of MMP-1 (TIMP-1) gene polymorphisms in generalized aggressive per

125 ICAM-1) and pro-fibrogenic (Col1, alpha-SMA, TIMP-1) genes.

126 GAgP) and to assess the effects of MMP-8 and TIMP-1 genotypes on the outcomes of non-surgical periodo

127 perior to tamoxifen in both the normal serum TIMP-1 group (median TTP, 11.8 v 8.6 months; P = .003) a

128 months; P = .003) and in the elevated serum TIMP-1 group (median, 6.1 v 3.2 months; P = .03) In mult

129 Patients with elevated serum TIMP-1 had a significantly reduced objective response ra

130 Patients with elevated pretreatment serum TIMP-1 had a significantly reduced response and survival

131 issue inhibitor of matrix-metalloprotease-1 (TIMP-1) had a 3.5-fold greater risk of fibrosis 1 year a

132 Only recently, TIMP-1 has been revealed as a signalling molecule that c

133 RNA interference of TIMP-1 has revealed that endogenous TIMP-1 suppresses th

134 ous tissue inhibitor of metalloproteinase-1 (TIMP-1) has a greater inhibitory effect on endogenously

135 he tissue inhibitor of metalloproteinases-1 (TIMP-1) has been suggested to be involved in the regulat

136 involved in the growth factor activities of TIMP-1, however, remain controversial.

137 TIMP-1(-/-) HSCs also display increased levels of p57, p

138 llularity and, consistent with this finding, TIMP-1(-/-) HSCs display reduced capability of long-term

139 Of note, TIMP-1(-/-) HSCs present decreased levels of CD44 glycop

140 bound in greater quantities to its inhibitor TIMP-1 in advanced versus early fibrosis.

141 The knockdown of TIMP-1 in hMSCs activated the Wnt/beta-catenin signaling

142 he levels of MMP-9 and its natural inhibitor TIMP-1 in maintaining the basement membrane integrity.

143 observation led us to hypothesize a role for TIMP-1 in oligodendrogenesis and CNS myelination.

144 keratitis, confirming findings for MMP-9 and TIMP-1 in other infectious keratitis models and suggesti

145 Our findings establish a role for TIMP-1 in regulating HSC function, suggesting a novel me

146 We investigated the role of MMP-9/TIMP-1 in regulating innate antitumor immunity in breast

147 For instance, MMP-independent actions of TIMP-1 in the central nervous system have been implicate

148 Upregulated MMPs and TIMP-1 in the corneal epithelium and stroma of infected

149 scribe a previously uncharacterized role for TIMP-1 in the regulation of oligodendrocytes and astrocy

150 Upon the overexpression of TIMP-1 in tumour cells, miR-210 was accumulated in exoso

151 MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in biofluids of women with gestational diabetes

152 translational levels of MMP-8, -9, -13, and TIMP-1 increase during the early stages of C. albicans k

153 The inability of TIMP-1(-/-) mice to express TIMP-1 increased the levels of active caspase-3 and depr

154 actor-beta (TGF-beta), upstream regulator of TIMP-1, increased with age but was attenuated by ET.

155 TIMP-1 induced P110/P85 PI3K-signalling and AKT phosphor

156 nd systemic depletion of neutrophils reduced TIMP-1-induced increased liver susceptibility towards me

157 rucial functional role of neutrophils in the TIMP-1-induced premetastatic niche.

158 Because TIMP-1 inhibits most matrix metalloproteases, which are

159 goal of this study was to determine whether TIMP-1 inhibits re-epithelialization through matrilysin.

160 We find that TIMP-1 inhibits the MMP-10cd with a K(i) of 1.1 x 10(-9)

161 Our data demonstrate that TIMP-1 interacts with matrix metalloproteinases and regu

162 2), tissue inhibitor of metalloproteinase 1 (TIMP-1), interleukin-6 (IL-6), and inducible nitric oxid

163 Our results demonstrate that TIMP-1 is a direct regulator of hMSC functions and revea

164 These data further suggest that TIMP-1 is a promising biomarker for assessing risk of he

165 This correlation seemed paradox as TIMP-1 is best described as an inhibitor of pro-tumourig

166 Expression of TIMP-1 is dramatically increased in response to a variet

167 ation constant and, in contrast with TIMP-2, TIMP-1 is inefficient against MT1-MMP.

168 Tissue inhibitor of metalloproteinases 1 (TIMP-1) is a matrix metalloproteinase (MMP)-independent

169 Tissue inhibitor of metalloproteinase-1 (TIMP-1) is an extracellular protein and endogenous regul

170 Tissue inhibitor of metalloproteinase-1 (TIMP-1) is the major endogenous regulator of matrix meta

171 data led us to propose a novel function for TIMP-1: its highly localized up-regulation might arrest

172 n of MT6-MMP was inhibited preferentially by TIMP-1 (K(i) = 0.2 nm) over TIMP-2 (K(i) = 2.0 nm), beca

173 We have previously reported that adult TIMP-1 knock-out (KO) mice exhibit poor myelin repair fo

174 Moreover, TIMP-1 knockdown cells exhibited enhanced beta-catenin t

175 Surprisingly, TIMP-1 knockout mice exhibited a profound attenuation of

176 The amelioration of disease in TIMP-1 knockout mice was not attributable to either an a

177 progenitor cells (neurosphere) cultures from TIMP-1 KO mice revealed a specific deficit of NG2(+) oli

178 myelin formation is significantly delayed in TIMP-1 KO mice, a situation that coincided with dramatic

179 n of recombinant murine TIMP-1 (rmTIMP-1) to TIMP-1 KO neurosphere cultures evoked a dose-dependent i

180 tors grown in conditioned media derived from TIMP-1 KO primary glial cultures resulted in reduced dif

181 High systemic TIMP-1 led to increased hepatic SDF-1 levels, which in t

182 an increase of both exogenous and endogenous TIMP-1 led to the upregulation of miR-210 in a CD63/PI3K

183 All study groups had similar serum TIMP-1 levels (P >0.05).

184 duced MMP-2 and MT1-MMP levels but increased TIMP-1 levels compared with unstimulated fibroblasts.

185 function of TIMP-1 may explain why elevated TIMP-1 levels in lung cancer patients are highly correla

186 In mice, high systemic TIMP-1 levels increased the liver susceptibility towards

187 Low MMP-8 and high TIMP-1 levels may indicate the role of the lozenges in r

188 tal cancer patients, tumor as well as plasma TIMP-1 levels were correlated with synchronous liver met

189 The TIMP-1 levels were decreased in SJS and OCP patients whe

190 Upon correction of VD levels, TGF-beta1 and TIMP-1 levels were decreased, and the MMP2 and MMP9 leve

191 MMP-8, MMP-9, and TIMP-1 levels were determined in gingival crevicular flu

192 Decreased GCF MMP-8 levels and increased TIMP-1 levels were found to be significant up to day 180

193 Serum MMP-8 levels and salivary TIMP-1 levels were higher in Gh compared with Hg group (

194 MMP activity was higher and TIMP-1 levels were lower in oGVHD than in control (P < .

195 ers between groups showed that TGF-beta1 and TIMP-1 levels were significantly decreased and the MMP2

196 A combined model including elevated OPN and TIMP-1 levels, age <57, and absence of diabetes had the

197 pared with patients with normal pretreatment TIMP-1 levels.

198 um tissue inhibitor of metalloproteinases-1 (TIMP-1) levels were measured using an enzyme-linked immu

199 Indeed, TIMP-1(-/-) livers were characterized by massive leukocy

200 9), tissue inhibitor of metalloproteinase-1 (TIMP-1), macrophage chemoattractant protein-1 (MCP-1), v

201 new pro-tumourigenic signalling function of TIMP-1 may explain why elevated TIMP-1 levels in lung ca

202 es, CVB3-induced myocarditis and, thus, that TIMP-1 may represent a target for the treatment of virus

203 on the surface of hMSCs is essential for the TIMP-1-mediated effects on Wnt/beta-catenin signaling.

204 sma tissue inhibitor of metalloproteinase-1 (TIMP-1), metalloproteinase-9 (MMP-9), and procollagen II

205 (-/-) mice died postreperfusion, whereas all TIMP-1(+/+) mice recovered and survived surgery.

206 led to lethal liver IRI, as over 60% of the TIMP-1(-/-) mice died postreperfusion, whereas all TIMP-

207 We found that TIMP-1(-/-) mice have decreased BM cellularity and, cons

208 Compared to wildtype mice, TIMP-1(-/-) mice showed further impaired liver function

209 The inability of TIMP-1(-/-) mice to express TIMP-1 increased the levels

210 We therefore hypothesized that TIMP-1 might be involved in the homeostatic regulation o

211 y and compared with published data for the N-TIMP-1/MMP-3cd interaction.

212 he serum levels of 25-hydroxy VD, TGF-beta1, TIMP-1, MMP2 and MMP9 were measured at baseline and at t

213 th Hg group (P <0.05) whereas salivary MMP-8/TIMP-1 molar ratio was lower in Gh compared with Hg grou

214 Serum MMP-8, MMP-9, TIMP-1, MPO, and NE levels in circulation were assessed

215 els but inhibited type I collagen, MMP 1 and TIMP 1 mRNA levels.

216 Also tissue inhibitor metalloproteinase 1 (TIMP-1) mRNA was increased to a much greater extent in t

217 derived from TIMP-3, we have also created a TIMP-1 mutant (K26/27/30 + K76 transplant) capable of EC

218 not inhibit MMP indicated that the effect of TIMP-1 on beta-catenin signaling is MMP independent.

219 development and provide a novel function for TIMP-1 on myelination in the developing CNS.

220 Furthermore, the binding of CD63 to TIMP-1 on the surface of hMSCs is essential for the TIMP

221 -induced aggrecan breakdown was inhibited by TIMP-1 or by the N-terminal portion of TIMP-3, although

222 inases (TIMP), was delivered in complex with TIMP-1 or in a mixture with TIMP-2, the protease failed

223 njections of adenoviruses carrying the human TIMP-1 or MMP-9 gene (AdMMP-9).

224 Neither TIMP-1 or TIMP-2 affected the onset of rejection patholo

225 Furthermore, we speculate that TIMP-1 overexpression restricts airway re-epithelializat

226 ratory distress syndrome, demonstrating that TIMP-1 oxidation occurs in vivo.

227 ever, only pre-LT plasma OPN (P = 0.009) and TIMP-1 (P = 0.019) levels were significantly higher in r

228 , osteopontin (p=0.0004), HGF (p=0.010), and TIMP-1 (p=0.006) had shorter PFS than did those with low

229 We specifically selected an MT1-MMP.TIMP-1 pair to test our hypothesis, because any improvem

230 The N-terminal cysteine of TIMP-1 plays a key role in the inhibitory activity of th

231 -MMP-9 was stoichiometrically complexed with TIMP-1, pointing to a direct role of the MMP-9 enzyme in

232 We related plasma TIMP-1, procollagen III N-terminal peptide, and MMP-9 to

233 both arginase activity (EC(50)=261.8 nM) and TIMP-1 production (EC(50)=80.67 nM), and both pharmacolo

234 being the result of defective stimulation of TIMP-1 promoter activity by TLRs.

235 tor forkhead box protein O1 to the MMP-9 and TIMP-1 promoters.

236 MMP-2 and MMP-9, and TIMP-1 protein levels were assessed by ELISA and zymogra

237 plus UVA also decreased MMP-1 and increased TIMP-1 protein levels.

238 In addition, MMP-2 and MMP-9/TIMP-1 protein ratios were significantly lower in murine

239 However, MMP-9 and TIMP-1 protein, determined by western blot, were similar

240 h the previously solved structure of MMP-3cd.TIMP-1 (Protein Data Bank entry 1UEA), we see substantia

241 racellular MMP-9 activity with its inhibitor TIMP-1 provides evidence that local MMP-9 activity in th

242 chemical markers, i.e., MMP-3, CTX-II, COMP, TIMP-1, Pyr, and Glc-Gal-Pyr, correlated significantly w

243 ichiasis was associated with a reduced MMP-1/TIMP-1 ratio (P = 0.029).

244 There was no significant difference in MMP-8/TIMP-1 ratio among the study groups (P >0.05).

245 parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically healthy patients (P <0.05).

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

247 MMP-9/TIMP-1 ratio was significantly higher in patients with h

248 ted EAE mice had a significantly lower MMP-9/TIMP-1 ratio, and significantly lower MCT-1 and CD98 lev

249 iasis was associated with a reduced MMP-1 to TIMP-1 ratio, which may favor the accumulation of fibrot

250 ized the LV and right ventricular (RV) MMP-1/TIMP-1 ratio.

251 romoting a synergistic decrease in the MMP-1/TIMP-1 ratio.

252 1beta and CsA showed a decrease in the MMP-1/TIMP-1 ratio.

253 The MMP-8-to-TIMP-1 and MMP-9-to-TIMP-1 ratios were markedly elevated in SJS and OCP tear

254 livary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, were higher in the systemically healthy w

255 Tissue inhibitor of metalloproteinases-1 (TIMP-1) recently emerged as a pro-metastatic factor high

256 ed O1(+) oligodendrocytes, while antisera to TIMP-1 reduced oligodendrocyte numbers.

257 and NECA were less efficacious in augmenting TIMP-1 release by A(2A) receptor-deficient than control

258 o the adenosine augmentation of IL-4-induced TIMP-1 release, as both adenosine and NECA were less eff

259 03) In multivariate analysis, elevated serum TIMP-1 remained an independent predictor of both shorter

260 P-2) and of MMP-9 (that forms a complex with TIMP-1) replaced the original PEX in the MT1-MMP structu

261 Application of recombinant murine TIMP-1 (rmTIMP-1) to TIMP-1 KO neurosphere cultures evok

262 st after its complexing with TIMP-1, whereas TIMP-1 silencing in M0/M1 macrophages rendered them both

263 rmed by administering, to wild-type animals, TIMP-1-specific siRNA or polyclonal antisera, both of wh

264 nterestingly, the cell cycle distribution of TIMP-1(-/-) stem cells appears distorted, with a dysregu

265 rence of TIMP-1 has revealed that endogenous TIMP-1 suppresses the proliferation, metabolic activity,

266 Individuals in the top TIMP-1 tertile had a 2.15-fold increased risk of hyperte

267 Pro-fibrogenic gene expressions (COL1, TIMP-1, TGF-beta1, alpha-SMA) and protein expression of

268 An analysis of a mutant form of TIMP-1 that cannot inhibit MMP indicated that the effect

269 In parallel, UDCA upregulates TIMP-1 that in turn inhibits matrix metalloproteinases,

270 -9, and -24 as well as TIMP-1 through -4.

271 a two-step mechanism, whereby LfcinB induces TIMP-1 through an IL-11-dependent pathway involving tran

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

273 sue inhibitor of matrix metalloproteinase 1 (TIMP-1), TIMP-2, and hypoxanthine phosphoribosyl transfe

274 9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, CD68, and caspase 3.

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

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

277 y was used for the protein detection of EGF, TIMP-1, TIMP-2, HGF, angiopn-1, angiopn-2, VEGF-A, IP-10

278 ed between HCV cirrhosis and HCV-HCC groups (TIMP-1, TIMP-2, HGF, angiopn-1, angiopn-2, VEGF-A, IP-10

279 , MMP-9, p16, p21ras, p21WAF1, p27kip1, p53, TIMP-1, TIMP-2, vascular endothelial growth factor (VEGF

280 etalloproteinase 7 (MMP-7) and its inhibitor TIMP-1 (tissue inhibitor of matrix metalloproteinase 1)

281 -10, IL12p40, indoleamine-2,3-dioxidase, and TIMP-1 (tissue inhibitor of matrix metalloproteinases).

282 There are four mammalian TIMPs (TIMP-1 to -4) but only TIMP-3 is sequestered to the extr

283 Timed additions of TIMP-1 to the onplants containing TIMP-free neutrophil p

284 MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP-1 using multianalyte bead-based enzyme-linked immun

285 Serum TIMP-1 was an independent predictive and prognostic fact

286 ultivariable models, a 1-SD increment of log-TIMP-1 was associated with a 50% higher incidence of hyp

287 TIMP-1 was associated with induced melanoma cell prolife

288 rats, MMP-9 was activated and expression of TIMP-1 was decreased in the retina and its microvasculat

289 Pretreatment serum TIMP-1 was elevated in 120 (23%) of 522 patients.

290 s) -2 and -3 blocked transmigration, whereas TIMP-1 was ineffective.

291 TIMP-1 was produced in all cell lines.

292 crophages were nonangiogenic, although their TIMP-1 was severely downregulated.

293 TIMP-1 was significantly higher in PACG (p = 0.049) and

294 Tissue inhibitor of MMP (TIMP-1) was elevated with age but protected by ET.

295 day p.i., MMP-8, -9, -10, -12, -13, -19, and TIMP-1 were significantly upregulated from fivefold to 3

296 and tissue inhibitor of metalloproteinase-1 (TIMP-1) were increased.

297 l MMP-9 activation and its tissue inhibitor, TIMP-1, were quantified in streptozotocin-induced diabet

298 proMMP-9 was lost after its complexing with TIMP-1, whereas TIMP-1 silencing in M0/M1 macrophages re

299 Comparing our structure of MMP-10cd.TIMP-1 with the previously solved structure of MMP-3cd.T

300 and tissue inhibitor of metalloproteinase 1 (TIMP-1), with the latter being the result of defective s