ライフサイエンスコーパス: TIMP-1

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

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

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

4 or tissue inhibitor of metalloproteinases-1 (TIMP-1).

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

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

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

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

9 n activity and osteogenic differentiation by TIMP-1.

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

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

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

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

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

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

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

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

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

19 eased tissue inhibitor of metalloproteinases TIMP-1,2, which caused transient inhibition of MMP-2 act

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

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

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

23 TIMP-1 also inhibited matrilysin-mediated cell migration

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

25 A novel form of TIMP-1 (an inhibitor of soluble MMPs) is rapidly express

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

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

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

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

30 1, -3, and -9 also decreased while PAI-1 and TIMP-1 and -3 increased.

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

32 th doses of luteolin significantly increased TIMP-1 and BMP-2 expressions and decreased MMP-8 levels.

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

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

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

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

37 studies demonstrated increased expression of TIMP-1 and its association with poor prognosis in cancer

38 metalloprotease inhibitor TIMP-4, but not by TIMP-1 and less efficiently by TIMP-2 and TIMP-3.

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

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

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

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

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

44 asp" formed between the N-terminal domain of TIMP-1 and proximal MMP-3 interface and by changes in se

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

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

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

48 that the 9 C-terminal amino acid residues of TIMP-1 and the large extracellular loop of CD63 are requ

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

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

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

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

53 TIMP-1 and TIMP-2 were also found to increase the affini

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

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

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

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

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

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

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

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

62 Saliva MMP-8, MMP-9, TIMP-1, and MPO concentrations distinguished periodontit

63 pack years of smoking, whereas saliva MMP-9, TIMP-1, and MPO were mostly affected by time since cessa

64 At baseline, higher values of sST-2, TIMP-1, and PIIINP were associated with higher primary o

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

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

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

68 A, HSP-47, extracellular matrix (MMP7, 9 and TIMP-1), angiogenesis and lymphangiogenesis for AR compa

69 on-MMP-inhibitory and oncogenic functions of TIMP-1 are mediated by induction of intracellular signal

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

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

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

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

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

75 /-) murine PMNs; and 3) binding of exogenous Timp-1 (but not Timp-2) to Timp-1(-/-) murine PMNs recon

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

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

78 by changes in secondary structure within the TIMP-1 C-terminal domain that stabilize interdomain inte

79 Importantly, our analysis includes TIMP-1/CD63 interactions at the cell surface of live cel

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

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

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

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

84 In vivo, TIMP-1 deficiency completely abolished spontaneous remye

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

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

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

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

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

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

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

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

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

94 Astrocyte-derived TIMP-1 drove differentiation of oligodendrocyte precurso

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

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

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

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

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

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

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

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

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

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

105 g antibodies against the C-terminal motif of TIMP-1 for disruption of TIMP-1 interaction with CD63 an

106 gates the structure-function relationship of TIMP-1 for its interaction with CD63, which may eventual

107 he profibrotic biomarkers aldosterone, sST2, TIMP-1, Gal-3, PINP, and PIIINP were higher, and biomark

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

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

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

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

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

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

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

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

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

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

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

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

120 en together, OSM and its downstream mediator TIMP-1 have the therapeutic potential to boost remyelina

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 C-terminal motif of TIMP-1 for disruption of TIMP-1 interaction with CD63 and the subsequent signal t

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

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

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

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

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

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

152 While TIMP-1 is primarily known as an endogenous inhibitor of

153 e MMP-8 and -9 as shown by the following: 1) TIMP-1 is strikingly colocalized with MMP-8 and -9 on ac

154 Considering that the N-terminal half of TIMP-1 is sufficient for TIMP-1's MMP-inhibitory activit

155 Membrane-bound TIMP-1 is the PMN receptor for pro- and active MMP-8 and

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

157 Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a pleiotropic protein, promoting both tumor-s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 nd tissue inhibitor of metalloproteinases-1 [TIMP-1] levels, age < 57, no diabetes).

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

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

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

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

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

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

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

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

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

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

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

196 nths after randomization, aldosterone, sST2, TIMP-1, MMP-9, PINP, and PIIINP had decreased more in th

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

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

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

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

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

202 ding of exogenous Timp-1 (but not Timp-2) to Timp-1(-/-) murine PMNs reconstitutes the binding of exo

203 p-9 are detected on the surface of activated Timp-1(-/-) murine PMNs; and 3) binding of exogenous Tim

204 variants revealed conformational changes in TIMP-1 near the cooperative mutation sites.

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

206 required for their binding to membrane-bound Timp-1 on murine PMNs.

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

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

209 sidues are a potentially targetable motif of TIMP-1 oncogenic activity.

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

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

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

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

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

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

216 -8 and MMP-9 to PMN surfaces, membrane-bound TIMP-1 plays a counterintuitive role in promoting PMN pe

217 us pro-Mmp-8 and pro-Mmp-9 to the surface of Timp-1(-/-) PMNs.

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

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

220 p-HGFR-p-Akt-p-p65, driving CXCL1, CCL2, and TIMP-1 production.

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

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

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

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

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

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

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

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

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

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

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

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

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

234 MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature-induc

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

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

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

238 1beta and CsA showed a decrease in the MMP-1/TIMP-1 ratio.

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

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

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

242 with elevated pre-LT serum levels of OPN and TIMP-1, recovery of renal function correlated with decre

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

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

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

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

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

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

249 N-terminal half of TIMP-1 is sufficient for TIMP-1's MMP-inhibitory activity, we propose that those

250 y help design a novel approach for targeting TIMP-1's pro-oncogenic activity without interfering its

251 y providing feedback which affects MMP-9 and TIMP-1 secretion, which may become dysregulated in fibro

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

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

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

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

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

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

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

259 low tissue inhibitor of metalloproteinase 1 (TIMP-1), the endogenous inhibitor of the matrix metallop

260 secretion, and also upregulate secretion of TIMP-1, though not its expression.

261 -9, and -24 as well as TIMP-1 through -4.

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

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

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

265 9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, CD68, and caspase 3.

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

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

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

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

270 -10, IL12p40, indoleamine-2,3-dioxidase, and TIMP-1 (tissue inhibitor of matrix metalloproteinases).

271 ch as MMP-8 (matrix metalloproteinase-8) and TIMP-1 (tissue inhibitor of metalloproteinases 1); false

272 for directed evolution of full-length human TIMP-1 to develop MMP-3-targeting ultrabinders.

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

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

275 Crystal structures of MMP-3 complexes with TIMP-1 variants revealed conformational changes in TIMP-

276 idual and paired mutations from the selected TIMP-1 variants revealed cooperative effects between dis

277 g diversity into both domains, we identified TIMP-1 variants that were up to 10-fold improved in bind

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

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

280 TIMP-1 was associated with induced melanoma cell prolife

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

282 Astrocytic TIMP-1 was demonstrated to play a pivotal role in OSM-me

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

284 Finally, TIMP-1 was expressed by human astrocytes in demyelinated

285 TIMP-1 was produced in all cell lines.

286 = 77 subset), the largest decline in OPN and TIMP-1 was seen in the rAKI group.

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

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

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

290 anges from baseline to 8 months in sST-2 and TIMP-1 were associated with change in outcomes.

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

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

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

294 NA expressions of IL-1beta, iNOS, COX-2, and TIMP-1 when compared to vehicle alone in the ligature gr

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

296 ion for p38alpha promoting the expression of TIMP-1, which in turn stimulates cell proliferation in a

297 smoke upregulates colocalized expression of TIMP-1 with MMP-8 and MMP-9 on peripheral blood PMN surf

298 achieve this by fusing T1(TACE), a designer TIMP-1 with superb affinities for MT1-MMP and TACE, to t

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

301 d improved in binding MMP-3 compared with WT TIMP-1, with inhibition constants (K(i) ) in the low pic