ライフサイエンスコーパス: TIMP

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

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

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

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

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

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

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

8 TIMP-3 K26A/K45A retained higher affinity for sulfated g

9 TIMP-3 similarly bridged binding of MMP-13 and MMP-14 to

10 TIMP-GLIA did not increase markers of maturation on cult

11 TIMPs from invertebrates also inhibit metalloproteinases

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

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

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

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

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

17 9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, CD68, and caspase 3.

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

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

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

21 e (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patients with polycystic ovary syndrome

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

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

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

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

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

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

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

29 a K(D) of 34.6 nM for LRP-1, while the MMP-1/TIMP-3 complex had a sevenfold higher affinity (K(D) = 4

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

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

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

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

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

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

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

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

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

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

40 Tissue inhibitor of metalloproteinases-3 (TIMP-3) is a central inhibitor of matrix-degrading and s

41 of tissue inhibitor of metalloproteinases 4 (TIMP-4).

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

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

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

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

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

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

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

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

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

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

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

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

54 LRP-1 and a number of MMPs, ADAMs, ADAMTSs, TIMPs and metalloproteinase/TIMP complexes.

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

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

57 Among the proteins analyzed, TIMP-3 bound to LRP-1 with highest affinity (K(D) = 1.68

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

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

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

61 nhibitor of metalloproteinase 1 (TIMP-1) and TIMP-3/4 as assessed by zymography and reverse zymograph

62 ibitor of metalloproteinases 1 (TIMP-1), and TIMP-4.

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

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

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

66 ed that CTGF-induced expression of IL-10 and TIMP-3 in CD146(+) TSCs are regulated by JNK/signal tran

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

68 by TIMP-1 and less efficiently by TIMP-2 and TIMP-3.

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

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

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

72 ed morphine-induced alterations in MMP-9 and TIMP expression and identified organs, including the liv

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

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

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

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

77 By enabling profiling of active and TIMP-bound MMPs, our novel method may open opportunities

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

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

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

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

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

83 association of adipose metalloproteinase and TIMP expression with whole-body lipid distribution and i

84 studies strongly supports a role for MMP and TIMP genes as candidate genes for non-syndromic cleft li

85 -group differences were observed for MMP and TIMP.

86 were performed to assess changes in MMP and TIMP.

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

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

89 = 77 subset), the largest decline in OPN and TIMP-1 was seen in the rAKI group.

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

91 Several MMPs, ADAMTSs and TIMPs have been reported to be endocytosed by the low-de

92 results suggest that metalloproteinases and TIMPs regulate adipose tissue remodelling and distributi

93 an adipocytes express metalloproteinases and TIMPs, and that their expression varies with inflammator

94 We found altered levels of MMPs and TIMPs as well as imbalance of MMP:TIMP ratios in the aqu

95 In this study, levels of specific MMPs and TIMPs in the aqueous humour of primary angle-closure gla

96 As TIMP-4 expression is prevalent in cardiovascular tissues

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

98 matrix metalloproteinase inhibitors, such as TIMP-4, holds promise as a means to interrupt the progre

99 ssion of endogenous MMP-2 inhibitors such as TIMPs and/or the acute phase reactant alpha-2-macroglobu

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

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

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

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

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

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

106 -8 and MMP-9 to PMN surfaces, membrane-bound TIMP-1 plays a counterintuitive role in promoting PMN pe

107 4, but not by TIMP-1 and less efficiently by TIMP-2 and TIMP-3.

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

109 The broad-spectrum inhibition of MMPs by TIMPs and their N-domains (NTIMPs) is consistent with th

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

111 Furthermore, individual and combinatorial TIMP-deficient mice demonstrate the redundancy of metall

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

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

114 ar cells, were cultured in medium containing TIMP-GLIA, anti-CD3 antibody, or lipopolysaccharide (con

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

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

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

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

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

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

121 findings suggest new strategies to engineer TIMP proteins for therapeutic applications, and our dire

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

123 0 were 24-hour urinary creatinine excretion, TIMP-2/mOsm, and total warm ischemia time with an AUC of

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

125 og of suramin, has an increased affinity for TIMP-3 and increased ability to inhibit TIMP-3 endocytos

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

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

128 ody quadruple-knockout mice lacking all four TIMPs have growth plate closure in long bones, precipita

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

130 ion fraction was improved with either Ad-GFP-TIMP-4 or hTIMP-4exp.

131 lenocytes from HLA-DQ8 transgenic mice given TIMP-GLIA nanoparticles, but not control nanoparticles,

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

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

134 cent protein (GFP) and the full-length human TIMP-4 (Ad-GFP-TIMP4) or GFP.

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

136 We also identify TIMP-4 as a likely physiological ADAMTS7 inhibitor.

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

138 We identify TIMP/FGF-2/IHH as a novel nexus underlying bone lengthen

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

140 TIMP-3 levels was independent of changes in TIMP-3 mRNA levels, but correlated with shedding of LRP1

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

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

143 ur findings may provide a new perspective in TIMP targeting that could be exploited to halt metastati

144 ), seems to provide a snapshot of a stage in TIMP evolution preceding the third gene duplication.

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

146 evelopment of novel therapeutics to increase TIMP-3 levels and inhibit cartilage degradation in osteo

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

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

149 oteinase)-3 and MMP-8 synthesis and inducing TIMP (tissue inhibitor of metalloproteinases)-1.

150 for TIMP-3 and increased ability to inhibit TIMP-3 endocytosis and protect cartilage.

151 report that the endogenous ADAM17 inhibitor TIMP-3 inhibits ADAM17 activity only when it is bound to

152 of the TACE (also known as ADAM17) inhibitor TIMP-3, and lead to the inhibition of tumor necrosis fac

153 y inhibited by the metalloprotease inhibitor TIMP-4, but not by TIMP-1 and less efficiently by TIMP-2

154 alloproteinases (MMPs) and their inhibitors (TIMPs).

155 alloproteinases and their tissue inhibitors (TIMPs) have been implicated in human adipose tissue remo

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

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

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

159 at the tissue inhibitors of metalloprotease (TIMP) gene family is essential for normal bone growth af

160 Tissue inhibitor of metalloprotease (TIMP)-3 was expressed in CD146(+) TSCs at 1 wk with CTGF

161 not by tissue inhibitor of metalloproteases (TIMP)-1, TIMP-2, or the N-terminal inhibitory domain of

162 issue inhibitor of matrix metalloproteinase (TIMP)-1 were analyzed using multianalyte bead-based ELIS

163 issue inhibitor of matrix metalloproteinase (TIMP)-1, matrix metalloproteinase (MMP)-2, MMP-9, Galect

164 n of tissue inhibitors of metalloproteinase (TIMP) -1 and TIMP-2.

165 9 and tissue inhibitor of metalloproteinase (TIMP)-1 and -2 and also increased collagen and galectin-

166 lpha, tissue inhibitor of metalloproteinase (TIMP)-1 and collagen-I, which were blocked by HIF-1alpha

167 MP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and myeloperoxidase (MPO).

168 8 and tissue inhibitor of metalloproteinase (TIMP)-1 by enzyme-linked immunosorbent assay.

169 9 and tissue inhibitor of metalloproteinase (TIMP)-1 were obtained through reverse transcription poly

170 MP-1, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 levels increased across all particip

171 , and tissue inhibitor of metalloproteinase (TIMP)-2 increased, and the expression of TIMP3 declined.

172 ADAMs, ADAMTSs, TIMPs and metalloproteinase/TIMP complexes.

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

174 e of tissue inhibitor of metalloproteinases (TIMP) 2 in the context of hepatocellular carcinoma (HCC)

175 ses, tissue inhibitor of metalloproteinases (TIMP)-1 has been thought to suppress tumor metastasis.

176 and tissue inhibitor of metalloproteinases (TIMP)-2 complex.

177 tor, tissue inhibitor of metalloproteinases (TIMP)-3, through blocking its interaction with the endoc

178 tive tissue inhibitor of metalloproteinases (TIMP)-resistant forms.

179 sue inhibitors of matrix metalloproteinases (TIMPs) and is associated with adverse left ventricular (

180 Tissue inhibitors of metalloproteinases (TIMPs) are natural inhibitors of matrix metalloproteinas

181 our tissue inhibitors of metalloproteinases (TIMPs) are potent inhibitors of the many matrixins (MMPs

182 and tissue inhibitors of metalloproteinases (TIMPs) in the aqueous humour of primary open-angle glauc

183 rs, tissue inhibitors of metalloproteinases (TIMPs), is abnormal in BOS.

184 and tissue inhibitors of metalloproteinases (TIMPs), leading to the accumulation of collagen in the a

185 e 4 tissue inhibitors of metalloproteinases (TIMPs), multifunctional proteins that all inhibit member

186 of tissue inhibitors of metalloproteinases (TIMPs).

187 as tissue inhibitors of metalloproteinases (TIMPs).

188 MMP-1, -2 -7, -9, tissue inhibitor of MMP (TIMP) -1, and-2 were measured at baseline and post-inter

189 proteinase (MMP)-8, tissue inhibitor of MMP (TIMP)-1, receptor activator of nuclear factor kappaB lig

190 A role for MMP/TIMP balance in dolichoectasia appears more prominent in

191 f MMPs and TIMPs as well as imbalance of MMP:TIMP ratios in the aqueous humour of PACG eyes that were

192 and reduction in tissue inhibitors of MMPs (TIMPs) plays a role in ischemia/reperfusion (I/R) injury

193 ta1, and enzymes, tissue inhibitors of MMPs (TIMPs).

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

195 The two mutants (TIMP-3 K26A/K45A and K42A/K110A) with lowest rates of up

196 he N-terminal inhibitory domain of TIMP-3 (N-TIMP-3).

197 However, N-TIMP-3 displayed profound inhibitory activity against th

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

199 wk with CTGF, in contrast to control with no TIMP-3 expression.

200 ng the functional properties of nonmammalian TIMPs.

201 ade of LRP1 inhibited endocytic clearance of TIMP-3, leading to an increase in cell surface levels of

202 s that contribute to CNV as a consequence of TIMP-3 mutations will provide insight into the pathophys

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

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

205 MP-2, or the N-terminal inhibitory domain of TIMP-3 (N-TIMP-3).

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

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

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

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

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

211 cal insight into the cooperative function of TIMP domains and the significance of peripheral TIMP epi

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

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

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

215 mice with gliadin sensitivity, injection of TIMP-GLIA nanoparticles induced unresponsiveness to glia

216 ce were given 1 or 2 tail-vein injections of TIMP-GLIA or control nanoparticles.

217 of celiac disease, intravenous injections of TIMP-GLIA significantly decreased gliadin-specific T-cel

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

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

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

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

222 RP1, thus increasing extracellular levels of TIMP-3 and inhibiting cartilage degradation by the TIMP-

223 cell surface and that cell surface levels of TIMP-3 in endotoxin-activated human macrophages are dyna

224 However, BAL levels of TIMP-bound MMP-8 and -9 were higher in BOS than in good

225 served in good outcome recipients, levels of TIMP-bound MMP-8 and -9 were higher in BOS.

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

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

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

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

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

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

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

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

234 This suggests that LRP-1 scavenging of TIMP/metalloproteinase complexes may be a general mechan

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

236 This review examines the structures of TIMPs from different vertebrate orders using information

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

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

239 P domains and the significance of peripheral TIMP epitopes in MMP recognition.

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

241 % CI, 0.80-0.90 for clinical variables plus [TIMP-2].[IGFBP7]).

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

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

244 Here, we used molecular modeling to predict TIMP-3 residues potentially involved in binding to LRP1

245 nanoparticles encapsulating gliadin protein (TIMP-GLIA) in 3 mouse models of celiac disease.

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

247 cts of intracoronary delivery of recombinant TIMP-3 (rTIMP-3) on I/R injury.

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

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

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

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

252 Similarly, TIMP-3 expression was detected only when treated with CT

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

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

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

256 Following LPS stimulation, TIMP-3 levels on the surface of macrophages increased 4-

257 This dynamic regulation of cell surface TIMP-3 levels was independent of changes in TIMP-3 mRNA

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

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

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

261 nt residues located on the N- and C-terminal TIMP domains, positioned on opposite sides of the intera

262 Additionally, we found that TIMP-3 can facilitate the clearance of its target metall

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

264 t in cardiovascular tissues, we propose that TIMP-4 represents the primary endogenous ADAMTS7 inhibit

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

266 TIMP1-4) family of proteins, suggesting that TIMPs may possess anti-tumor activity.

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

268 The TIMP N-terminal domain binds and inhibits an MMP catalyt

269 ignificantly down-regulated member among the TIMP family in human HCCs.

270 and inhibiting cartilage degradation by the TIMP-3 target enzyme, adamalysin-like metalloproteinase

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

272 an MMP catalytic domain, but the role of the TIMP C-terminal domain in MMP inhibition is poorly under

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

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

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

276 overed that suramin (C51H40N6O23S6) bound to TIMP-3 with a KD value of 1.9 +/- 0.2 nM and inhibited i

277 Elevated MMP-to-TIMP ratios and MMP activity suggest an imbalance in tea

278 concentrations and for longer than wild-type TIMP-3, indicating that their increased half-lives impro

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

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

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

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

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

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

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

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

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

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

289 uring their evolutionary divergence, various TIMPs lost inhibitory activity toward some metalloprotei

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

291 e not orthologs of any particular vertebrate TIMP.

292 phylogeny analyses indicate that vertebrate TIMP genes arose from an invertebrate ancestor through 3

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

294 ovel nexus underlying bone lengthening where TIMPs negatively regulate the release of FGF-2 from chon

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

296 resistant or ADAMTS-resistant aggrecans with TIMP deficiency, we uncouple growth plate activity in ax

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

298 a from healthy volunteers was incubated with TIMP-GLIA, and hemolysis, platelet activation and aggreg

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

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