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1 MPs) is relatively unopposed by the specific tissue inhibitors of metalloproteinases.
2 e metalloproteinase interaction sites of the tissue inhibitors of metalloproteinases.
3 alloproteinases in a manner analogous to the tissue inhibitors of metalloproteinases.
4 flections on the evolution of the vertebrate tissue inhibitors of metalloproteinases.
5 f action of the NP mimics that of endogenous tissue inhibitors of metalloproteinases.
6 transforming growth factor beta1 (P=0.0004), tissue inhibitor of metalloproteinase 1 (P=0.0009), gran
7 91(phox(-/-) ) than in WT mice after CCl(4.) Tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
8 oteinase 9 (MMP-9) and increased circulating tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
9 including COX-2 itself, lipocalin 2 (LCN2), tissue inhibitor of metalloproteinase 1 (TIMP-1), interl
10 e describe a novel approach that would allow tissue inhibitor of metalloproteinase 1 (TIMP-1), the en
11 expression of fibrogenic genes IL-1beta and tissue inhibitor of metalloproteinase 1 (TIMP-1), with t
12 oducts (collagen type 1 alpha 1 (CoL1A1) and tissue inhibitor of metalloproteinase 1 (TIMP1)) were al
14 8 (IL-8), human beta-defensin 1 (hBD-1), and tissue inhibitor of metalloproteinase 1 and 2 (TIMP-1 an
15 MP-1 was up-regulated, whereas expression of tissue inhibitor of metalloproteinase 1 decreased before
16 factor-beta1, alpha-smooth muscle actin, and tissue inhibitor of metalloproteinase 1 expression and a
17 ries of Dicer(d/d) mice partially normalized tissue inhibitor of metalloproteinase 1 expression and C
18 s after biliary decompression, both MMP3 and tissue inhibitor of metalloproteinase 1 expression decli
19 the eye, and the imbalance between MMP-1 and tissue inhibitor of metalloproteinase 1 may play a role
20 broblasts, reduced hepatic procollagen I and tissue inhibitor of metalloproteinase 1 messenger RNA ex
22 , including transforming growth factor beta, tissue inhibitor of metalloproteinase 1, and connective
24 minotransferase, gamma-glutamyl transferase, tissue inhibitor of metalloproteinase 1, C-reactive prot
25 ns of prostaglandin-endoperoxide synthase 2, tissue inhibitor of metalloproteinase 1, Dpp4, nitric ox
26 increased messenger RNA levels of collagen, tissue inhibitor of metalloproteinase 1, matrix metallop
27 ote fibrosis (collagen type I alpha 1 chain, tissue inhibitor of metalloproteinase 1, platelet-derive
31 lloproteinase 1 [MMP-1], MMP-13, and MMP-3), tissue inhibitor of metalloproteinases 1 (TIMP-1), and c
32 smosine, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 1 (TIMP-1), and T
33 d wine and ethanol upregulated expression of tissue inhibitor of metalloproteinases 1 (TIMP-1), downr
34 invasion assay in the presence or absence of tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-
35 r metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-
36 faip6), matrix metalloproteinase 19 (Mmp19), tissue inhibitor of metalloproteinases 1 (Timp1), and po
37 MMP-9), and the inhibitors of these enzymes (tissue inhibitor of metalloproteinases 1 [TIMP-1] and TI
38 prometastatic matrix metalloproteinase 8 and tissue inhibitor of metalloproteinases 1 in metastatic n
39 DAMTS-5 increased approximately 40-fold, and tissue inhibitor of metalloproteinases 1 increased appro
40 mor necrosis factor receptor 2 or IL-10, and tissue inhibitor of metalloproteinases 1) were identifie
41 P-8 (matrix metalloproteinase-8) and TIMP-1 (tissue inhibitor of metalloproteinases 1); false discove
42 st up-regulated genes (e.g., caspase-3, p21, tissue inhibitor of metalloproteinases 1, 2, and 3, and
43 ulmonary and activation-regulated chemokine, tissue inhibitor of metalloproteinases 1, and soluble CD
44 scores with the lowest levels of IFN-alpha, tissue inhibitor of metalloproteinases 1, and vascular e
45 enic factors (eg, ANG [angiogenin], TIMP1/2 [tissue inhibitor of metalloproteinases 1/2], and RANTES
46 kin 6 [IL-6]; stromal cell-derived factor 1; tissue inhibitor of metalloproteinases 1; and vascular c
47 3 (IL-23), IL-1 receptor I (IL-1RI), IL-17R, tissue inhibitors of metalloproteinase 1 and 2 (TIMP-1 a
48 increased in TAA tissue homogenates, whereas tissue inhibitors of metalloproteinases 1 and 4 decrease
50 03), MMP-2 (p = 0.06), MMP-3 (p = 0.02), and tissue inhibitor of metalloproteinase-1 (p = 0.04) in el
55 lagen I type I, fibronectin, COL1alpha1, and tissue inhibitor of metalloproteinase-1 (TIMP-1) were in
56 treated with IL-1beta express high levels of tissue inhibitor of metalloproteinase-1 (TIMP-1), an imp
57 rix metalloproteinase-2 and 9 (MMP-2 and 9), tissue inhibitor of metalloproteinase-1 (TIMP-1), macrop
58 who underwent routine measurements of plasma tissue inhibitor of metalloproteinase-1 (TIMP-1), metall
61 smooth muscle actin (alphaSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIMP1) and tran
62 plored whether OGG1 recruited to intron 1 of tissue inhibitor of metalloproteinase-1 (TIMP1) gene and
63 ed by elevated MMP-1, -2, -3, -7, and -8 and tissue inhibitor of metalloproteinase-1 and -2; and depr
64 -type plasminogen activator while increasing tissue inhibitor of metalloproteinase-1 and plasminogen
65 th a balance between metalloproteinase-8 and tissue inhibitor of metalloproteinase-1 expressions.
66 ase-8 expression and decreased expression of tissue inhibitor of metalloproteinase-1 in pulmonary acu
69 , whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regula
70 owth factor receptor beta, desmin, vimentin, tissue inhibitor of metalloproteinase-1) and fibrosis (r
71 and Lix/CXCL-5), matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and apoptosis r
72 s syndrome); and matrix metalloproteinase-3, tissue inhibitor of metalloproteinase-1, and CXCL13 in A
74 with gene expression for alpha2(I) collagen, tissue inhibitor of metalloproteinase-1, and transformin
75 n expression of MMP-1, collagen type 1alpha, tissue inhibitor of metalloproteinase-1, and vascular re
76 nogen activator inhibitor (PAI)-1, vimentin, tissue inhibitor of metalloproteinase-1, fibronectin, gr
82 is via its transcriptional regulation of the tissue inhibitor of metalloproteinases-1 (TIMP-1) gene.
83 role in extracellular matrix remodeling, the tissue inhibitor of metalloproteinases-1 (TIMP-1) has be
91 al injury including Cystatin C, Osteopontin, Tissue Inhibitor of Metalloproteinases-1 (TIMP1), beta2-
92 splant [REVERSE]: high osteopontin [OPN] and tissue inhibitor of metalloproteinases-1 [TIMP-1] levels
94 protein-10 (IP-10), interleukin (IL)-6, and tissue inhibitor of metalloproteinases-1 on days 8-9 aft
95 to analyze serum levels of hyaluronic acid, tissue inhibitor of metalloproteinases-1, and propeptide
100 ating factor, stromal cell-derived factor-1, tissue inhibitor of metalloproteinase 2, and von Willebr
101 rofibrotic (transforming growth factor beta, tissue inhibitor of metalloproteinase 2, collagen type I
104 ulinlike growth factor-binding protein 7 and tissue inhibitor of metalloproteinases 2 after surgery (
105 urnover: matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 2, C-terminal typ
107 ling was associated with decreased levels of tissue inhibitors of metalloproteinase 2, -3, and -4 and
110 nase-2/-9 exhibited little change, the large tissue inhibitor of metalloproteinase-2 (TIMP-2) increas
111 zymography), and cellular contents of MMP2, tissue inhibitor of metalloproteinase-2 (TIMP2), and pho
112 within 12 hours after admission, and urinary tissue inhibitor of metalloproteinase-2 and insulin-like
113 oduct of the G1-cell cycle arrest biomarkers tissue inhibitor of metalloproteinase-2 and insulin-like
115 r operating characteristic curve (95% CI) of tissue inhibitor of metalloproteinase-2 and insulin-like
116 the effect of nonrenal organ dysfunction on tissue inhibitor of metalloproteinase-2 and insulin-like
117 for each patient on enrollment and compared tissue inhibitor of metalloproteinase-2 and insulin-like
120 In multivariate analysis, the addition of tissue inhibitor of metalloproteinase-2 and insulin-like
121 he performance of the model with and without tissue inhibitor of metalloproteinase-2 and insulin-like
122 nfirmed the involvement of the MT1-MMP/MMP-2/tissue inhibitor of metalloproteinase-2 complex in this
124 these, matrix metalloproteinase-2 (MMP2) and tissue inhibitor of metalloproteinase-2 were down-regula
125 Our aim was to evaluate the performance of tissue inhibitor of metalloproteinase-2 x insulin-like g
126 tic performance of renal resistive index and tissue inhibitor of metalloproteinase-2 x insulin-like g
129 The performance of the urinary biomarker, tissue inhibitor of metalloproteinase-2 x insulin-like g
131 oMTb decreased expression of the inhibitors, tissue inhibitor of metalloproteinase-2, -3, and -4.
132 ne domain in the biosensor or treatment with tissue inhibitor of metalloproteinase-2, a cell-impermea
133 a membrane-associated factor, inhibited with tissue inhibitor of metalloproteinase-2, and abolished w
134 content, potentially through an increase in tissue inhibitor of metalloproteinase-2, and transmigrat
135 inhibition of proMMP-2 cleavage; recombinant tissue inhibitor of metalloproteinase-2, which binds to
136 crossed with transgenic mice overexpressing tissue inhibitor of metalloproteinase-2-a natural MMP in
138 y analysis examined the relationship between tissue inhibitor of metalloproteinases-2 ([TIMP-2]) and
141 an archetype member of the MMP family, binds tissue inhibitor of metalloproteinases-2 (TIMP-2), activ
144 to patients who exhibit an increased urinary tissue inhibitor of metalloproteinases-2 and insulin-lik
147 ischemic preconditioning to induce required [tissue inhibitor of metalloproteinases-2]*[insulin-like
149 e interventional part was change in urinary [tissue inhibitor of metalloproteinases-2]*[insulin-like
150 te ischemic preconditioning could stimulate [tissue inhibitor of metalloproteinases-2]*[insulin-like
151 esponse relationship on absolute changes in [tissue inhibitor of metalloproteinases-2]*[insulin-like
152 mic preconditioning significantly increased [tissue inhibitor of metalloproteinases-2]*[insulin-like
153 ic response in human articular chondrocytes, tissue inhibitor of metalloproteinase 3 (TIMP-3) inducti
156 ically, d-flow-induced miR-712 downregulates tissue inhibitor of metalloproteinase 3 (TIMP3) expressi
158 1 (ADAMTS1) and downregulated its inhibitor, tissue inhibitor of metalloproteinase 3 (TIMP3) in respo
159 in natural regulator of TACE activity is the tissue inhibitor of metalloproteinase 3 (Timp3), we hypo
160 e-wide association study; the locus near the tissue inhibitor of metalloproteinase 3 was corroborated
162 ecanase activity with monoclonal antibodies, tissue inhibitor of metalloproteinases 3 (TIMP-3), and c
163 recognized aggrecanases and their inhibitor, tissue inhibitor of metalloproteinases 3 (TIMP-3), in hu
169 ents with active AAV, but those of ADAM10 or tissue inhibitor of metalloproteinases 3, which inhibits
171 usly demonstrated in vitro that a variant of tissue inhibitor of metalloproteinase-3 ([-1A]TIMP3) inh
172 erative disorder, caused by mutations in the Tissue Inhibitor of Metalloproteinase-3 (TIMP3) gene.
173 ogenic effects by upregulating expression of tissue inhibitor of metalloproteinase-3 (TIMP3) in a P53
174 ssion events by delivering molecules such as tissue inhibitor of metalloproteinase-3 and angiopoietin
175 afforded by miR-181b inhibition are largely tissue inhibitor of metalloproteinase-3 dependent, while
176 To investigate whether miR-181b regulates tissue inhibitor of metalloproteinase-3 expression and a
177 hat miR-181b negatively regulates macrophage tissue inhibitor of metalloproteinase-3 expression and v
178 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
179 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
180 l-specific molecule-1, 5'-ecto-nucleotidase, tissue inhibitor of metalloproteinase-3, epidermal growt
181 uble Pref-1A is inhibited by TAPI-0 and by a tissue inhibitor of metalloproteinase-3, TIMP-3, that ca
187 ddition, CaPPS increased cartilage levels of tissue inhibitor of metalloproteinases-3 (TIMP-3), an en
188 ith pan-metalloproteinase inhibitors or with tissue inhibitors of metalloproteinase-3 reduced neurite
189 yl oxidase, adamalysin metalloproteinase-17, tissue inhibitors of metalloproteinase-3, c-Met and CXCR
192 and alterations in matrix metalloproteinase/tissue inhibitors of metalloproteinase abundance, consis
195 jor regulators of MMP-2 activity such as the tissue inhibitors of metalloproteinases and MMP-14.
196 e MMP-9 much less sensitive to inhibition by tissue inhibitors of metalloproteinases and synthetic in
197 cium-binding S100, matrix metalloproteinase, tissue inhibitor of metalloproteinase, and ion channel f
198 ring wing maturation, the Timp gene product, tissue inhibitor of metalloproteinases, and probably oth
199 reduced, pulmonary expression of collagens, tissue inhibitors of metalloproteinases, and fibrogenic
200 hich was caused by the reduced expression of tissue inhibitors of metalloproteinases as well as incre
201 ion of selected matrix metalloproteinases or tissue inhibitors of metalloproteinases between the woun
202 proteins (eg, matrix metalloproteinases and tissue inhibitor of metalloproteinases) compared with wi
203 f invasion-related genes including increased tissue inhibitors of metalloproteinases, decreased metal
205 isintegrin and metalloproteinase domain, and tissue inhibitors of metalloproteinases in M. tuberculos
206 hibition of metalloproteinases in mice using tissue inhibitors of metalloproteinases increases plaque
207 emically characterized MT6-MMP, profiled its tissue inhibitor of metalloproteinase inhibitory spectru
208 reover, small but significant alterations in tissue inhibitors of metalloproteinase levels also occur
209 otoxin variants or suggested by analogy with tissue inhibitors of metalloproteinases, progressively e
210 effects dependent on increased expression of tissue inhibitor of metalloproteinase-sensitive protease
211 inally, studies that either removed or added tissue inhibitor of metalloproteinases species in the my
213 1, matrix metalloproteinase (MMP)-2, MMP-14, tissue inhibitor of metalloproteinase (TIMP) -1, and TIM
214 and activity, concomitant with increases in tissue inhibitor of metalloproteinase (TIMP) 1 and E-cad
216 hemokine, and matrix metalloproteinase (MMP)/tissue inhibitor of metalloproteinase (TIMP) expression.
217 BARX2 also increases the expression of the tissue inhibitor of metalloproteinase (TIMP) genes, TIMP
218 ray Human MMP/TIMP Array to quantify MMP and tissue inhibitor of metalloproteinase (TIMP) production
219 between matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 and -2 an
221 ocyte chemoattractant protein (MCP)-1, IL-8, tissue inhibitor of metalloproteinase (TIMP)-1 and -2, a
222 increased the protein levels of HIF-1alpha, tissue inhibitor of metalloproteinase (TIMP)-1 and colla
223 rs, matrix metalloproteinase (MMP)-8, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and myelo
224 ysis of matrix metalloproteinase (MMP)-8 and tissue inhibitor of metalloproteinase (TIMP)-1 by enzyme
228 COX)-2, matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 were obta
230 e activation states of hepatic MMP-9, MMP-2, tissue inhibitor of metalloproteinase (TIMP)-1, TGF-beta
231 xpression of fibrin, collagen, TGF-beta, and tissue inhibitor of metalloproteinase (TIMP)-2 increased
232 mall interfering RNA suppression of pericyte tissue inhibitor of metalloproteinase (TIMP)-3 (a known
233 ition of TACE activity by specific inhibitor tissue inhibitor of metalloproteinase (TIMP)-3 at dosage
235 s of the matrix metalloproteinase inhibitor, tissue inhibitor of metalloproteinase (TIMP)-4, are asso
236 t growth factor (FGF)-3, its receptor FGFR3, tissue inhibitor of metalloproteinase (TIMP)-4, laminin
237 MP-9 enzyme were critically dependent on the tissue inhibitor of metalloproteinase (TIMP)-free status
240 if neutrophil proMMP-9, naturally devoid of tissue inhibitor of metalloproteinases (TIMP), was deliv
241 bit prometastatic matrix metalloproteinases, tissue inhibitor of metalloproteinases (TIMP)-1 has been
242 terleukin 8, hepatocyte growth factor (HGF), tissue inhibitor of metalloproteinases (TIMP)-1, and E-s
243 O), and matrix metalloproteinase (MMP)-2 and tissue inhibitor of metalloproteinases (TIMP)-2 complex.
247 the endogenous metalloproteinase inhibitor, tissue inhibitor of metalloproteinases (TIMP)-3, through
249 utrophil proMMP-9 required activation of the tissue inhibitor of metalloproteinases (TIMP)-free zymog
250 ng to PMN surfaces in a catalytically active tissue inhibitor of metalloproteinases (TIMP)-resistant
251 antitative real-time PCR analysis, levels of tissue inhibitor of metalloproteinases (TIMP-1 and TIMP-
252 , i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors of metalloproteinase (TIMP) -1 and TIM
253 P. acnes induced the mRNA expression of tissue inhibitors of metalloproteinase (TIMP)-1, the mai
256 ilizing a rat model of lung transplantation, tissue inhibitors of metalloproteinases (TIMP-1 and TIMP
257 ted lipocalin, cystatin C, trefoil factor 3, tissue inhibitor of metalloproteinase [TIMP]-1, and beta
258 MMP enzymatic activity is inhibited by the tissue inhibitor of metalloproteinase (TIMP1-4) family o
259 trix metalloproteinases (MMPs 12 and 13) and tissue inhibitor of metalloproteinases (TIMP1), as well
260 talloproteinase MMP2, in the presence of the tissue inhibitor of metalloproteinases TIMP2, constitute
261 ix metalloproteinases (MMPs) 1, 2, 3, and 9; tissue inhibitor of metalloproteinases (TIMPs) 1, 2, and
262 ed MT6-MMPs were found to be associated with tissue inhibitor of metalloproteinases (TIMPs) and did n
265 e expression of their natural inhibitor, the tissue inhibitor of metalloproteinases (TIMPs), are pote
266 , we profiled MMPs and their inhibitors, the tissue inhibitor of metalloproteinases (TIMPs), in sputu
267 pression of MT1-MMP in ECs or by addition of tissue inhibitor of metalloproteinases (TIMPs)-2, -3, an
270 derived matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinase (TIMPs) in cancer
271 MMP10, MMP13, and trypsin; inhibition by the tissue inhibitors of metalloproteinases (TIMPs) 1 and 2;
272 x metalloproteinases (MMPs) 1, 3, and 13 and tissue inhibitors of metalloproteinases (TIMPs) 1 and 3
277 sion of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) during t
280 pecific matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in the a
283 etalloproteinases (MMPs) and the activity of tissue inhibitors of metalloproteinases (TIMPs) is impli
284 vels of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) of HGFs
287 alloproteinases (Mmps) regulated by secreted tissue inhibitors of metalloproteinases (Timps), cleave
288 proteinases (MMPs) and their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), in the
289 and binding to their endogenous inhibitors, tissue inhibitors of metalloproteinases (TIMPs), is abno
290 between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), leading
291 Jawed vertebrates (Gnathostomes) have 4 tissue inhibitors of metalloproteinases (TIMPs), multifu
293 To understand the regulation of MMP-10 by tissue inhibitors of metalloproteinases (TIMPs), we have
299 s may be an effective method for discovering tissue inhibitor of metalloproteinase variants that disc
300 nes involved in tumor cell migration such as tissue inhibitors of metalloproteinases, were also incre