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1 e metalloproteinase interaction sites of the tissue inhibitors of metalloproteinases.
2 alloproteinases in a manner analogous to the tissue inhibitors of metalloproteinases.
3 MPs) is relatively unopposed by the specific tissue inhibitors of metalloproteinases.
4 transforming growth factor beta1 (P=0.0004), tissue inhibitor of metalloproteinase 1 (P=0.0009), gran
5 oteinase 9 (MMP-9) and increased circulating tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
6 91(phox(-/-) ) than in WT mice after CCl(4.) Tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
8 including COX-2 itself, lipocalin 2 (LCN2), tissue inhibitor of metalloproteinase 1 (TIMP-1), interl
9 expression of fibrogenic genes IL-1beta and tissue inhibitor of metalloproteinase 1 (TIMP-1), with t
11 oducts (collagen type 1 alpha 1 (CoL1A1) and tissue inhibitor of metalloproteinase 1 (TIMP1)) were al
13 8 (IL-8), human beta-defensin 1 (hBD-1), and tissue inhibitor of metalloproteinase 1 and 2 (TIMP-1 an
14 MP-1 was up-regulated, whereas expression of tissue inhibitor of metalloproteinase 1 decreased before
15 factor-beta1, alpha-smooth muscle actin, and tissue inhibitor of metalloproteinase 1 expression and a
16 ries of Dicer(d/d) mice partially normalized tissue inhibitor of metalloproteinase 1 expression and C
17 s after biliary decompression, both MMP3 and tissue inhibitor of metalloproteinase 1 expression decli
18 ate cells (HSCs) were activated and produced tissue inhibitor of metalloproteinase 1 in a sphingosine
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 ns of prostaglandin-endoperoxide synthase 2, tissue inhibitor of metalloproteinase 1, Dpp4, nitric ox
25 increased messenger RNA levels of collagen, tissue inhibitor of metalloproteinase 1, matrix metallop
26 reases levels of their endogenous inhibitor, tissue inhibitor of metalloproteinase 1, resulting in ma
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 explants induced synthesis and secretion of tissue inhibitor of metalloproteinases 1 (TIMP-1), which
37 faip6), matrix metalloproteinase 19 (Mmp19), tissue inhibitor of metalloproteinases 1 (Timp1), and po
38 MMP-9), and the inhibitors of these enzymes (tissue inhibitor of metalloproteinases 1 [TIMP-1] and TI
39 prometastatic matrix metalloproteinase 8 and tissue inhibitor of metalloproteinases 1 in metastatic n
40 DAMTS-5 increased approximately 40-fold, and tissue inhibitor of metalloproteinases 1 increased appro
41 mor necrosis factor receptor 2 or IL-10, and tissue inhibitor of metalloproteinases 1) were identifie
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
49 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
51 is substantially resistant to inhibition by tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIM
56 lagen I type I, fibronectin, COL1alpha1, and tissue inhibitor of metalloproteinase-1 (TIMP-1) were in
57 treated with IL-1beta express high levels of tissue inhibitor of metalloproteinase-1 (TIMP-1), an imp
58 rix metalloproteinase-2 and 9 (MMP-2 and 9), tissue inhibitor of metalloproteinase-1 (TIMP-1), macrop
59 who underwent routine measurements of plasma tissue inhibitor of metalloproteinase-1 (TIMP-1), metall
60 sults, in part, from increased expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), which
64 smooth muscle actin (alphaSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIMP1) and tran
66 -type plasminogen activator while increasing tissue inhibitor of metalloproteinase-1 and plasminogen
67 teinase-2 and -9 but was linked to decreased tissue inhibitor of metalloproteinase-1 and plasminogen
68 th a balance between metalloproteinase-8 and tissue inhibitor of metalloproteinase-1 expressions.
69 ase-8 expression and decreased expression of tissue inhibitor of metalloproteinase-1 in pulmonary acu
72 , whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regula
73 owth factor receptor beta, desmin, vimentin, tissue inhibitor of metalloproteinase-1) and fibrosis (r
74 and Lix/CXCL-5), matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and apoptosis r
75 s syndrome); and matrix metalloproteinase-3, tissue inhibitor of metalloproteinase-1, and CXCL13 in A
77 with gene expression for alpha2(I) collagen, tissue inhibitor of metalloproteinase-1, and transformin
78 n expression of MMP-1, collagen type 1alpha, tissue inhibitor of metalloproteinase-1, and vascular re
79 nogen activator inhibitor (PAI)-1, vimentin, tissue inhibitor of metalloproteinase-1, fibronectin, gr
87 is via its transcriptional regulation of the tissue inhibitor of metalloproteinases-1 (TIMP-1) gene.
88 role in extracellular matrix remodeling, the tissue inhibitor of metalloproteinases-1 (TIMP-1) has be
94 al injury including Cystatin C, Osteopontin, Tissue Inhibitor of Metalloproteinases-1 (TIMP1), beta2-
96 protein-10 (IP-10), interleukin (IL)-6, and tissue inhibitor of metalloproteinases-1 on days 8-9 aft
97 to analyze serum levels of hyaluronic acid, tissue inhibitor of metalloproteinases-1, and propeptide
103 ating factor, stromal cell-derived factor-1, tissue inhibitor of metalloproteinase 2, and von Willebr
104 rofibrotic (transforming growth factor beta, tissue inhibitor of metalloproteinase 2, collagen type I
106 proteinases (MT1-MMP) in the presence of the tissue inhibitor of metalloproteinases 2 (TIMP2) in a bu
108 ulinlike growth factor-binding protein 7 and tissue inhibitor of metalloproteinases 2 after surgery (
109 urnover: matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 2, C-terminal typ
111 ling was associated with decreased levels of tissue inhibitors of metalloproteinase 2, -3, and -4 and
114 nase-2/-9 exhibited little change, the large tissue inhibitor of metalloproteinase-2 (TIMP-2) increas
115 zymography), and cellular contents of MMP2, tissue inhibitor of metalloproteinase-2 (TIMP2), and pho
117 r operating characteristic curve (95% CI) of tissue inhibitor of metalloproteinase-2 and insulin-like
118 the effect of nonrenal organ dysfunction on tissue inhibitor of metalloproteinase-2 and insulin-like
119 for each patient on enrollment and compared tissue inhibitor of metalloproteinase-2 and insulin-like
122 In multivariate analysis, the addition of tissue inhibitor of metalloproteinase-2 and insulin-like
123 he performance of the model with and without tissue inhibitor of metalloproteinase-2 and insulin-like
124 nfirmed the involvement of the MT1-MMP/MMP-2/tissue inhibitor of metalloproteinase-2 complex in this
126 fibronectin, matrix metalloproteinase-2, and tissue inhibitor of metalloproteinase-2 was studied with
127 these, matrix metalloproteinase-2 (MMP2) and tissue inhibitor of metalloproteinase-2 were down-regula
128 oMTb decreased expression of the inhibitors, tissue inhibitor of metalloproteinase-2, -3, and -4.
129 ne domain in the biosensor or treatment with tissue inhibitor of metalloproteinase-2, a cell-impermea
130 a membrane-associated factor, inhibited with tissue inhibitor of metalloproteinase-2, and abolished w
131 content, potentially through an increase in tissue inhibitor of metalloproteinase-2, and transmigrat
132 inhibition of proMMP-2 cleavage; recombinant tissue inhibitor of metalloproteinase-2, which binds to
133 crossed with transgenic mice overexpressing tissue inhibitor of metalloproteinase-2-a natural MMP in
137 an archetype member of the MMP family, binds tissue inhibitor of metalloproteinases-2 (TIMP-2), activ
144 ic response in human articular chondrocytes, tissue inhibitor of metalloproteinase 3 (TIMP-3) inducti
146 ically, d-flow-induced miR-712 downregulates tissue inhibitor of metalloproteinase 3 (TIMP3) expressi
148 1 (ADAMTS1) and downregulated its inhibitor, tissue inhibitor of metalloproteinase 3 (TIMP3) in respo
150 in natural regulator of TACE activity is the tissue inhibitor of metalloproteinase 3 (Timp3), we hypo
151 e-wide association study; the locus near the tissue inhibitor of metalloproteinase 3 was corroborated
153 ecanase activity with monoclonal antibodies, tissue inhibitor of metalloproteinases 3 (TIMP-3), and c
154 recognized aggrecanases and their inhibitor, tissue inhibitor of metalloproteinases 3 (TIMP-3), in hu
160 ents with active AAV, but those of ADAM10 or tissue inhibitor of metalloproteinases 3, which inhibits
162 se inhibitor-2 (TAPI-2), phenanthroline, and tissue inhibitor of metalloproteinase-3 (TIMP-3) but not
164 ogenic effects by upregulating expression of tissue inhibitor of metalloproteinase-3 (TIMP3) in a P53
165 ssion events by delivering molecules such as tissue inhibitor of metalloproteinase-3 and angiopoietin
166 afforded by miR-181b inhibition are largely tissue inhibitor of metalloproteinase-3 dependent, while
167 To investigate whether miR-181b regulates tissue inhibitor of metalloproteinase-3 expression and a
168 hat miR-181b negatively regulates macrophage tissue inhibitor of metalloproteinase-3 expression and v
169 ive CXCR2 ligand GROalpha (10 ng/ml) induced tissue inhibitor of metalloproteinase-3 expression, mark
171 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
172 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
173 l-specific molecule-1, 5'-ecto-nucleotidase, tissue inhibitor of metalloproteinase-3, epidermal growt
174 uble Pref-1A is inhibited by TAPI-0 and by a tissue inhibitor of metalloproteinase-3, TIMP-3, that ca
181 ddition, CaPPS increased cartilage levels of tissue inhibitor of metalloproteinases-3 (TIMP-3), an en
183 ith pan-metalloproteinase inhibitors or with tissue inhibitors of metalloproteinase-3 reduced neurite
184 yl oxidase, adamalysin metalloproteinase-17, tissue inhibitors of metalloproteinase-3, c-Met and CXCR
187 trix metalloproteinase-2 (MMP-2), MMP-9, and tissue inhibitor of metalloproteinase-4 (TIMP-4) in lung
188 and alterations in matrix metalloproteinase/tissue inhibitors of metalloproteinase abundance, consis
191 jor regulators of MMP-2 activity such as the tissue inhibitors of metalloproteinases and MMP-14.
192 e MMP-9 much less sensitive to inhibition by tissue inhibitors of metalloproteinases and synthetic in
193 cium-binding S100, matrix metalloproteinase, tissue inhibitor of metalloproteinase, and ion channel f
194 ring wing maturation, the Timp gene product, tissue inhibitor of metalloproteinases, and probably oth
195 reduced, pulmonary expression of collagens, tissue inhibitors of metalloproteinases, and fibrogenic
196 hich was caused by the reduced expression of tissue inhibitors of metalloproteinases as well as incre
197 ion of selected matrix metalloproteinases or tissue inhibitors of metalloproteinases between the woun
198 proteins (eg, matrix metalloproteinases and tissue inhibitor of metalloproteinases) compared with wi
199 lated by M. tuberculosis, and no increase in tissue inhibitor of metalloproteinase expression occurs
201 isintegrin and metalloproteinase domain, and tissue inhibitors of metalloproteinases in M. tuberculos
202 hibition of metalloproteinases in mice using tissue inhibitors of metalloproteinases increases plaque
203 emically characterized MT6-MMP, profiled its tissue inhibitor of metalloproteinase inhibitory spectru
204 reover, small but significant alterations in tissue inhibitors of metalloproteinase levels also occur
205 otoxin variants or suggested by analogy with tissue inhibitors of metalloproteinases, progressively e
206 effects dependent on increased expression of tissue inhibitor of metalloproteinase-sensitive protease
207 inally, studies that either removed or added tissue inhibitor of metalloproteinases species in the my
208 1, matrix metalloproteinase (MMP)-2, MMP-14, tissue inhibitor of metalloproteinase (TIMP) -1, and TIM
209 and activity, concomitant with increases in tissue inhibitor of metalloproteinase (TIMP) 1 and E-cad
211 radation, matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) expression,
212 hemokine, and matrix metalloproteinase (MMP)/tissue inhibitor of metalloproteinase (TIMP) expression.
213 it differential inhibition by members of the tissue inhibitor of metalloproteinase (TIMP) family.
214 BARX2 also increases the expression of the tissue inhibitor of metalloproteinase (TIMP) genes, TIMP
215 ray Human MMP/TIMP Array to quantify MMP and tissue inhibitor of metalloproteinase (TIMP) production
216 between matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 and -2 an
218 ocyte chemoattractant protein (MCP)-1, IL-8, tissue inhibitor of metalloproteinase (TIMP)-1 and -2, a
219 increased the protein levels of HIF-1alpha, tissue inhibitor of metalloproteinase (TIMP)-1 and colla
220 ysis of matrix metalloproteinase (MMP)-8 and tissue inhibitor of metalloproteinase (TIMP)-1 by enzyme
225 e activation states of hepatic MMP-9, MMP-2, tissue inhibitor of metalloproteinase (TIMP)-1, TGF-beta
226 lysis revealed a selective downregulation of tissue inhibitor of metalloproteinase (TIMP)-2 in PmAF a
227 xpression of fibrin, collagen, TGF-beta, and tissue inhibitor of metalloproteinase (TIMP)-2 increased
228 mall interfering RNA suppression of pericyte tissue inhibitor of metalloproteinase (TIMP)-3 (a known
229 ition of TACE activity by specific inhibitor tissue inhibitor of metalloproteinase (TIMP)-3 at dosage
231 s of the matrix metalloproteinase inhibitor, tissue inhibitor of metalloproteinase (TIMP)-4, are asso
232 t growth factor (FGF)-3, its receptor FGFR3, tissue inhibitor of metalloproteinase (TIMP)-4, laminin
233 MP-9 enzyme were critically dependent on the tissue inhibitor of metalloproteinase (TIMP)-free status
235 (uPA), matrix metalloproteinase (MMP)14, and tissue inhibitor of metalloproteinase (TIMP-2) were cons
237 if neutrophil proMMP-9, naturally devoid of tissue inhibitor of metalloproteinases (TIMP), was deliv
238 bit prometastatic matrix metalloproteinases, tissue inhibitor of metalloproteinases (TIMP)-1 has been
239 terleukin 8, hepatocyte growth factor (HGF), tissue inhibitor of metalloproteinases (TIMP)-1, and E-s
241 O), and matrix metalloproteinase (MMP)-2 and tissue inhibitor of metalloproteinases (TIMP)-2 complex.
245 the endogenous metalloproteinase inhibitor, tissue inhibitor of metalloproteinases (TIMP)-3, through
247 utrophil proMMP-9 required activation of the tissue inhibitor of metalloproteinases (TIMP)-free zymog
248 antitative real-time PCR analysis, levels of tissue inhibitor of metalloproteinases (TIMP-1 and TIMP-
249 , i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors of metalloproteinase (TIMP) -1 and TIM
250 P. acnes induced the mRNA expression of tissue inhibitors of metalloproteinase (TIMP)-1, the mai
252 balance between metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) has been
254 ilizing a rat model of lung transplantation, tissue inhibitors of metalloproteinases (TIMP-1 and TIMP
255 ted lipocalin, cystatin C, trefoil factor 3, tissue inhibitor of metalloproteinase [TIMP]-1, and beta
256 trix metalloproteinases (MMPs 12 and 13) and tissue inhibitor of metalloproteinases (TIMP1), as well
257 talloproteinase MMP2, in the presence of the tissue inhibitor of metalloproteinases TIMP2, constitute
258 ix metalloproteinases (MMPs) 1, 2, 3, and 9; tissue inhibitor of metalloproteinases (TIMPs) 1, 2, and
259 ed MT6-MMPs were found to be associated with tissue inhibitor of metalloproteinases (TIMPs) and did n
262 e expression of their natural inhibitor, the tissue inhibitor of metalloproteinases (TIMPs), are pote
263 , we profiled MMPs and their inhibitors, the tissue inhibitor of metalloproteinases (TIMPs), in sputu
264 pression of MT1-MMP in ECs or by addition of tissue inhibitor of metalloproteinases (TIMPs)-2, -3, an
267 derived matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinase (TIMPs) in cancer
268 MMP10, MMP13, and trypsin; inhibition by the tissue inhibitors of metalloproteinases (TIMPs) 1 and 2;
269 x metalloproteinases (MMPs) 1, 3, and 13 and tissue inhibitors of metalloproteinases (TIMPs) 1 and 3
275 sion of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) during t
279 pecific matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in the a
282 etalloproteinases (MMPs) and the activity of tissue inhibitors of metalloproteinases (TIMPs) is impli
283 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 2)-induced decrease in lymphocyte-associated tissue inhibitors of metalloproteinases (TIMPs), resulti
293 To understand the regulation of MMP-10 by tissue inhibitors of metalloproteinases (TIMPs), we have
298 metalloproteinases (MMPs), their inhibitors (tissue inhibitors of metalloproteinases; TIMPs), and the
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
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