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1 stent with the properties of a membrane type matrix metalloprotease.
2 analysis suggests that the enzyme was a non-matrix metalloprotease.
3 grading the matrix through the activation of matrix metalloproteases.
4 ttractants, leukocyte adhesion proteins, and matrix metalloproteases.
5 wo compounds known as specific inhibitors of matrix metalloproteases.
6 ored precursor by incompletely characterized matrix metalloproteases.
7 n of p87 and was suppressed by inhibitors of matrix metalloproteases.
8 cluding decorin, collagens, fibronectin, and matrix metalloproteases.
9 d to inflammatory response and inhibition of matrix metalloproteases.
10 cleavage takes place on the cell surface by matrix metalloproteases.
11 epend on actin cytoskeletal dynamics but not matrix metalloproteases.
12 lation of miR-34a also altered expression of matrix metalloproteases 1 and 2, the mediators involved
14 roles of the upstream proteases thrombin and matrix metalloprotease-1 (MMP-1) in triggering PAR1-medi
19 tween the catalytic and hemopexin domains of matrix metalloprotease-1 (MMP1) on type 1 collagen fibri
21 ased levels of mRNA for two PAR1 activators, matrix metalloprotease-1 and Factor Xa, suggesting a mec
22 r necrosis factor-alpha-induced collagenase (matrix metalloprotease-1) gene expression in dermal fibr
23 in the expression of alpha1 type I collagen, matrix metalloprotease-1, and platelet-derived growth fa
24 fficiently secreted (>80%); are cleaved with matrix metalloprotease-1; inhibit NF-kappaB driven trans
25 ividuals with detectable tissue inhibitor of matrix-metalloprotease-1 (TIMP-1) had a 3.5-fold greater
29 obstruction of airways and higher levels of matrix metalloprotease-12 in sputa, suggesting that Pneu
33 dependent fashion, whereas it down-regulated matrix metalloprotease-13 (MMP13), thus favoring scarrin
34 ion markers, including alkaline phosphatase, matrix metalloproteases-13, osteocalcin, and runx2, and
35 at L1 interacts with the ANT binding partner matrix metalloprotease 14 (MMP14) and that the ANT prote
36 of ADAM17 (TNF-alpha converting enzyme) and matrix metalloprotease 14 caused by a reduction in the e
37 including Cadherin 6, CollagenXXValpha1, and Matrix metalloprotease 17, that are selectively expresse
39 h the activated form of purified recombinant matrix metalloprotease 2 (MMP-2) and had type IV collage
41 to a bioactive variant by incorporation of a matrix metalloprotease 2 (MMP-2) specific cleavage site
42 ed invadopodium function via upregulation of matrix metalloprotease 2 (MMP2) and MMP9 expression leve
43 loprotease 9 (MMP9) as well as activation of matrix metalloprotease 2 (MMP2) and MMP9, whereas the ED
44 MMP-12 inhibitor, was derived from a potent matrix metalloprotease 2 and 13 inhibitor via lead optim
45 sulted in decreased alphavbeta3 integrin and matrix metalloprotease 2, suggesting that the leptin sig
47 ion kinase phosphorylation and expression of matrix metalloproteases 2 and 9, both downstream mediato
50 tric oxide (NO) production, which stimulates matrix metalloprotease-2 (MMP-2) and MMP-9 activity in t
51 te an annexin V-dependent externalization of matrix metalloprotease-2 (MMP-2) for reconfiguring the e
52 gments (Fn-f) associated with the proform of matrix metalloprotease-2 (MMP-2) in conditioned medium o
56 Specific cleavage of laminin-5 (Ln-5) by matrix metalloprotease-2 (MMP2) was shown to induce migr
59 s of angiogenesis, including angiopoietin-1, matrix metalloprotease-2, and hypoxia-inducible factor 1
60 tified five common targets: tenascin-C(TNC), matrix metalloprotease-2, collagen-6-A1, mannosidase-alp
61 xpression of alpha-SMA, collagen alpha1 (I), matrix metalloprotease-2, or tissue inhibitor of metallo
64 orylation and slow degradation of lamin-A by matrix-metalloprotease-2 (MMP2), and inhibition of this
67 n is critically regulated by the activity of matrix metalloprotease 3 (MMP-3), in contrast to NMDAR-d
68 he nuclear factor kB-dependent activation of matrix metalloprotease 3 (MMP3/stromelysin1) was replica
71 ted by the use of inhibitors directed toward matrix metalloprotease 8, matrix metalloprotease 9, or p
72 The enzymes responsible for generating PGP, matrix metalloproteases 8 and -9 and prolyl endopeptidas
73 d in PGP generation from collagen, involving matrix metalloproteases 8 and 9 and prolyl endopeptidase
78 production, NO-dependent S-nitrosylation of matrix metalloprotease 9 (MMP9) as well as activation of
79 unteracted the effects of TGF-B1 by inducing matrix metalloprotease 9 (MMP9) expression while repress
82 ed an angiogenic response by upregulation of matrix metalloprotease 9 and endothelial and mesangial m
84 on, activation of p38MAPK, and production of matrix metalloprotease 9 are possible mechanisms for pro
85 (1607)-T(1608) peptide bond; cathepsin G and matrix metalloprotease 9 cleave VWF substrates at the Y(
86 ancer cells with a corresponding increase in matrix metalloprotease 9 enhanced hypoxia-induced GLUT1
88 , anti-inflammatory (IL-10), and fibrogenic (matrix metalloprotease 9) gene expression was increased
89 giogenic proteins like Galectin 3 and MMP-9 (Matrix Metalloprotease 9) in cervical carcinoma cells.
91 kout mouse, oxidative stress activated MMP9 (matrix metalloprotease 9) via its redox-responsive regul
92 P2 undergoes activity-dependent ES via MMP9 (matrix metalloprotease 9), and CNTNAP2-ecto levels are r
94 y response genes, including TNF-alpha, CCL3, matrix metalloprotease 9, integrin alpha(M), and Bcl-X i
97 regulating the Mr 92,000 type IV collagenase matrix metalloprotease-9 (MMP-9) and in vitro invasivene
98 d using BrdU incorporation and both TrkA and matrix metalloprotease-9 (MMP-9) expression were measure
99 sent study, we investigate the potential for matrix metalloprotease-9 (MMP-9), an endopeptidase secre
101 ressed the DMBA-induced cyclooxygenase-2 and matrix metalloprotease-9 expression in the breast tumor.
103 Infected Wsh mice had reduced amounts of matrix metalloprotease-9 in BALF and were resistant to e
105 vivo, sIL-6R and LPS augmented amniochorion matrix metalloprotease-9 release, whereas sgp130 opposed
107 [VEGF-A], stromal cell-derived factor-1, and matrix metalloprotease-9) and proangiogenic macrophage/m
111 sential for the efficient early induction of matrix metalloprotease-9, a known mediator of extracellu
112 xpression of basic fibroblast growth factor, matrix metalloprotease-9, and matrix metalloprotease-2.
113 ced NF-kappaB-dependent reporter gene and of matrix metalloprotease-9, cyclooxygenase-2, and cyclin D
115 as also necessary for TNF-induced release of matrix metalloprotease-9, thought to be an essential reg
120 pwise cascade of protease activation wherein matrix metalloproteases activate effector caspases, lead
122 uring invasion in Matrigel, the secretion of matrix metalloprotease activity and migration in a modif
123 Because osteonectin specifically enhances matrix metalloprotease activity in prostate and breast c
124 ficantly reduced tumor cell invasiveness and matrix metalloprotease activity in the coculture superna
125 Treatment with IL-1 significantly increased matrix metalloprotease activity in the conditioned media
126 astic fiber disruption with age, and vaginal matrix metalloprotease activity was increased significan
127 nse to TSP1 or its EGF-like repeats required matrix metalloprotease activity, including activity of m
130 The EGFR ligands are known substrates of the matrix metalloprotease ADAM17, suggesting stretch activa
131 e levels of collagenolytic activity of MMPs (matrix metalloproteases), along with a significant reduc
132 joints as well as by increased expression of matrix metalloproteases and bone-specific proteases.
134 th fibrosis and tissue remodeling, including matrix metalloproteases and collagen, were upregulated i
135 ctin-rich protrusive organelles that secrete matrix metalloproteases and degrade the extracellular ma
136 innate immune cells, elevated activities of matrix metalloproteases and increased angiogenesis and v
137 oactivator p300, preventing the induction of matrix metalloproteases and other p300-dependent genes r
138 facilitating invasion through expression of matrix metalloproteases and synthesis of interleukin 6 (
140 gment is generated at the plasma membrane by matrix metalloproteases and transferred to the cell nucl
141 en engineered requirements for activation by matrix metalloproteases and urokinase plasminogen activa
142 ystems-BMP-1/TLD (tolloid) (astacins), MMPs (matrix metalloproteases) and the ADAMs (disintegrin/meta
143 inly in the connective tissue (predominantly matrix metalloproteases) and, to some extent, in the epi
145 tin, TGF-beta1, collagen I, fibronectin, and matrix metalloproteases, and plasma PAI-1 levels correla
146 against other zinc-dependent enzymes such as matrix metalloproteases, and possessed limited cytotoxic
147 n and LPS up-regulate chemokines, cytokines, matrix metalloproteases, and PTGS/COX2, consistent with
148 expression of the M-CSF receptor c-Fms by a matrix metalloprotease- and MAPK-dependent mechanism.
150 nitiate dendrite breakage, and extracellular matrix metalloproteases are required to degrade the seve
152 g., for the thrombin receptor, inhibition of matrix metalloproteases blocked IL-8-mediated cell migra
153 ue-specific proteases, including complement, matrix metalloproteases, caspases, and granzymes, and ca
156 ted through an autocrine mechanism involving matrix metalloprotease-dependent release of heparin-bind
157 rends and selectivity profiles against other matrix metalloproteases despite their close structural s
158 o breach basement membrane in the absence of matrix metalloproteases during its developmental invasio
159 promoted invasiveness indirectly by inducing matrix metalloprotease enzyme 9 production, whereas drug
160 is a glycosylphosphatidyl inositol-anchored matrix metalloprotease expressed on the surface of cance
161 NF-a inhibited ND- and T2DM-DF migration and matrix metalloprotease expression to the same degree, al
162 geting metastatic spread using inhibitors of matrix metalloproteases failed to deliver the promise of
163 is cleaved by members of the disintegrin and matrix-metalloprotease family that are increased in the
164 os-dependent transcriptional activation of a matrix metalloprotease gene mmp1 downstream of JNK.
166 gh the role of selected serine proteases and matrix metalloproteases in chemokine processing has long
167 ermore, RNF213 down-regulated expressions of matrix metalloproteases in endothelial cells, but not in
168 strated that TWEAK induced the production of matrix metalloproteases in human chondrocytes and potent
170 uggest that although activation of all known matrix metalloproteases in vitro is accomplished by prot
171 nally, studies using selective inhibitors of matrix metalloproteases indicated that they and heparin-
172 s, we found that targeting the extracellular matrix metalloprotease inducer (EMMPRIN) by injecting na
173 y mediators that stimulate the production of matrix metalloprotease, inflammatory cell recruitment, a
174 -plasmin, an inhibitor of plasmin, or by the matrix metalloprotease inhibitor 1,10 phenanthroline.
175 A key intermediate in the synthesis of a matrix metalloprotease inhibitor has been achieved using
181 e relationship of Pneumocystis colonization, matrix metalloprotease levels in sputum, and airway obst
182 regulatory pathways involving inhibition of matrix metalloproteases, liver X receptor/retinoid X rec
183 e proteins in PDAC tumours and revealed that matrix-metalloprotease-mediated shedding of the AXL rece
184 urther analysis highlighted induction of the matrix metalloprotease MMP-10 and the extracellular matr
188 showed that exogenous addition of activated matrix metalloprotease (MMP) 2 stimulates migration onto
189 lox/flox) mice is characterized by excessive matrix metalloprotease (MMP) activity, reduced lung elas
190 onents of the plasminogen activator (PA) and matrix metalloprotease (MMP) cascade have been character
191 d according to the need of the cell by using matrix metalloprotease (MMP) cleavable peptide sequences
192 we explored how the epigenome contributes to matrix metalloprotease (MMP) dysregulation impacting tum
194 Young and aged mice were treated with a matrix metalloprotease (MMP) inhibitor and systemic sFas
195 howed that cold causes actin disassembly and matrix metalloprotease (MMP) secretion by SEC, we also q
197 We now identify the metalloprotease MT1-matrix metalloprotease (MMP), an integral membrane prote
198 vity caused the expression and activation of matrix metalloprotease (MMP)-1 and MMP-9, which in turn
203 on of angiogenesis ( approximately 40%) in a matrix metalloprotease (MMP)-2-deficient mouse compared
204 oth the expression and enzymatic activity of matrix metalloprotease (MMP)-9 and MMP-2, two pro-angiog
206 onths and were analysed for a panel of novel matrix metalloprotease (MMP)-degraded ECM proteins, by E
208 cell interfaces accompanied by inhibition of matrix metalloprotease (MMP)-dependent shedding of the D
209 In response to PR-induced Wnt-1 signaling, matrix metalloprotease (MMP)-mediated membrane-proximal
210 ole of biomaterial design in BMP delivery, a matrix metalloprotease (MMP)-sensitive hyaluronic acid (
215 ibition results in a significant increase in matrix metalloproteases (MMP)-2 and membrane-type 1-MMP
222 increase in the activity of membrane type-1 matrix metalloprotease (MMP14, MT1-MMP) by heterotrimeri
223 ribes the characterization of the Drosophila matrix metalloprotease Mmp2 as an extracellular inhibito
224 markers FN, Snail, N-cadherin, vimentin, the matrix metalloprotease MMP2, alpha-smooth muscle actin a
225 matory responses such as upregulation of the matrix metalloprotease MMP9, and increases angiogenesis
227 ulated induction, in cardiac fibroblasts, of matrix metalloproteases (MMPs) 9 and 13-MMPs linked to g
229 atrix-degrading enzyme expression, including matrix metalloproteases (MMPs) and a disintegrin-like an
247 an-1 cleavage is mediated by upregulation of matrix metalloproteases (MMPs) that accompanies higher H
248 ACE inhibition, but reducing potency against matrix metalloproteases (MMPs) thus increasing overall s
251 been synthesized, evaluated as inhibitors of matrix metalloproteases (MMPs), and found to display rem
253 d t-SP depends on extracellular signaling by matrix metalloproteases (MMPs), but it is unknown how th
254 rface of cells is sensitive to cleavage with matrix metalloproteases (MMPs), this study examined whet
256 arge variety of mediators, including several matrix metalloproteases (MMPs), which participate in fib
260 ate the extracellular levels of gelatinases (matrix metalloproteases, MMPs) and potentially influence
261 ses, including neutrophil elastase and MMPs (matrix metalloproteases), modulate cell signaling, infla
262 anges in macrophage cytokine, chemokine, and matrix metalloprotease mRNA, and protein-inducing mediat
266 crovesicle cargo such as the membrane-type 1 matrix metalloprotease (MT1-MMP) to shedding microvesicl
267 n secretion from the cell by membrane type 1 matrix metalloprotease (MT1-MMP), affording the 8 and 5
268 ity, dependent on the enzyme membrane type I matrix metalloprotease (MT1-MMP), and that DC transientl
269 s (EECs) of critical cargos (membrane-type 1 matrix metalloprotease [MT1-MMP] and beta3 integrin) req
270 b27-dependent recycling of the transmembrane matrix metalloprotease, MT1-MMP to promote invasive beha
272 ed to serine hydrolases, cysteine proteases, matrix metalloproteases, nitrilases, caspases, and histo
274 ificantly inhibit the 10 most abundant human matrix metalloproteases or complement-mediated cell lysi
277 mitogenesis of articular cells and stimulate matrix metalloprotease production, thus promoting degrad
279 in vivo and that inhibition of ROCK but not matrix-metalloproteases reduces cancer cell motility in
282 cue-induced synaptic enlargement depends on matrix metalloprotease signaling in the extracellular ma
284 ptides, peptide hormones, growth factors and matrix metalloprotease substrates, neuropeptides, amyloi
287 Type IV 72-kDa collagenase is one of the matrix metalloproteases that has been implicated in diff
289 imilar to that found in tissue inhibitors of matrix metalloproteases (TIMPs) and in complement factor
290 I), as well as by an endogenous inhibitor of matrix metalloproteases, tissue inhibitor of metalloprot
291 ate that NG2+ cells, but not astrocytes, use matrix metalloproteases to extend across a region of inh
292 d their shared susceptibility to cleavage by matrix metalloproteases to generate circulating collagen
295 s, including chemokines, growth factors, and matrix metalloproteases, was increased, a signature rese
296 pus, including the up-regulation of multiple matrix metalloproteases, which are known to be critical
298 phosphorylation of DDRs is known to activate matrix metalloproteases, which in turn cleave the ECM.
300 ealed that the protrusion is enriched in the matrix metalloprotease ZMP-1 and transiently expands AC