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1 d increases in the elastin-degrading enzyme, matrix metalloproteinase 2.
2 ail1, plasminogen activator inhibitor 1, and matrix metalloproteinase 2.
3 ated with reduction of the metalloproteinase matrix metalloproteinase 2.
4 y cell migration through upregulation of pro-matrix metalloproteinase 2.
5  with cellular retinol-binding protein 1 and matrix metalloproteinase 2.
6 wth factor receptor-1, protein kinase C, and matrix metalloproteinase 2.
7 egulators C-terminal tensin-like protein and matrix metalloproteinase 2.
8 and metastasis and inhibited the activity of matrix metalloproteinase-2.
9 ation sphingolipid G-protein receptor-1, and matrix metalloproteinase-2.
10 oproteinase inducer), to activate Akt1/2 and matrix metalloproteinase-2.
11 stant to breakdown by both collagenase D and matrix metalloproteinase-2.
12 trix metalloproteinase-2/tissue inhibitor of matrix metalloproteinase-2.
13 d beta3 integrins, and the production of pro-matrix metalloproteinase-2.
14 g upregulation of its downstream target gene matrix metalloproteinase-2.
15 increased fibrosis and altered expression of matrix metalloproteinase-2.
16 tracellular signal-regulated kinase 1/2, and matrix metalloproteinase-2.
17 17.8 [14.1-22.8] ng/mL) were higher, and for matrix metalloproteinase-2 (188 [155.5-230.6] ng/mL) low
18 r, double knockouts of apolipoprotein E with matrix metalloproteinase 2, 3, 7, 9, 12, and 13 have mor
19 ion of exogenous metalloproteases, including matrix metalloproteinases 2, 3, 8, 9, 12, and 13 and agg
20 , along with early upregulated expression of matrix metalloproteinases-2, -3, -9, -13, -14, and their
21 reased expression of messenger RNAs encoding matrix metalloproteinase-2, -9, and -12, and cathepsins
22 tions in strial expression of mRNAs encoding matrix metalloproteinases-2, -9, -12, and -14.
23 y decreased by pharmacological inhibition of matrix metalloproteinase 2/9 activity.
24 lution in vivo using a fluorescent probe for matrix metalloproteinase-2/9 activity, fluorescein isoth
25  changes appear to be caused by increases in matrix metalloproteinase-2/9 secretion and transforming
26 sion was associated with increased levels of matrix metalloproteinase-2/9 transcripts.
27  eHsp90 promoted cell motility in an ERK and matrix metalloproteinase-2/9-dependent manner, and shift
28 e senescence-associated secretory phenotype (matrix metalloproteinases-2/9, C-X-C motif chemokine lig
29                       Although activation of matrix metalloproteinase-2/-9 exhibited little change, t
30 actor (EGF) receptor, and (ii) expression of matrix metalloproteinase 2, a pro-invasive factor for tu
31                                 Furthermore, matrix metalloproteinase-2, a downstream target of beta-
32 nd was associated with the downregulation of matrix metalloproteinase-2, a known FoxM1 target.
33 aphy indicated increased secretion of active matrix metalloproteinase-2, a mediator of cell migration
34    As fibrillar type I collagen promotes pro-matrix metalloproteinase 2 activation by membrane type 1
35  cultures with 14G2a mAb showed decreases in matrix metalloproteinase-2 activation, a process regulat
36                Blockade of TFPI-2 suppressed matrix metalloproteinase-2 activation, and, therefore, T
37 beta responses, but inhibited leptin-induced matrix metalloproteinase-2 activation.
38 lar CypA are required for ROS generation and matrix metalloproteinase-2 activation.
39 at correlated with significant decreased pro-matrix metalloproteinase-2 activation.
40  asphyxiated neonates and is associated with matrix metalloproteinase-2 activation.
41 nds and is required for motility by inducing matrix metalloproteinase 2 activity, but phospho-extrace
42 se 1 messenger RNA expression, and increased matrix metalloproteinase 2 activity.
43 pendent mitochondrial Ca(2+) uptake promotes matrix metalloproteinase-2 activity and cell motility by
44 ese aneurysms and is associated with reduced matrix metalloproteinase-2 activity and diminished plasm
45 fter aortic cross-clamp release to determine matrix metalloproteinase-2 activity and troponin I level
46 cycline-treated piglets had lower myocardial matrix metalloproteinase-2 activity compared with contro
47 wed EGCG inhibits IL-6/soluble IL-6R-induced matrix metalloproteinase-2 activity in RA synovial fibro
48 ycline group (p = 0.01), and the increase of matrix metalloproteinase-2 activity in the placebo group
49 h cardiopulmonary bypass, it reduced cardiac matrix metalloproteinase-2 activity in these patients.
50 ndary to edema, we found that suppression of matrix metalloproteinase-2 activity is sufficient to abr
51  demonstrate elevated PI3K/Akt signaling and matrix metalloproteinase-2 activity that culminates in e
52 ith cardiopulmonary bypass, increased atrial matrix metalloproteinase-2 activity was inversely correl
53                               Cardiac 72-kDa matrix metalloproteinase-2 activity was lower upon reper
54                                   Myocardial matrix metalloproteinase-2 activity was quantified by ge
55 addition, aortic macrophage infiltration and matrix metalloproteinase-2 activity were reduced in apoE
56 n kinase C activation, actin polymerization, matrix metalloproteinase-2 activity, and astrocytoma mot
57 ymographic analysis and quantified by active matrix metalloproteinase-2 activity, as well as apoptosi
58 radiation concomitant with the inhibition of matrix metalloproteinase-2 activity, down-regulation of
59 f alternative activation, iii) cytokine, iv) matrix metalloproteinase-2 activity, v) fibrosis, and vi
60 crotaline-induced matrix metalloproteinase-9/matrix metalloproteinase-2 activity.
61 proteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degrad
62 sulted in the upregulation of genes, such as matrix metalloproteinase-2, alkaline phosphatase, and tr
63 sed expression and proteolytic activities of matrix metalloproteinase-2, an enzyme that releases angi
64 mals (P < 0.05), resulting in a reduction of matrix metalloproteinase 2 and 9 activity in resolvin-tr
65 s markers for cell proliferation, as well as matrix metalloproteinase 2 and 9 for invasion.
66 on, extracellular matrix reorganization, and matrix metalloproteinase 2 and hyaluronic acid productio
67                              Upregulation of matrix metalloproteinase 2 and proinflammatory cytokines
68 a) gene and protein expression and decreased matrix metalloproteinase 2 and tissue inhibitor of matri
69 ons with half-maximal inhibition (IC(50)) of matrix metalloproteinase- 2 and -9 (MMP-2 and -9).
70 TSP1) repeats are CCN1 degradome products by matrix metalloproteinase-2 and -14.
71 f ARF1 and Arfaptin2 leading to secretion of matrix metalloproteinase-2 and -7.
72  Near-apneic group showed significantly less matrix metalloproteinase-2 and -9 activity.
73  myocardial collagen content and accentuated matrix metalloproteinase-2 and -9 activity.
74 ardial fibrosis, downregulated expression of matrix metalloproteinase-2 and -9 and decreased gelatina
75 xplained by changes in mRNA of TGF-beta1 and matrix metalloproteinase-2 and -9 but was linked to decr
76  complex directly induced gene expression of matrix metalloproteinase-2 and -9 in vitro, which requir
77   A monoclonal antibody was raised against a matrix metalloproteinase-2 and -9 specific cleavage site
78          Enzyme zymography showed attenuated matrix metalloproteinase-2 and -9 up-regulation post-MI
79 ssue growth factor, fibronectin, collagen-1, matrix metalloproteinase-2 and -9), enhanced cell death
80 tor stimulation increased activation of both matrix metalloproteinase-2 and -9.
81                                Expression of matrix metalloproteinase-2 and 9 (MMP-2 and 9), tissue i
82 -1 signals, transcripts for the AP-1 target, matrix metalloproteinase-2 and associated invasive behav
83            Patients with HFpEF showed higher matrix metalloproteinase-2 and C-terminal propeptide of
84 ine called S-SDF-1(S4V) that is resistant to matrix metalloproteinase-2 and exopeptidase cleavage but
85 lls with a trend for decreased expression of matrix metalloproteinase-2 and increased expression of t
86     RAD001 also attenuated the expression of matrix metalloproteinase-2 and inhibited the invasivenes
87 ow-mediated dilation of the brachial artery, matrix metalloproteinase-2 and matrix metalloproteinase-
88 structure content, the col 2 domain of human matrix metalloproteinase-2 and the kringle 2 domain of h
89 ls via reduced transcriptional activities of matrix metalloproteinase-2 and urokinase-type plasminoge
90 lanoma cells by modulating the activities of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).
91 tility of prostate tumor cells by activating matrix metalloproteinases 2 and 9 (MMP2 and MMP9) in vit
92 -derived growth factor D, Pdgfrb, Itga2, and matrix metalloproteinases 2 and 9 expression in aortic l
93 or dimerization, and increased expression of matrix metalloproteinases 2 and 9 in an EGF receptor-dep
94 expression was accompanied by an increase of matrix metalloproteinases 2 and 9 in mice treated with a
95           We also observed the activation of matrix metalloproteinases 2 and 9 upon CXCL12 stimulatio
96 xenografted with human tumor cells secreting matrix metalloproteinases 2 and 9, ACPPs bearing a far-r
97 ssion of urokinase plasminogen activator and matrix metalloproteinases 2 and 9, and increased podocyt
98 ificantly attenuated the increased levels of matrix metalloproteinases 2 and 9, chemokines (KC, TARC)
99 osure to tumor-associated proteases, such as matrix metalloproteinases 2 and 9, the coiled-coil pepti
100 including collagen 1 and 3, fibronectin, and matrix metalloproteinases 2 and 9, were up-regulated in
101               The expression and activity of matrix metalloproteinases 2 and 9, which participate in
102 protein kinase A, protein phosphatase-1, and matrix metalloproteinases 2 and 9.
103 a signaling pathway in a mechanism involving matrix metalloproteinases 2 and 9.
104 factor, urokinase plasminogen activator, and matrix metalloproteinases 2 and 9.
105 creased the tubulointerstitial expression of matrix metalloproteinases 2 and 9.
106 l growth factor (VEGF) A, interleukin-8, and matrix metalloproteinases-2 and -9 and had a high vascul
107 s (vascular endothelial growth factor, VEGF; matrix metalloproteinases-2 and -9), and nucleolin (a nu
108 es, contractile myofibroblasts, glial cells, matrix metalloproteinases-2 and -9, and collagen type I,
109 ns COX-2, cyclin D1, cytosolic beta-catenin, matrix metalloproteinases-2 and -9, and vascular endothe
110  as striking reductions in the production of matrix metalloproteinases-2 and -9.
111 ntervening linker is cut by tumor-associated matrix metalloproteinases-2 and 9 (MMP2,9) or elastases.
112 ed by augmented expression of extracellular (matrix metalloproteinase-2) and intracellular (ubiquitin
113 MMP-2, BSP, and natural (tissue inhibitor of matrix metalloproteinase-2) and synthetic (ilomastat and
114 rowth factor beta1, collagen type 4 alpha 1, matrix metalloproteinase 2, and alpha-smooth muscle acti
115 otein levels; increased expression of SNAIL, matrix metalloproteinase 2, and integrin beta1; and incr
116 en, tissue inhibitor of metalloproteinase 1, matrix metalloproteinase 2, and matrix metalloproteinase
117 eukin-1 receptor family member), galectin-3, matrix metalloproteinase-2, and collagen III N-terminal
118 reatment resulted in decreased expression of matrix metalloproteinase-2, and decreased vascularizatio
119  remodeling, collagen content, expression of matrix metalloproteinase-2, and increased levels of tiss
120 pression of TGF-beta, collagen, fibronectin, matrix metalloproteinase-2, and tissue inhibitor of meta
121 nd reduced ECM turnover due to inhibition of matrix metalloproteinase 2 by EFEMP1(R345W) and C3a.
122 reased expression of metalloproteinase-9 and matrix metalloproteinase-2 by sinusoidal endothelial cel
123 tin and large amounts of collagen type I and matrix metalloproteinase-2, characteristic features of m
124 resistant to dipeptidylpeptidase IV/CD26 and matrix metalloproteinase-2 cleavage and delivered by nan
125 tant to both dipeptidylpeptidase IV/CD26 and matrix metalloproteinase-2 cleavage, was active in vitro
126 ion, cellular retinol-binding protein 1, and matrix metalloproteinase 2, compared to term and preterm
127 xidative stress, fibrosis, and intracellular matrix metalloproteinase 2 content.
128 epsin B and cathepsin L, tissue inhibitor of matrix metalloproteinase 2, cytochrome c oxidase, and al
129                                 With repair, matrix metalloproteinase-2 decreased to < or = 50% that
130 s, LAP cleavage is shown to be predominantly matrix metalloproteinase 2 dependent.
131 nregulation of bone morphogenesis protein 4, matrix metalloproteinase 2, endothelial plasminogen acti
132           Zymographic analysis revealed that matrix metalloproteinase-2 enzymatic activity was elevat
133                                              Matrix metalloproteinase 2 expression is observed associ
134  signal-regulated kinase 1/2 activation, and matrix metalloproteinase 2 expression, all of which are
135                                              Matrix metalloproteinase-2 expression and activation by
136 on with repressed elastin mRNA and increased matrix metalloproteinase-2 expression and activity, both
137 ing the PKC-Raf/MEK/ERK pathways controlling matrix metalloproteinase-2 expression and podosome forma
138 ndothelial growth factor, interleukin-8, and matrix metalloproteinase-2 expression levels, as well as
139                             p38 MAPK induces matrix metalloproteinase-2 expression to cleave E-cadher
140    LV collagen synthesis and maturation, and matrix metalloproteinase-2 expression, were more importa
141 ERK pathway, resulting in down-regulation of matrix metalloproteinase-2 expression.
142 pression, and decreasing tissue inhibitor of matrix metalloproteinase-2 expression.
143 evels, reduced nitrosative stress, and lower matrix metalloproteinase-2 expression.
144  well as connective tissue growth factor and matrix metalloproteinase-2 expression.
145  failed to induce alpha-smooth muscle actin, matrix metalloproteinase-2, fibronectin, and integrin-li
146 ix metalloproteinase 9 and 13 expression and matrix metalloproteinase 2 gelatinase activity were sign
147 wever, SDF-1 is cleaved by exopeptidases and matrix metalloproteinase-2, generating a neurotoxin impl
148 ors of IPAH patients secreted high levels of matrix metalloproteinase-2, had greater affinity for ang
149 , granulocyte colony-stimulating factor, and matrix metalloproteinase 2 in STZ-induced diabetic bone
150 vels in ESA-treated animals revealed reduced matrix metalloproteinase 2 in the borderzone (P<0.05), w
151 ell as enhanced synthesis of fibronectin and matrix metalloproteinase-2 in a PAR-2- and ERK1/2-depend
152            Pathogenic rise of collagenolytic matrix metalloproteinase-2 in biofilm-infected wound-edg
153  upregulation of beta-catenin, vimentin, and matrix metalloproteinase-2 in hepatoma cells.
154 ter activity and the collagenase activity of matrix metalloproteinase-2 in human melanoma cells, resu
155 e-9 and a later, lower-magnitude increase of matrix metalloproteinase-2 in the liver.
156 atrix metalloproteinase inhibitor, prevented matrix metalloproteinase-2-induced troponin I cleavage i
157 extracellular matrix synthesis and decreased matrix metalloproteinase-2 levels as well as cell hypert
158 necrosis factor-alpha, interferon-gamma, and matrix metalloproteinase-2 levels.
159 characterization revealed that the levels of matrix metalloproteinase-2, matrix metalloproteinase-9,
160            Gelatin zymography indicated that matrix metalloproteinase 2 (MMP-2) and MMP-9 activities
161  invasion through the down-regulation of the matrix metalloproteinase 2 (MMP-2) and MMP-9 expression.
162                                              Matrix metalloproteinase 2 (MMP-2) contains three fibron
163 ascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP-2) expression in brain c
164                                We found that matrix metalloproteinase 2 (MMP-2) facilitated invasion
165                                Activation of matrix metalloproteinase 2 (MMP-2) has been shown to pla
166  the following markers of collagen turnover: matrix metalloproteinase 2 (MMP-2), tissue inhibitor of
167 e 1 collagen (ICTP), collagen VI, desmosine, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of
168           Fibroblasts constitutively express matrix metalloproteinase 2 (MMP-2), which specifically c
169 d and evaluated the biological properties of matrix metalloproteinase 2 (MMP-2)-responsive N-(2-hydro
170 novel markers such as HER2/neu, survivin and matrix metalloproteinase 2 (MMP-2).
171 llular [3H]-proline incorporation, increased matrix metalloproteinase-2 (MMP-2) activity and protein,
172 pithelial cells were found to have increased matrix metalloproteinase-2 (MMP-2) activity indicating t
173                               Acquisition of matrix metalloproteinase-2 (MMP-2) activity is temporall
174 ype 1 matrix metalloproteinase (MT1-MMP) and matrix metalloproteinase-2 (MMP-2) activity, critical in
175       The present study assessed the role of matrix metalloproteinase-2 (MMP-2) and -9 in synapse los
176    Neutrophils may be an important source of matrix metalloproteinase-2 (MMP-2) and matrix metallopro
177                                              Matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA increa
178 y and invasion, the latter via activation of matrix metalloproteinase-2 (MMP-2) and MMP-9.
179                                              Matrix metalloproteinase-2 (MMP-2) and transforming grow
180                     Levels of the proteinase matrix metalloproteinase-2 (MMP-2) are highly increased
181 ic binding to cancer cells is facilitated by matrix metalloproteinase-2 (MMP-2) as evidenced by reduc
182 howed 3-5-fold increase in the expression of matrix metalloproteinase-2 (MMP-2) as well as other inva
183 ases cellular invasive potential by inducing matrix metalloproteinase-2 (MMP-2) expression and activi
184 nase activities, as well as higher levels of matrix metalloproteinase-2 (MMP-2) expression and activi
185                                 In addition, matrix metalloproteinase-2 (MMP-2) expression in the iri
186                                              Matrix metalloproteinase-2 (MMP-2) expression is often u
187  adhesion molecule-1 (PECAM-1) and decreased matrix metalloproteinase-2 (MMP-2) expression.
188                            The expression of matrix metalloproteinase-2 (MMP-2) has been linked with
189                                              Matrix metalloproteinase-2 (MMP-2) has pivotal role in t
190 scular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2) in vivo and in vitro.
191           Selective small-interfering RNA to matrix metalloproteinase-2 (MMP-2) inhibited endothelium
192                                              Matrix metalloproteinase-2 (MMP-2) is a protease related
193    FRNK-expressing cells exhibited decreased matrix metalloproteinase-2 (MMP-2) mRNA levels and MMP-2
194                                              Matrix metalloproteinase-2 (MMP-2) plays an essential ro
195                                              Matrix metalloproteinase-2 (MMP-2) plays important roles
196                                              Matrix metalloproteinase-2 (MMP-2) rates of hydrolysis f
197                                              Matrix metalloproteinase-2 (MMP-2) was increased by Nox1
198 gamma) treatment showed that the activity of matrix metalloproteinase-2 (MMP-2) was increased in lung
199 wth factor (VEGF), Interleukin 6 (IL-6), and matrix metalloproteinase-2 (MMP-2) were measured using a
200                              Interactions of matrix metalloproteinase-2 (MMP-2) with native and denat
201 induce limited gelatinase activity in latent matrix metalloproteinase-2 (MMP-2) without removal of th
202 TG2 regulates the expression and function of matrix metalloproteinase-2 (MMP-2), a critical mediator
203 bility to inhibit cell-surface activation of matrix metalloproteinase-2 (MMP-2), a potent mediator of
204      Sensors showed a negligible response to matrix metalloproteinase-2 (MMP-2), a protease which may
205                             More IL-8, VEGF, matrix metalloproteinase-2 (MMP-2), and microvessel dens
206  of metalloproteinases-2 (TIMP-2), activates matrix metalloproteinase-2 (MMP-2), and stimulates cell
207 ession profoundly affected the expression of matrix metalloproteinase-2 (MMP-2), basic fibroblast gro
208                   We find that expression of matrix metalloproteinase-2 (MMP-2), known in other syste
209 branching and increased levels of Cyclin D1, matrix metalloproteinase-2 (MMP-2), matrix metalloprotei
210 collagen, transforming growth factor-beta 1, matrix metalloproteinase-2 (MMP-2), MMP-13, and interfer
211 TGF-beta1), connective tissue growth factor, matrix metalloproteinase-2 (MMP-2), MMP-14, endoglin (EN
212 egulation of FoxM1 reduced the expression of matrix metalloproteinase-2 (MMP-2), MMP-9 and vascular e
213 ipeptidyl peptidase-IV, neutrophil elastase, matrix metalloproteinase-2 (MMP-2), MMP-9, and cathepsin
214 omerular gelatinase expression, specifically matrix metalloproteinase-2 (MMP-2), MMP-9, and MMP-14, w
215 0/CCL6 decreased the levels of mRNA encoding matrix metalloproteinase-2 (MMP-2), MMP-9, and tissue in
216  Numbers of infiltrating cells and levels of matrix metalloproteinase-2 (MMP-2), nitric oxide (NO), a
217 pha), stromal cell derived factor-1 (SDF-1), matrix metalloproteinase-2 (MMP-2), vascular endothelial
218 scular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2), which are upregulate
219 2 (VEGFR2) signaling and decreased levels of matrix metalloproteinase-2 (MMP-2), with no effect on le
220 ensor, we have demonstrated the detection of matrix metalloproteinase-2 (MMP-2)-an important gelatina
221 Previous work has shown that BSP can bind to matrix metalloproteinase-2 (MMP-2).
222 okinase-type plasminogen activator (uPA) and matrix metalloproteinase-2 (MMP-2).
223 asion, including cyclooxgenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2).
224 Golgi network leading to an inactive form of matrix metalloproteinase-2 (MMP-2).
225   In vitro, Meg3 regulated the production of matrix metalloproteinase-2 (MMP-2).
226 x receptor on the surface of glioma cells as matrix metalloproteinase-2 (MMP-2).
227 B/urokinase-type plasminogen activator (uPA)/matrix metalloproteinase-2 (MMP-2).
228 n the activation of paxillin, NF-kappaB, and matrix metalloproteinase-2 (MMP-2).
229                                              Matrix metalloproteinase-2 (MMP-2; gelatinase A) is know
230 e genes regulated by them, ie, the genes for matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) and ti
231  matrix degradation and cytokine processing (matrix metalloproteinase 2 [MMP-2] and MMP-9), and the i
232 nism by which LRP1 induces the expression of matrix metalloproteinase 2 (MMP2) and MMP9 and thereby p
233 oactivator and formed complexes with PEA3 on matrix metalloproteinase 2 (MMP2) and MMP9 promoters to
234 (rhEPO) significantly increased secretion of matrix metalloproteinase 2 (MMP2) and MMP9.
235                           Then we identified matrix metalloproteinase 2 (MMP2) as a direct target of
236                  The inhibition mechanism of matrix metalloproteinase 2 (MMP2) by the selective inhib
237 ormonal induction of fat body remodeling and Matrix metalloproteinase 2 (MMP2) expression in the fat
238 reviously, we demonstrated the importance of matrix metalloproteinase 2 (MMP2) for airway egression o
239 ng is essential for the proper activation of matrix metalloproteinase 2 (Mmp2) for follicle rupture.
240                                          The matrix metalloproteinase 2 (MMP2) gene has been identifi
241 ms in the estrogen receptor alpha (ESR1) and matrix metalloproteinase 2 (MMP2) genes are associated w
242 st time that alphavbeta6 selectively induces matrix metalloproteinase 2 (MMP2) in vitro in multiple p
243 lly-active laminin-111 fragment generated by matrix metalloproteinase 2 (MMP2) processing, which is h
244                                              Matrix metalloproteinase 2 (MMP2) was shown to be expres
245                            We show here that matrix metalloproteinase 2 (MMP2), as part of an interle
246 or beta1 (Tgf-beta1), collagen 1a1 (Col1A1), matrix metalloproteinase 2 (Mmp2), cytokeratin 19, alpha
247 tress kinase JNK mediate the accumulation of matrix metalloproteinase 2 (Mmp2), damaging the BM, whic
248 ed to the PDL-MSCs, and higher expression of matrix metalloproteinase 2 (MMP2), interleukin (IL)-6, i
249 lay increased expression of Slug, Twist, and matrix metalloproteinase 2 (MMP2), loss of E-cadherin, a
250                                              Matrix metalloproteinase 2 (MMP2), which degrades Type I
251 on subverted lung T cell priming by inducing matrix metalloproteinase 2 (MMP2), which impaired the ac
252 ich contained a polyethylene glycol (PEG), a matrix metalloproteinase 2 (MMP2)-sensitive peptide link
253 therapeutic, a nanopreparation composed of a matrix metalloproteinase 2 (MMP2)-sensitive self-assembl
254 , and its transcriptional targets, including matrix metalloproteinase 2 (MMP2).
255 forming growth factor-beta1 (TGF-beta1), and matrix metalloproteinase 2 (MMP2).
256 ADP(+) and ATP contents (spectrophotometry), matrix metalloproteinase-2 (MMP2) activities (gelatin zy
257 p, and Reck could suppress the expression of matrix metalloproteinase-2 (Mmp2) and Mmp9, which could
258                                    Of these, matrix metalloproteinase-2 (MMP2) and tissue inhibitor o
259  assays, the expression of the gene encoding matrix metalloproteinase-2 (MMP2) in GBM cell lines grow
260 f retinal progenitor cells induced increased matrix metalloproteinase-2 (MMP2) secretion, partly from
261                                            A matrix metalloproteinase-2 (MMP2) sensitive self-assembl
262  enhances the activity but not expression of matrix metalloproteinase-2 (MMP2), the target substrate
263 , tissue plasminogen activator (tPA), and/or matrix metalloproteinase-2 (MMP2).
264  describing the proteolysis of collagen I by matrix metalloproteinases 2 (MMP2) and membrane type 1 m
265 ulocyte-colony-stimulating factor) and MMP2 (matrix metalloproteinase 2), MMP3, MMP9 and MMP13.
266 s, which correlated with a decrease in MMP2 (matrix metalloproteinase 2), MMP9, and ADAM10 (ADAM meta
267 ha(+)/CD44(+)/matrix metalloproteinase-14(+)/matrix metalloproteinase-2(+) myofibroblasts, which secr
268 mice were unable to induce OX40 and OX40L by matrix metalloproteinase-2 on splenic dendritic cells.
269 ctivation of the PI3K-integrin-linked kinase-matrix metalloproteinase 2 pathway was detected mainly i
270 Inhibition of matrix metalloproteinase-9 and matrix metalloproteinase-2 prevents the development of s
271 ndothelial growth factor A, which stimulates matrix metalloproteinase 2 production and the invasive m
272 then recruit and activate Akt2, resulting in matrix metalloproteinase-2 production.
273  surface MT1-MMP-catalyzed activation of pro-matrix metalloproteinase-2 (proMMP-2) required proper gl
274 red for DDR2-mediated transactivation of the matrix metalloproteinase-2 promoter.
275 growth-regulated oncogene (GRO), CX3CL1, and matrix metalloproteinase-2 protein and cyclooxygenase-2
276 n deposition, together with increased latent matrix metalloproteinase-2 protein and reduction in smoo
277                                              Matrix metalloproteinase-2 proteolyzes intracellular pro
278 ted the promoter and collagenase activity of matrix metalloproteinase 2, resulting in decreased invas
279                          PRL-3 also enhanced matrix metalloproteinase-2 secretion and cellular invasi
280 el invasion and migration, and a decrease in matrix metalloproteinase-2 secretion by HUVEC.
281                          Tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) belongs to a small f
282 of angiogenesis known as tissue inhibitor of matrix metalloproteinase-2 (TIMP-2), characterized for i
283  enable disengagement of tissue inhibitor of matrix metalloproteinase 2 (TIMP2) and tumor invasion.
284 Type 1 MMP (MT1-MMP) and tissue inhibitor of matrix metalloproteinase 2 (TIMP2).
285  previously inhibited by tissue inhibitor of matrix metalloproteinase-2 (TIMP2).
286 ng (procollagen type III N-terminal peptide, matrix metalloproteinase-2, tissue inhibitor of matrix m
287 ibrosis, myocyte apoptosis, and the ratio of matrix metalloproteinase-2/tissue inhibitor of matrix me
288  proliferation, migration, and production of matrix metalloproteinase 2; treatment with MDM2 inhibito
289 he expression of genes encoding cathepsin D; matrix metalloproteinase 2; urokinase plasminogen activa
290 odulating expression of genes, such as IL-8, matrix metalloproteinase-2, vascular endothelial growth
291 ed for the in vitro and in vivo detection of matrix metalloproteinases-2 via a MMP-2-specific peptide
292                      Decreased expression of matrix metalloproteinase 2 was also observed in the impl
293                                     Further, matrix metalloproteinase-2 was up regulated within these
294 of the extracellular matrix-degrading enzyme matrix metalloproteinase-2 were increased by thymosin be
295                   Levels of IL-10, IL-6, and matrix metalloproteinase-2 were significantly increased,
296 ptor, vascular cell adhesion molecule 1, and matrix metalloproteinase 2, were significantly associate
297  of fibroblast activation markers, including matrix metalloproteinase 2, were significantly increased
298 emodeling requires mesenchymal expression of matrix metalloproteinase 2, which is necessary for branc
299 n of phosphatidylserine (PS), annexin A6 and matrix metalloproteinase-2, which converts exosomes into
300 mpared with sham, and its activation induced matrix metalloproteinase-2, which enhanced GB pathogenes

 
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