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1  the activity of matrix metalloproteinase 9 (MMP-9).
2  L, and matrix metalloproteinases (MMP-2 and MMP-9).
3 etic ablation of matrix metalloproteinase-9 (MMP-9).
4 ) and a protease, matrix metallopeptidase 9 (MMP-9).
5 clastogenesis is matrix metalloproteinase 9 (MMP-9).
6 rget gene encoding matrix metalloprotease 9 (MMP-9).
7 ity of secreted matrix metalloproteinases 9 (MMP-9).
8 matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).
9 contrast to NMDAR-dependent LTP regulated by MMP-9.
10 e rescued by exogenous application of active MMP-9.
11  eIF4E phosphorylation and the expression of MMP-9.
12 tly inhibited in vivo expression of FGF2 and MMP-9.
13 A1 region, whereas nmdaLTP depends solely on MMP-9.
14 n and specifically preventing its binding to MMP-9.
15 DC/NHS for immobilization of monoclonal anti-MMP-9.
16 ionally activating E-cadherin and repressing MMP-9.
17 vity of matrix metalloproteinase (MMP)-3 and MMP-9.
18  observed within 5 min after the addition of MMP-9.
19 parallel cell-specific activity of MMP-2 and MMP-9.
20  that the improved outcomes are mediated via MMP-9.
21  oxidase-derived reactive oxygen species and MMP-9.
22 s increased expression of p16Ink4a, p21, and MMP-9.
23 1beta, and the pro-invasive metalloprotease, MMP-9.
24 rescein-conjugated gelatin by MMP-2, but not MMP-9.
25 ase-1 and -2; and depressed active and total MMP-9.
26                       Recombinant human (rh) MMP-9 (10 or 20 mul; 0, 12.5, 25, 50, 100, 200, 500, and
27 th expression of matrix metalloproteinase 9 (MMP-9), a marker of fast MNs.
28                  Pharmacologic inhibition of MMP-9 abrogated the difference in chemotactic attraction
29 plasticity of dendritic spines by triggering MMP-9 activation and ECM remodelling.
30                  Liver metastasis along with MMP-9 activation and the production of inflammatory cyto
31  BV2 mouse microglia cell line and inhibited MMP-9 activation in primary microglia.
32         Our study shows that MCV sT-mediated MMP-9 activation is driven through the LSD, a known E3 l
33 ain Results: Neutrophil elastase, MMP-2, and MMP-9 activities and protein levels were equally elevate
34 0-60 min, likely independent of gelatinase B/MMP-9 activities.
35 l as on the corresponding intrinsic cellular MMP-9 activities.
36 ing heroin-paired cues transiently increased MMP-9 activity around D1-MSN dendritic spines and synaps
37 s from eight selected legume species towards MMP-9 activity in colon carcinoma cells.
38 mulates matrix metalloprotease-2 (MMP-2) and MMP-9 activity in the extracellular space.
39 t toward attenuating tumor progression where MMP-9 activity is strongly implicated.
40                                              MMP-9 activity is strongly related to cancer growth and
41 These findings suggest that increasing islet MMP-9 activity might be a strategy to limit beta-cell lo
42                   LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thal
43                                              MMP-9 activity was analyzed by zymography.
44 e-induced periodontitis (P > 0.05); however, MMP-9 activity was lower in the group treated with desip
45 nd breakdown of TJPs, secondary to increased MMP-9 activity which suggests that these pathways are po
46 y addition of exogenous Shh, or neutralizing MMP-9 activity, decreased permeability and increased TJP
47 hness, and both appeared suitable to monitor MMP-9 activity.
48  the potential for matrix metalloprotease-9 (MMP-9), an endopeptidase secreted in response to neurona
49  the activity of matrix metalloproteinase 9 (MMP-9), an enzyme involved in extracellular matrix (ECM)
50 he conjoint increased expression of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist redu
51 n induced a significant increase in secreted MMP-9 and an accumulation of cytoplasmic MMP-2 over time
52 city (Rmax) and Gb values for interaction of MMP-9 and anti-MMP-9 were 0.4nM, 680 microRIU and -53.51
53 nosorbent assay was used to assess levels of MMP-9 and IL-1beta in peri-implant sulcular fluid.
54 ient was used to analyze for correlations of MMP-9 and IL-1beta levels with peri-implant parameters.
55               The differential expression of MMP-9 and its regulatory factors is also examined.
56 gulation of known downstream targets such as MMP-9 and KISS1.
57 ith the iNPH group (p < 0.001), while MMP-2, MMP-9 and MMP-12 did not differ between the groups.
58 development genes, matrix metalloproteinases mmp-9 and mmp-13, while cortisol led to stronger upregul
59    This study investigates the expression of MMP-9 and MMP-2 in aggressive extracranial AVMs.
60 n of matrix metalloproteinases (MMPs), i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors o
61                                        Serum MMP-9 and MPO levels were higher in women with PCOS and
62                                     Salivary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, wer
63 miscuous E3 ligases, including FBW7, a known MMP-9 and Snail regulator.
64 transition (EMT)-associated genes, including MMP-9 and Snail.
65     The increased and aberrant expression of MMP-9 and specific MMP-9 forms may help explain the cons
66 we confirmed morphine-induced alterations in MMP-9 and TIMP expression and identified organs, includi
67 mal DNA methylation and an imbalance between MMP-9 and TIMP-1 and -2 lead to ECM remodeling and renal
68 al rigidity providing feedback which affects MMP-9 and TIMP-1 secretion, which may become dysregulate
69                             Mechanistically, MMP-9 and VCAM-1 appear to be involved downstream of PDG
70  production of iNOS and arginase, as well as MMP-9 and VEGF.
71 ession of matrix metalloproteinase (MMP) -2, MMP-9 and vimentin.
72  (i.e., matrix metalloproteinase [MMP]-2 and MMP-9) and extracellular matrix metalloproteinase induce
73 ased circulating matrix metalloproteinase 9 (MMP-9) and increased circulating tissue inhibitor of met
74  catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by
75 matically active matrix metalloproteinase 9 (MMP-9), and were capable of mediating potent effects on
76 with a 2.3% decrease (95% CI: -4.3, -0.3) in MMP-9, and a 5% increase in %uMMA was associated with a
77 IL]-1beta, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels) evaluations were performe
78  stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that was significantly higher in the kid
79 cted to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significan
80 ed positively with the expressions of MMP-2, MMP-9, and EMMPRIN in gingiva.
81 ough inhibiting integrin alphavbeta6, MMP-2, MMP-9, and ERK phosphorylation by HT29.
82                        In particular, MMP-2, MMP-9, and MMP-14 have been reported to be crucial for t
83                                   NE, MMP-8, MMP-9, and MPO levels were elevated in oGVHD tears when
84                             In controls, NE, MMP-9, and MPO significantly correlated with each other
85 hat correlated strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic source and
86 on studies were performed between NE, MMP-8, MMP-9, and MPO within study groups.
87                                       MMP-8, MMP-9, and TIMP-1 levels were determined in gingival cre
88  levels of matrix metalloproteinase (MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in biofluid
89 tin by MMP-2, confirming that PEX9 is not an MMP-9 antagonist.
90                  Matrix metalloproteinase 9 (MMP-9) antisense oligonucleotides (ASO) or an MMP inhibi
91 studies of a potent difluorinated probe with MMP-9 are also disclosed and indicate that the structura
92 ) minimal immunoreactive and active Mmp-8 or Mmp-9 are detected on the surface of activated Timp-1(-/
93                                    MMP-2 and MMP-9 are detected using label free porous silicon (PSi)
94       FGF2 is a known mitogen, and both FGF2/MMP-9 are proangiogenic factors.
95 minal hemopexin domains of pro-Mmp-8 and pro-Mmp-9 are required for their binding to membrane-bound T
96 that MCV sT contributes to the activation of MMP-9 as a result of FBW7 targeting and increases the in
97 e data do not support the inclusion of serum MMP-9 as predictive biomarker for DMD patients.
98 s to investigate Matrix Metalloproteinase-9 (MMP-9) as predictive biomarker for Duchenne.
99 olytic cleavage of hepatic VEGF using either MMP-9 ASO or intraportal MMP inhibitor in 5-week and 10-
100 L-12p40 and high level of metalloprotease 9 (MMP-9) at the late stages of disease.
101       The PMN receptor(s) to which MMP-8 and MMP-9 bind(s) is not known.
102 tingly, late-phase LTP was also decreased by MMP-9 blockade.
103 0% in cellular assays, and IgG L13 inhibited MMP-9 but not MMP-2/-12/-14 and significantly relieved n
104 nstrate that mRNA and protein expressions of MMP-9, but not MMP-2, are significantly higher in AVM ti
105                           The serum level of MMP-9, but not MMP-2, is also elevated in AVM patients c
106               The tear film was analyzed for MMP-9 by a commercially available test (InflammaDry; Rap
107 nd achieve ultimate selectivity: They target MMP-9 by allosterically preventing activation of its zym
108                              Consistent with MMP-9 cleavage resulting in largely non-amyloidogenic de
109 tigated whether hIAPP fragments arising from MMP-9 cleavage retain the potential to aggregate and cau
110    GCF and serum MMP-8 concentrations, serum MMP-9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MM
111                                              MMP-9 decreased in parallel to clinical stabilization in
112 tro stimulation of isolated neutrophils with MMP-9 decreased neutrophil apoptosis, indicated by reduc
113 n of collagenases or selective inhibition of MMP-9 decreased pathological vascular permeability in a
114 ast 2-fold upregulated or downregulated with MMP-9 deletion (all P<0.05).
115                           These effects were MMP-9 dependent and were reversed in the presence of spe
116  collective results support the necessity of MMP-9-dependent H3NT proteolysis in regulating gene path
117 l mechanism of alcohol craving that involves MMP-9-dependent synaptic plasticity in CeA.
118 (MMP-2), a protease which may interfere with MMP-9 detection.
119                           GST-PEX9 inhibited MMP-9-driven gelatin proteolysis, measured by gelatin zy
120                                              MMP-9 efficiently degrades the extracellular matrix comp
121                                              MMP-9 expression and MMP-9/TIMP-1 ratio were similar amo
122 e show that fibrotic rigidities downregulate MMP-9 expression and secretion, and also upregulate secr
123  HFHF rats, the MMP inhibitor reduced active MMP-9 expression by 97%, ameliorated histologic evidence
124 ct volume, edema, inflammation, and vascular MMP-9 expression compared with IR and sham groups.
125 d epidermal growth factor receptor-regulated MMP-9 expression via ERK1/2, which resulted in cleavage
126                                    MMP-2 and MMP-9 expression was reduced in the skin of doxycycline-
127 ation accompanied by a decrease in MMP-2 and MMP-9 expression within the aortic wall in doxycycline-t
128 y, migration and invasion, reduced MMP-2 and MMP-9 expression, and reduced N-cadherin expression, but
129   XLOC_006277 knockdown suppressed MMP-8 and MMP-9 expression, both associated with heart lesions.
130 -9 gene at position -1562, which upregulates MMP-9 expression, correlated with increased motivation f
131 blasts, RHAMM promoted ERK1/2 activation and MMP-9 expression, whereas in keratinocytes, RHAMM suppre
132 g PMNs, and its removal by PMN-MP-associated MMP-9 facilitates PMN trafficking across epithelial laye
133 gated gains in secreted proteases, MMP-2 and MMP-9, following radiation.
134 nd aberrant expression of MMP-9 and specific MMP-9 forms may help explain the constitutive vascular r
135   These granules are involved in trafficking MMP-9 from the stroma to the epithelium to promote lumin
136 ix metalloproteinases (MMP)-1, MMP-3, MMP-8, MMP-9, from baseline to week 2; regulated on activation,
137  investigation of the effects of the loss of MMP-9 function on pancreatic islets uncovers a deteriora
138  (TIMP)-1, matrix metalloproteinase (MMP)-2, MMP-9, Galectin-3 (Gal-3), N-terminal propeptide of coll
139                 Finally, C/T polymorphism of MMP-9 gene at position -1562, which upregulates MMP-9 ex
140  primers, we found a significant increase in MMP-9 gene expression in the tumor-reactive stroma durin
141 etylation of H3K18 as a central regulator of MMP-9 H3NT protease activity both in vitro and at H3NT c
142                                              MMP-9 has been shown to play a detrimental role in many
143 dysregulation of matrix metalloproteinase-9 (MMP-9) has been implicated in multiple essential roles i
144 isease, involves matrix metalloproteinase 9 (MMP-9), IL-17, and IL-23 release from infiltrated inflam
145 this antiulcer drug reduces IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with induced periodont
146 the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.
147 er and induces reduction of IL-6, MMP-1, and MMP-9 immunoexpression, reinforcing the idea that the be
148 ocess surface and number of IL-6, MMP-1, and MMP-9-immunolabeled cells in the gingival mucosa were qu
149 AP-positive osteoclasts and IL-6, MMP-1, and MMP-9-immunolabeled cells was significantly lower than i
150 ation products, adenoviral overexpression of MMP-9 in amyloid-prone islets reduced amyloid deposition
151 d cause toxicity, and whether overexpressing MMP-9 in amyloid-prone islets reduces amyloid burden and
152 ether an 8-week HIIT intervention influences MMP-9 in breast cancer patients undergoing anthracycline
153 ators, TNF-alpha, IL-1 beta, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyperosmotic medium.
154                                        Thus, MMP-9 in particular could play a role in tubal scarring
155                             Concentration of MMP-9 in saliva samples was determined, with linearity i
156 ld be rescued by overexpression of exogenous MMP-9 in the central nucleus of the amygdala (CeA).
157                                              MMP-9 in the CON group was not significantly changed [11
158                  We aimed to validate a tear MMP-9 in-situ immunoassay (InflammaDry) and to identify
159                           The results of the MMP-9 in-situ immunoassay varied significantly depending
160 ible function of matrix metalloproteinase-9 (MMP-9) in alcohol addiction because this protein has rec
161 educed levels of matrix metalloproteinase-9 (MMP-9) in the plasma and brains at different time points
162 ysyl oxidase and a second metalloproteinase, MMP-9, in murine optic gliomas relative to normal non-ne
163 (MMP-14, a predominant target in metastasis; MMP-9, in neuropathic pain), beta-secretase 1 (BACE-1, a
164                                              MMP-9, in particular, is highly dynamically regulated in
165  matrix metalloproteinases (MMPs), MMP-8 and MMP-9, in the wounds of db/db mice.
166 GST-B1 also inhibited gelatin degradation by MMP-9, indicating that these regions are responsible for
167 show that the recombinant FN domain inhibits MMP-9-induced TGF-beta activation and fibroblast differe
168                We found that liver-selective MMP-9 inhibition accelerated liver regeneration after pa
169                Here, we investigated whether MMP-9 inhibition also interferes with threat memory reco
170                              Liver-selective MMP-9 inhibition enhances VEGF-sdf1 signaling and recrui
171                              Liver-selective MMP-9 inhibition largely abolished warm ischemia-reperfu
172                              Liver-selective MMP-9 inhibition markedly increased recruitment and engr
173                              Liver-selective MMP-9 inhibition may be a therapeutic tool for liver inj
174                              Liver-selective MMP-9 inhibition prevented VEGF cleavage and doubled pro
175  extended hepatectomy model, liver-selective MMP-9 inhibition restored liver sinusoidal endothelial c
176                              Liver-selective MMP-9 inhibition to protect against proteolytic cleavage
177 esis for this study was that liver-selective MMP-9 inhibition would protect the hepatic VEGF-sdf-1 si
178 nhibitor were used to induce liver-selective MMP-9 inhibition.
179                            Coinjection of an MMP-9 inhibitor, but not an MMP-2 inhibitor, reduced per
180       Lupin seeds contain the most efficient MMP-9 inhibitors of all legume seeds analyzed, inhibitin
181                                     Specific MMP-9 inhibitors would be a promising treatment for AVMs
182 min and globulin fractions were screened for MMP-9 inhibitors, using a fluorometric assay and gelatin
183 udies, we also report that the expression of MMP-9 is significantly decreased in activated HSCs in fi
184                  Matrix metalloproteinase-9 (MMP-9) is active in islets and cleaves hIAPP.
185                  Matrix metalloproteinase-9 (MMP-9) is required for structural synapse remodeling inv
186       These plastic changes were impaired in MMP-9 knockout mice.
187                        Mice devoid of MMP-9 (MMP-9 knockout) drank as much alcohol as wild-type anima
188  IL-6, matrix metalloproteinase (MMP)-8, and MMP-9 levels among habitual gutka chewers and non-chewer
189 ng clinical periodontal parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically heal
190    Autopsy-derived PFC samples show elevated MMP-9 levels in antidepressant-treated MDD patients comp
191                Chronic venlafaxine increases MMP-9 levels in murine cortex, and increases both pyrami
192 s of natural history cohorts showed elevated MMP-9 levels in patients and a significant increase over
193 ogen Screening, Inc, Sarasota, FL) detecting MMP-9 levels of more than 40 ng/ml.
194 ng clinical periodontal parameters and serum MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1
195 tension study clarified that the decrease in MMP-9 levels was not predictive of treatment response.
196 nd whole salivary IL-6, IL-1beta, MMP-8, and MMP-9 levels were higher among gutka chewers than non-ch
197                                        Serum MMP-9 levels were lower in healthy women with gingivitis
198 migration, and invasion, increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced E-cadheri
199                       Chemical treatments of MMP-9 markedly inhibited MCV sT-induced cell migration a
200 rom the C-terminal region, via the action of MMP-9 (matrix metalloproteinase 9).
201                                        Thus, MMP-9 may release netrin-1 fragments from the extracellu
202                                              MMP-9 may serve as the biochemical culprit to target and
203                               Mice devoid of MMP-9 (MMP-9 knockout) drank as much alcohol as wild-typ
204  markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondr
205                           Cells positive for MMP-9, MMP-13, and alpha-SMA expression were present at
206 -9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly higher in Gg
207 MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio.
208 hemopexin domain fail to bind to Mmp-8(-/-)x Mmp-9(-/-) murine PMNs.
209 ng of pro-Mmp-8 and pro-Mmp-9 to Mmp-8(-/-)x Mmp-9(-/-) murine PMNs.
210         Unlike full-length pro-Mmp-8 and pro-Mmp-9, mutant pro-Mmp proteins lacking the COOH-terminal
211  with controls were BPI, ITGAM, CAP37, PCM1, MMP-9, MZB1, UGTT1, PLG, RAB1B, HSP90B1.
212                                              MMP-9/neutrophil gelatinase-associated lipocalin (NGAL)
213 accumulation of apoptotic neutrophils in the MMP-9 null group compared with wild-type group.
214           Infarct regions from wild-type and MMP-9 null mice (n=8 per group) analyzed by glycoproteom
215 ified as having the highest fold increase in MMP-9 null mice.
216 SD-95 expression in the cortex of WT but not MMP-9-null mice.
217 ocalized expression of TIMP-1 with MMP-8 and MMP-9 on peripheral blood PMN surfaces.
218 esis-related factors (CD26, FGF, HGF, MMP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (IL-1ra, IL-16) in
219  post-myocardial infarction macrophages with MMP-9 or a CD36-blocking peptide reduced phagocytic capa
220 NJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not inhibit
221 y images showed uniform distribution of anti-MMP-9 over the sensor chip.
222  4 mm (P < 0.01), and mean concentrations of MMP-9 (P < 0.001) and IL-1beta (P < 0.01) were significa
223 ant positive correlations were found between MMP-9 (P = 0.0198) and IL-1beta (P = 0.0047) levels and
224   Seed proteins include potent inhibitors of MMP-9, particularly low molecular mass proteins.
225 mponent gelatin, and the hemopexin domain of MMP-9 (PEX9) inhibits this degradation.
226  between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologically or genetically is sufficient to
227 er randomization, aldosterone, sST2, TIMP-1, MMP-9, PINP, and PIIINP had decreased more in the sacubi
228                    The activity of MMP-2 and MMP-9, predicted to be decreased in DN, was investigated
229   In contrast to other known H3NT proteases, MMP-9 primarily cleaved H3K18-Q19 in vitro and in cells.
230 ration of peripheral immune cells, including MMP-9-producing neutrophils/macrophages, resulting in la
231 rophage expansion, inflammatory cytokine and MMP-9 production and mitigates AAA development.
232 It is likely that the aberrantly accelerated MMP-9 proteolysis during neurogenesis is a biochemical r
233                                        Using MMP-9 proteolysis of the wild-type, CIP, and control pep
234 nt sequence is severalfold more sensitive to MMP-9 proteolysis relative to the wild type.
235                                      Hepatic MMP-9 proteolytically cleaved VEGF after partial hepatec
236                                The MMP-2 and MMP-9 quantification correlated well with the ELISA.
237 ork, we addressed the potential relevance of MMP-9 recruitment to and activity at the surface of fibr
238 0, favor neutrophil- and monocyte-associated MMP-9 release and disease relapse and opened new therape
239 naling on neutrophils, resulting in enhanced MMP-9 release, and unexpectedly revealed genetic polymor
240            Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional p
241                                    Moreover, MMP-9 results correlated with the number of obstructed m
242                                    Thus, the MMP-9 results indicated a clinically significant inflamm
243                                          The MMP-9 results were increased significantly in women (P <
244  (40.4%) and in 3 of 54 controls (5.6%), the MMP-9 results were positive.
245 mphocytes, responded to CXCL10 by increasing MMP-9 secretion through the activation of extracellular
246                    Finally, CXCL10-increased MMP-9 secretion was inhibited by methylprednisolone and
247 c42 GTPase activity, MT1-MMP expression, and MMP-9 secretion.
248 ) expression and matrix metalloproteinase-9 (MMP-9) secretion by these cells.
249 nd inhibition of matrix metalloproteinase-9 (MMP-9) secretion.
250 ve binding experiments showed that Mmp-8 and Mmp-9 share binding sites on murine PMN surfaces.
251 promote invasion through a FAK>p130Cas>c-Jun>MMP-9 signaling axis.
252                                         High MMP-9 staining alone (P = .001) or coexistent with low T
253                                TNF-alpha and MMP-9 staining did not reveal any significant difference
254 rction, which identified CD36 as a candidate MMP-9 substrate.
255 EX9 did not prevent the degradation of other MMP-9 substrates, such as a fluorogenic peptide, alphaB
256 ing a low-cost, disposable sensor system for MMP-9 suitable for home-monitoring of inflammation.
257 e findings were correlated to results of the MMP-9 test in tears.
258 expectedly revealed genetic polymorphisms in MMP-9 that alter activity.
259 ur data reveal a new cell-signaling role for MMP-9 through CD36 degradation to regulate macrophage ph
260                                Saliva MMP-8, MMP-9, TIMP-1, and MPO concentrations distinguished peri
261 ted by pack years of smoking, whereas saliva MMP-9, TIMP-1, and MPO were mostly affected by time sinc
262 dontal parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically healthy patients (P <
263                         MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature
264 e-treated EAE mice had a significantly lower MMP-9/TIMP-1 ratio, and significantly lower MCT-1 and CD
265     Salivary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, were higher in the systemically hea
266 iomarkers, matrix metalloproteinase (MMP)-8, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 an
267 ined for metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1)
268                                          The MMP-9/ tissue inhibitor of metalloproteases-1 (TIMP-1) c
269 oxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patien
270 in inhibits the binding of pro-Mmp-8 and pro-Mmp-9 to Mmp-8(-/-)x Mmp-9(-/-) murine PMNs.
271                       By anchoring MMP-8 and MMP-9 to PMN surfaces, membrane-bound TIMP-1 plays a cou
272 r, we have demonstrated that the addition of MMP-9 to the blood diminishes the protective effect of t
273                  We show that recruitment of MMP-9 to the fibroblast cell surface occurs through its
274 s the binding of exogenous pro-Mmp-8 and pro-Mmp-9 to the surface of Timp-1(-/-) PMNs.
275 nal assays suggest that both pro- and active MMP-9 trigger alpha-smooth muscle actin expression in cu
276 , respectively), matrix metalloproteinase-9 (MMP-9), tumor necrosis factor-alpha, plasminogen activat
277 pression of downstream target genes DKK1 and MMP-9, two molecules that promote myeloma progression.
278 o costly MRI scans could be the detection of MMP-9, using a low-cost, disposable sensor system for MM
279 lso down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migra
280                 In HIV-positive individuals, MMP-9 was associated with dolichoectasia only when coexp
281                                              MMP-9 was confirmed in vitro and in vivo to proteolytica
282 tive correlation between IL-6/MMP-1 and IL-6/MMP-9 was detected in PDSG and PDCimG.
283                                              MMP-9 was expressed in Escherichia coli BL21 and purifie
284 egradation of Abeta(1-16) by either MMP-2 or MMP-9 was not observed even after prolonged incubation t
285            However, within-group decrease in MMP-9 was observed in the HIIT group [104.3(51.9) to 65.
286               A THPI selective for MMP-2 and MMP-9 was redesigned to incorporate non-native amino aci
287  Gb values for interaction of MMP-9 and anti-MMP-9 were 0.4nM, 680 microRIU and -53.51kJ/mol, respect
288                           Levels of VEGF and MMP-9 were consistently higher in VSP patients, with the
289 NA and protein levels of IL-6, TNFalpha, and MMP-9 were elevated in diabetic rats both 2 and 3 weeks
290     Elevated concentrations of GCF MMP-8 and MMP-9 were found in Gg compared with Gh group (P <0.05).
291  dichotomy, recombinant human (rh) MMP-2 and MMP-9 were incubated with Abeta40 and Abeta42, and the r
292                          When both MMP-3 and MMP-9 were inhibited, both early- and late-phase LTP was
293 upon by matrix metalloproteinases (MMP-2 and MMP-9), which are up-regulated in heart tissue post-myoc
294 combinant human matrix metalloproteinases-9 (MMP-9), which has been associated with malignant tumor p
295    The collagenase matrix metalloprotease 9 (MMP-9), which is increased in patients with diabetic mac
296 ndent genes, including the gene that encodes MMP-9, which we implicated as a regulator of integrin-de
297                                   Inhibiting MMP-9 with doxycycline is suggested to attenuate human t
298 ology successfully reduces the expression of MMP-9 within the wounds of diabetic mice, significantly
299 ective compound that inhibited activation of MMP-9 zymogen and subsequent generation of catalytically
300 with a structural pocket in proximity to the MMP-9 zymogen cleavage site near Arg-106, which is disti

 
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