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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.
33 ain Results: Neutrophil elastase, MMP-2, and MMP-9 activities and protein levels were equally elevate
36 ing heroin-paired cues transiently increased MMP-9 activity around D1-MSN dendritic spines and synaps
41 These findings suggest that increasing islet MMP-9 activity might be a strategy to limit beta-cell lo
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
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
54 ient was used to analyze for correlations of MMP-9 and IL-1beta levels with peri-implant parameters.
58 development genes, matrix metalloproteinases mmp-9 and mmp-13, while cortisol led to stronger upregul
60 n of matrix metalloproteinases (MMPs), i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors o
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
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
85 hat correlated strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic source and
88 levels of matrix metalloproteinase (MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in biofluid
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(-/
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
99 olytic cleavage of hepatic VEGF using either MMP-9 ASO or intraportal MMP inhibitor in 5-week and 10-
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
107 nd achieve ultimate selectivity: They target MMP-9 by allosterically preventing activation of its zym
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
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
116 collective results support the necessity of MMP-9-dependent H3NT proteolysis in regulating gene path
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
125 d epidermal growth factor receptor-regulated MMP-9 expression via ERK1/2, which resulted in cleavage
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
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
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
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
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
156 ld be rescued by overexpression of exogenous MMP-9 in the central nucleus of the amygdala (CeA).
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
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
175 extended hepatectomy model, liver-selective MMP-9 inhibition restored liver sinusoidal endothelial c
177 esis for this study was that liver-selective MMP-9 inhibition would protect the hepatic VEGF-sdf-1 si
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
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
192 s of natural history cohorts showed elevated MMP-9 levels in patients and a significant increase over
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
198 migration, and invasion, increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced E-cadheri
204 markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondr
206 -9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly higher in Gg
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
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
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
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
232 It is likely that the aberrantly accelerated MMP-9 proteolysis during neurogenesis is a biochemical r
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
245 mphocytes, responded to CXCL10 by increasing MMP-9 secretion through the activation of extracellular
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.
259 ur data reveal a new cell-signaling role for MMP-9 through CD36 degradation to regulate macrophage ph
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 <
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)
269 oxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patien
272 r, we have demonstrated that the addition of MMP-9 to the blood diminishes the protective effect of t
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
284 egradation of Abeta(1-16) by either MMP-2 or MMP-9 was not observed even after prolonged incubation t
287 Gb values for interaction of MMP-9 and anti-MMP-9 were 0.4nM, 680 microRIU and -53.51kJ/mol, respect
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
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
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