ライフサイエンスコーパス: MMP-9

1 ) and a protease, matrix metallopeptidase 9 (MMP-9).

2 clastogenesis is matrix metalloproteinase 9 (MMP-9).

3 the activity of matrix metalloproteinase 9 (MMP-9).

4 L, and matrix metalloproteinases (MMP-2 and MMP-9).

5 etic ablation of matrix metalloproteinase-9 (MMP-9).

6 n and specifically preventing its binding to MMP-9.

7 DC/NHS for immobilization of monoclonal anti-MMP-9.

8 ionally activating E-cadherin and repressing MMP-9.

9 vity of matrix metalloproteinase (MMP)-3 and MMP-9.

10 observed within 5 min after the addition of MMP-9.

11 reasing the levels and activity of MMP-3 and MMP-9.

12 or for fast and straightforward detection of MMP-9.

13 y tumor-resident, but not blood-circulating, MMP-9.

14 in-mediated expression of COX-2, SOCS-3, and MMP-9.

15 tides containing specific cleavage sites for MMP-9.

16 ctors, including HIF1alpha, VEGFR, and MMP-2/MMP-9.

17 including collagenase MMP-13 and gelatinase MMP-9.

18 which is regulated by the metalloproteinase MMP-9.

19 tially suppressed IL-6-mediated induction of MMP-9.

20 matrix metalloproteinases (MMPs): MMP-2 and MMP-9.

21 contrast to NMDAR-dependent LTP regulated by MMP-9.

22 e rescued by exogenous application of active MMP-9.

23 eIF4E phosphorylation and the expression of MMP-9.

24 tly inhibited in vivo expression of FGF2 and MMP-9.

25 A1 region, whereas nmdaLTP depends solely on MMP-9.

26 e associated with a significant reduction in MMP-9/-3, less peripheral neutrophil infiltration, and a

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 rotection that could be mediated via reduced MMP-9 activation and myelin degradation as well as inhib

31 BV2 mouse microglia cell line and inhibited MMP-9 activation in primary microglia.

32 0-60 min, likely independent of gelatinase B/MMP-9 activities.

33 l as on the corresponding intrinsic cellular MMP-9 activities.

34 s from eight selected legume species towards MMP-9 activity in colon carcinoma cells.

35 on in the eyelid margin and conjunctiva, and MMP-9 activity in tears.

36 mulates matrix metalloprotease-2 (MMP-2) and MMP-9 activity in the extracellular space.

37 t toward attenuating tumor progression where MMP-9 activity is strongly implicated.

38 MMP-9 activity is strongly related to cancer growth and

39 These findings suggest that increasing islet MMP-9 activity might be a strategy to limit beta-cell lo

40 LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thal

41 Change in tear MMP-9 activity was similar to the pattern of MMP-9 trans

42 nd breakdown of TJPs, secondary to increased MMP-9 activity which suggests that these pathways are po

43 y addition of exogenous Shh, or neutralizing MMP-9 activity, decreased permeability and increased TJP

44 hness, and both appeared suitable to monitor MMP-9 activity.

45 , in part, via regulation of osteopontin and MMP-9 activity.

46 ction to measure matrix metalloproteinase 9 (MMP-9) activity were performed once in 8 asymptomatic he

47 the activity of matrix metalloproteinase 9 (MMP-9), an enzyme involved in extracellular matrix (ECM)

48 he conjoint increased expression of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist redu

49 n induced a significant increase in secreted MMP-9 and an accumulation of cytoplasmic MMP-2 over time

50 city (Rmax) and Gb values for interaction of MMP-9 and anti-MMP-9 were 0.4nM, 680 microRIU and -53.51

51 with an increased basal release of IL-8 and MMP-9 and expressed a corticosteroid resistance molecula

52 Co-incubation of MMP-9 and fragment 16-37 ablated amyloidogenicity, sugge

53 ions of human neutrophils, such as elastase, MMP-9 and IL-8 production.

54 The differential expression of MMP-9 and its regulatory factors is also examined.

55 gulation of known downstream targets such as MMP-9 and KISS1.

56 development genes, matrix metalloproteinases mmp-9 and mmp-13, while cortisol led to stronger upregul

57 in order to investigate its binding mode to MMP-9 and MMP-14.

58 This study investigates the expression of MMP-9 and MMP-2 in aggressive extracranial AVMs.

59 n of matrix metalloproteinases (MMPs), i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors o

60 Serum MMP-9 and MPO levels were higher in women with PCOS and

61 Salivary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, wer

62 Further, validation of MMP-9 and SDC1 3'-untranslated region (3'-UTR) targets w

63 The increased and aberrant expression of MMP-9 and specific MMP-9 forms may help explain the cons

64 Synthetic hIAPP was incubated with MMP-9 and the major hIAPP fragments observed by MS compr

65 we confirmed morphine-induced alterations in MMP-9 and TIMP expression and identified organs, includi

66 mal DNA methylation and an imbalance between MMP-9 and TIMP-1 and -2 lead to ECM remodeling and renal

67 production of iNOS and arginase, as well as MMP-9 and VEGF.

68 ession of matrix metalloproteinase (MMP) -2, MMP-9 and vimentin.

69 (i.e., matrix metalloproteinase [MMP]-2 and MMP-9) and extracellular matrix metalloproteinase induce

70 ased circulating matrix metalloproteinase 9 (MMP-9) and increased circulating tissue inhibitor of met

71 elective inhibitor of gelatinases (MMP-2 and MMP-9) and MMP-14, accelerates diabetic wound healing by

72 matically active matrix metalloproteinase 9 (MMP-9), and were capable of mediating potent effects on

73 with a 2.3% decrease (95% CI: -4.3, -0.3) in MMP-9, and a 5% increase in %uMMA was associated with a

74 of a normal islet matrix turnover exerted by MMP-9, and concomitant release of paracrine factors sequ

75 ed positively with the expressions of MMP-2, MMP-9, and EMMPRIN in gingiva.

76 ough inhibiting integrin alphavbeta6, MMP-2, MMP-9, and ERK phosphorylation by HT29.

77 In particular, MMP-2, MMP-9, and MMP-14 have been reported to be crucial for t

78 A nanomolar MMP-2, MMP-9, and MMP-14 inhibitor was identified, compound 3,

79 h improved inhibitory activity toward MMP-2, MMP-9, and MMP-14 with respect to the previously discove

80 NE, MMP-8, MMP-9, and MPO levels were elevated in oGVHD tears when

81 In controls, NE, MMP-9, and MPO significantly correlated with each other

82 hat correlated strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic source and

83 on studies were performed between NE, MMP-8, MMP-9, and MPO within study groups.

84 ta, matrix metalloproteinase (MMP)-3, MMP-8, MMP-9, and neutrophil gelatinase-associated lipocalin (N

85 tor-alpha, matrix metalloproteinase (MMP)-8, MMP-9, and plasminogen activator inhibitor-1 levels were

86 cessing of elevated osteopontin by activated MMP-9, and subsequent macrophage recruitment.

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 MMP-2 and MMP-9 are detected using label free porous silicon (PSi)

91 FGF2 is a known mitogen, and both FGF2/MMP-9 are proangiogenic factors.

92 e data do not support the inclusion of serum MMP-9 as predictive biomarker for DMD patients.

93 s to investigate Matrix Metalloproteinase-9 (MMP-9) as predictive biomarker for Duchenne.

94 In biochemical system, MMP-2, MMP-3, and MMP-9 bind with high affinity to, and are activated by,

95 (pro)MMP-9 binds to CLL cells through the PEX9 domain and con

96 tingly, late-phase LTP was also decreased by MMP-9 blockade.

97 nstrate that mRNA and protein expressions of MMP-9, but not MMP-2, are significantly higher in AVM ti

98 The serum level of MMP-9, but not MMP-2, is also elevated in AVM patients c

99 The tear film was analyzed for MMP-9 by a commercially available test (InflammaDry; Rap

100 nd achieve ultimate selectivity: They target MMP-9 by allosterically preventing activation of its zym

101 e a collagen Ialpha1 C-1158/59 fragment, and MMP-9 can further degrade it.

102 Consistent with MMP-9 cleavage resulting in largely non-amyloidogenic de

103 tigated whether hIAPP fragments arising from MMP-9 cleavage retain the potential to aggregate and cau

104 P R907Q mutation overlaps with the predicted MMP-9 cleavage site sequence.

105 37 ablated amyloidogenicity, suggesting that MMP-9 cleaves hIAPP 16-37 into non-amyloidogenic fragmen

106 ys clusters may diminish potential MMP-2 and MMP-9 collagenolytic activity.

107 GCF and serum MMP-8 concentrations, serum MMP-9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MM

108 MMP-9 decreased in parallel to clinical stabilization in

109 tro stimulation of isolated neutrophils with MMP-9 decreased neutrophil apoptosis, indicated by reduc

110 n of collagenases or selective inhibition of MMP-9 decreased pathological vascular permeability in a

111 Remarkably, MMP-9 deficiency also corrected non-neural features of F

112 ast 2-fold upregulated or downregulated with MMP-9 deletion (all P<0.05).

113 These effects were MMP-9 dependent and were reversed in the presence of spe

114 collective results support the necessity of MMP-9-dependent H3NT proteolysis in regulating gene path

115 l mechanism of alcohol craving that involves MMP-9-dependent synaptic plasticity in CeA.

116 (MMP-2), a protease which may interfere with MMP-9 detection.

117 GST-PEX9 inhibited MMP-9-driven gelatin proteolysis, measured by gelatin zy

118 stence of a novel regulatory mechanism where MMP-9 drives the suppression of miR-494, resulting in en

119 -specifically macroorchidism-indicating that MMP-9 dysregulation contributes to FXS-associated abnorm

120 MMP-9 efficiently degrades the extracellular matrix comp

121 st time that ionizing radiation (IR)-induced MMP-9 enhances SDC1 shedding, corroborating to tube-indu

122 In the presence of mutant SOD1, MMP-9 expressed by fast motor neurons themselves enhance

123 ct volume, edema, inflammation, and vascular MMP-9 expression compared with IR and sham groups.

124 MMP-9 expression increases during melanoma progression a

125 Thus, IL-6-induced MMP-9 expression is dependent on the activation of MAPK(

126 -induced phosphorylation of MAPK(erk1/2) and MMP-9 expression without affecting the phosphorylation o

127 MMP-9 expression, about which still discords exists, was

128 -9 gene at position -1562, which upregulates MMP-9 expression, correlated with increased motivation f

129 In addition, IL-6 induced MMP-9 expression, suggesting that the observed proteinas

130 ntraction alongside suppression of MMP-2 and MMP-9 expression.

131 g PMNs, and its removal by PMN-MP-associated MMP-9 facilitates PMN trafficking across epithelial laye

132 oblast cell surface and demonstrate that the MMP-9 FN domain is essential for the interaction.

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 smooth muscle actin expression by displacing MMP-9 from the fibroblast cell surface.

136 investigation of the effects of the loss of MMP-9 function on pancreatic islets uncovers a deteriora

137 Finally, C/T polymorphism of MMP-9 gene at position -1562, which upregulates MMP-9 ex

138 primers, we found a significant increase in MMP-9 gene expression in the tumor-reactive stroma durin

139 of the analysis to chromosome 20, where the MMP-9 gene is located, suggesting that SNP-specific miRN

140 etylation of H3K18 as a central regulator of MMP-9 H3NT protease activity both in vitro and at H3NT c

141 Matrix metalloproteases (MMPs) MMP-2 and MMP-9 have been implicated in the physiological cataboli

142 isease, involves matrix metalloproteinase 9 (MMP-9), IL-17, and IL-23 release from infiltrated inflam

143 this antiulcer drug reduces IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with induced periodont

144 the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.

145 er and induces reduction of IL-6, MMP-1, and MMP-9 immunoexpression, reinforcing the idea that the be

146 ocess surface and number of IL-6, MMP-1, and MMP-9-immunolabeled cells in the gingival mucosa were qu

147 AP-positive osteoclasts and IL-6, MMP-1, and MMP-9-immunolabeled cells was significantly lower than i

148 ation products, adenoviral overexpression of MMP-9 in amyloid-prone islets reduced amyloid deposition

149 d cause toxicity, and whether overexpressing MMP-9 in amyloid-prone islets reduces amyloid burden and

150 pha augments expression of MMP-1, MMP-3, and MMP-9 in decidual cells to interfere with normal stepwis

151 ize expression and localization of MMP-2 and MMP-9 in early postnatal and adult rat hippocampus.

152 ators, TNF-alpha, IL-1 beta, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyperosmotic medium.

153 Thus, MMP-9 in particular could play a role in tubal scarring

154 Concentration of MMP-9 in saliva samples was determined, with linearity i

155 ld be rescued by overexpression of exogenous MMP-9 in the central nucleus of the amygdala (CeA).

156 The detrimental role of MMP-9 in the pathology of diabetic wounds was confirmed

157 l types secrete higher amounts of MMP-2 than MMP-9 in their stimulated state, with RPE cells producin

158 ible function of matrix metalloproteinase-9 (MMP-9) in alcohol addiction because this protein has rec

159 sed expression of matrix metallopeptidase 9 (MMP-9) in mice exhibiting positive responses to MSV-EphA

160 ysyl oxidase and a second metalloproteinase, MMP-9, in murine optic gliomas relative to normal non-ne

161 MMP-9, in particular, is highly dynamically regulated in

162 common source of elevated enzymes, including MMP-9, in SJS and OCP tears.

163 matrix metalloproteinases (MMPs), MMP-8 and MMP-9, in the wounds of db/db mice.

164 tors interleukin 1beta (IL-1beta), IL-8, and MMP-9 increased to 13.26 (4.33; 11.14-15.38; P < .001),

165 GST-B1 also inhibited gelatin degradation by MMP-9, indicating that these regions are responsible for

166 er, the recombinant FN domain inhibited both MMP-9-induced TGF-beta activation and alpha-smooth muscl

167 show that the recombinant FN domain inhibits MMP-9-induced TGF-beta activation and fibroblast differe

168 Coinjection of an MMP-9 inhibitor, but not an MMP-2 inhibitor, reduced per

169 Lupin seeds contain the most efficient MMP-9 inhibitors of all legume seeds analyzed, inhibitin

170 Specific MMP-9 inhibitors would be a promising treatment for AVMs

171 min and globulin fractions were screened for MMP-9 inhibitors, using a fluorometric assay and gelatin

172 ally cancelled this process, suggesting that MMP-9 is also de novo synthesized in response to stimuli

173 These findings establish that MMP-9 is critical to the mechanisms responsible for neur

174 We show that MMP-9 is released by neutrophils, but not by eosinophils

175 MMP-9 is upregulated in a panel of rounded-amoeboid comp

176 Matrix metalloproteinase-9 (MMP-9) is active in islets and cleaves hIAPP.

177 ve evidence that matrix metalloproteinase-9 (MMP-9) is necessary to the development of FXS-associated

178 One of these, matrix metalloproteinase-9 (MMP-9), is expressed only by fast motor neurons, which a

179 These plastic changes were impaired in MMP-9 knockout mice.

180 Mice devoid of MMP-9 (MMP-9 knockout) drank as much alcohol as wild-type anima

181 s confirmed further by the study of diabetic MMP-9-knockout mice, which exhibited wounds more prone t

182 atures indicative of EMT, whereas those from MMP-9 KO mice did not acquire a mesenchymal phenotype.

183 nd whole salivary IL-1beta, IL-6, MMP-8, and MMP-9 levels among habitual gutka chewers and controls.

184 IL-6, matrix metalloproteinase (MMP)-8, and MMP-9 levels among habitual gutka chewers and non-chewer

185 ng clinical periodontal parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically heal

186 Across all study groups, MMP-9 levels correlated strongly with MMP-8 and MPO leve

187 s of natural history cohorts showed elevated MMP-9 levels in patients and a significant increase over

188 ogen Screening, Inc, Sarasota, FL) detecting MMP-9 levels of more than 40 ng/ml.

189 ng clinical periodontal parameters and serum MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1

190 tension study clarified that the decrease in MMP-9 levels was not predictive of treatment response.

191 nd whole salivary IL-6, IL-1beta, MMP-8, and MMP-9 levels were higher among gutka chewers than non-ch

192 Serum MMP-9 levels were lower in healthy women with gingivitis

193 e LV, at levels that inversely correlated to MMP-9 levels.

194 Thus, MMP-9 may release netrin-1 fragments from the extracellu

195 he secretion of many proteins, abolished the MMP-9-mCherry secretion, demonstrating the utility of th

196 In MMP-9(-/-) mice, a Th1-inducing condition could maintain

197 Mice devoid of MMP-9 (MMP-9 knockout) drank as much alcohol as wild-typ

198 ed for levels of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP-1 using multianalyte bead-b

199 markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondr

200 Cells positive for MMP-9, MMP-13, and alpha-SMA expression were present at

201 -9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly higher in Gg

202 MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio.

203 Levels of IL-1beta, IL-8, and MMP-9 mRNA remained suppressed, although they rebounded

204 MMP-9/neutrophil gelatinase-associated lipocalin (NGAL)

205 pment, we also explored ICAM-5 expression in MMP-9 null animals.

206 accumulation of apoptotic neutrophils in the MMP-9 null group compared with wild-type group.

207 Infarct regions from wild-type and MMP-9 null mice (n=8 per group) analyzed by glycoproteom

208 ified as having the highest fold increase in MMP-9 null mice.

209 lts uncover LH3 as a new docking receptor of MMP-9 on the fibroblast cell surface and demonstrate tha

210 yme gelatinase B/matrix metalloproteinase-9 (Mmp-9) on islet function in mice.

211 esis-related factors (CD26, FGF, HGF, MMP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (IL-1ra, IL-16) in

212 post-myocardial infarction macrophages with MMP-9 or a CD36-blocking peptide reduced phagocytic capa

213 NJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not inhibit

214 y images showed uniform distribution of anti-MMP-9 over the sensor chip.

215 1), IL-1beta (P <0.01), MMP-8 (P <0.01), and MMP-9 (P <0.01) concentrations.

216 Seed proteins include potent inhibitors of MMP-9, particularly low molecular mass proteins.

217 mponent gelatin, and the hemopexin domain of MMP-9 (PEX9) inhibits this degradation.

218 between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologically or genetically is sufficient to

219 matrix metalloproteinases (MMPs), including MMP-9, play a prominent role.

220 Matrix metalloproteinase-9 (MMP-9) plays an important role in both physiological and

221 The activity of MMP-2 and MMP-9, predicted to be decreased in DN, was investigated

222 In contrast to other known H3NT proteases, MMP-9 primarily cleaved H3K18-Q19 in vitro and in cells.

223 ration of peripheral immune cells, including MMP-9-producing neutrophils/macrophages, resulting in la

224 It is likely that the aberrantly accelerated MMP-9 proteolysis during neurogenesis is a biochemical r

225 Using MMP-9 proteolysis of the wild-type, CIP, and control pep

226 nt sequence is severalfold more sensitive to MMP-9 proteolysis relative to the wild type.

227 Nav1.7 sodium channel is highly sensitive to MMP-9 proteolysis.

228 The MMP-2 and MMP-9 quantification correlated well with the ELISA.

229 ork, we addressed the potential relevance of MMP-9 recruitment to and activity at the surface of fibr

230 Recent evidence indicates that MMP-9 recruitment to the tumor cell surface enhances tum

231 0, favor neutrophil- and monocyte-associated MMP-9 release and disease relapse and opened new therape

232 were in vitro stimulated, and the levels of MMP-9 release were measured in the cell culture supernat

233 naling on neutrophils, resulting in enhanced MMP-9 release, and unexpectedly revealed genetic polymor

234 lity to detect picogram amounts of MMP-2 and MMP-9 released by primary retinal pigment epithelial (RP

235 Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional p

236 Matrix metalloproteinase-9 (MMP-9) represents one of the most prominent proteins ass

237 Moreover, MMP-9 results correlated with the number of obstructed m

238 Thus, the MMP-9 results indicated a clinically significant inflamm

239 The MMP-9 results were increased significantly in women (P <

240 (40.4%) and in 3 of 54 controls (5.6%), the MMP-9 results were positive.

241 tumor angiogenesis is associated with higher MMP-9-SDC1 interactions on both the cell surface and ext

242 mphocytes, responded to CXCL10 by increasing MMP-9 secretion through the activation of extracellular

243 Finally, CXCL10-increased MMP-9 secretion was inhibited by methylprednisolone and

244 c42 GTPase activity, MT1-MMP expression, and MMP-9 secretion.

245 ) expression and matrix metalloproteinase-9 (MMP-9) secretion by these cells.

246 nd inhibition of matrix metalloproteinase-9 (MMP-9) secretion.

247 s identified 41 SNP-specific miRNA targeting MMP-9 SNPs, mostly in the coding exon and an extension o

248 High MMP-9 staining alone (P = .001) or coexistent with low T

249 TNF-alpha and MMP-9 staining did not reveal any significant difference

250 rction, which identified CD36 as a candidate MMP-9 substrate.

251 EX9 did not prevent the degradation of other MMP-9 substrates, such as a fluorogenic peptide, alphaB

252 R-494-mediated regulation of SDC1 but not of MMP-9, suggesting that the 3'-UTR of SDC1 mRNA is a dire

253 ing a low-cost, disposable sensor system for MMP-9 suitable for home-monitoring of inflammation.

254 e findings were correlated to results of the MMP-9 test in tears.

255 expectedly revealed genetic polymorphisms in MMP-9 that alter activity.

256 ur data reveal a new cell-signaling role for MMP-9 through CD36 degradation to regulate macrophage ph

257 dontal parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically healthy patients (P <

258 MMP-9/TIMP-1 ratio was significantly higher in patients

259 e-treated EAE mice had a significantly lower MMP-9/TIMP-1 ratio, and significantly lower MCT-1 and CD

260 Salivary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, were higher in the systemically hea

261 ed abnormal DNA methylation and restored the MMP-9/TIMP-1, -2 balance.

262 ined for metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1)

263 The MMP-9/ tissue inhibitor of metalloproteases-1 (TIMP-1) c

264 oxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patien

265 We show that recruitment of MMP-9 to the fibroblast cell surface occurs through its

266 MMP-9 activity was similar to the pattern of MMP-9 transcripts.

267 nal assays suggest that both pro- and active MMP-9 trigger alpha-smooth muscle actin expression in cu

268 , respectively), matrix metalloproteinase-9 (MMP-9), tumor necrosis factor-alpha, plasminogen activat

269 pression of downstream target genes DKK1 and MMP-9, two molecules that promote myeloma progression.

270 ming growth factor-beta1 (TGF-beta1) induces MMP-9 upregulation in pericytes via p38 mitogen-activate

271 o costly MRI scans could be the detection of MMP-9, using a low-cost, disposable sensor system for MM

272 lso down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migra

273 could indirectly inhibit the proteolysis of MMP-9 via allosteric modulation exclusively at the ligan

274 In HIV-positive individuals, MMP-9 was associated with dolichoectasia only when coexp

275 MMP-9 was confirmed in vitro and in vivo to proteolytica

276 tive correlation between IL-6/MMP-1 and IL-6/MMP-9 was detected in PDSG and PDCimG.

277 MMP-9 was expressed in Escherichia coli BL21 and purifie

278 egradation of Abeta(1-16) by either MMP-2 or MMP-9 was not observed even after prolonged incubation t

279 A THPI selective for MMP-2 and MMP-9 was redesigned to incorporate non-native amino aci

280 basic protein was increased, and activity of MMP-9 was reduced in ischemic rat brains after MMP-12 kn

281 MMP-9 was successfully detected in a clinically relevant

282 (TNF-alpha) and matrix metalloproteinase-9 (MMP-9) was performed on the stomach and rectosigmoid are

283 Gb values for interaction of MMP-9 and anti-MMP-9 were 0.4nM, 680 microRIU and -53.51kJ/mol, respect

284 Elevated concentrations of GCF MMP-8 and MMP-9 were found in Gg compared with Gh group (P <0.05).

285 dichotomy, recombinant human (rh) MMP-2 and MMP-9 were incubated with Abeta40 and Abeta42, and the r

286 When both MMP-3 and MMP-9 were inhibited, both early- and late-phase LTP was

287 Levels of IL-6, IL-1beta, MMP-8, and MMP-9 were measured in UWS using an enzyme-linked immuno

288 d TNF-alpha enhancement of MMP-1, MMP-3, and MMP-9, whereas IFN-gamma inhibited p38 mitogen-activated

289 upon by matrix metalloproteinases (MMP-2 and MMP-9), which are up-regulated in heart tissue post-myoc

290 combinant human matrix metalloproteinases-9 (MMP-9), which has been associated with malignant tumor p

291 The collagenase matrix metalloprotease 9 (MMP-9), which is increased in patients with diabetic mac

292 5 and the endopeptidase metalloproteinase-9 (MMP-9), which mediates ICAM-5 cleavage following glutama

293 , that C3f peptides can act as substrates of MMP-9, which cleaves C3f at L1311-L1312 into two peptide

294 trophils to allergens leads to generation of MMP-9, which may then lead to remodelling in asthma.

295 ndent genes, including the gene that encodes MMP-9, which we implicated as a regulator of integrin-de

296 sors detected the presence of both MMP-2 and MMP-9 while zymography could only detect MMP-2.

297 @C82(OH)22 can effectively inhibit MMP-2 and MMP-9 with high antitumoral efficacy.

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