ライフサイエンスコーパス: MMP

1 MMP activation was imaged by in vivo small-animal SPECT/

2 MMP activity differed between HIV-1-infected and -uninfe

3 MMP activity in TB differs by HIV-1 status and compartme

4 MMP inhibition is a potential host-directed therapy stra

5 MMP-1 is activated by mast cell tryptase resulting in a

6 MMP-1 protein and activity were assessed.

7 MMP-10 secretion increased by 90% with binding to type I

8 MMP-28 is expressed by the pulmonary epithelium and macr

9 MMP-9 decreased in parallel to clinical stabilization in

10 MMPs (1, 2, 3, 7, 8, 9, 12), MPO, and tissue inhibitor o

11 MMPs are upregulated at all stages of expression in canc

12 One factor, matrix metalloproteinase-1 (MMP-1), is induced in Drosophila ensheathing glia respon

13 mmatory markers (matrix metalloproteinase 1 [MMP-1] and heme oxygenase 1 [HO-1]), and proinflammatory

14 JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and di

15 and (S)-17b) of matrix metalloproteinase 13 (MMP-13).

16 , which stimulates matrix metalloprotease-2 (MMP-2) and MMP-9 activity in the extracellular space.

17 e growth factor, matrix metalloproteinase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase

18 he production of matrix metalloproteinase-2 (MMP-2).

19 ivator (uPA) and matrix metalloproteinase-2 (MMP-2).

20 factor, matrix metalloproteinase-2 (MMP-2), MMP-14, endoglin (ENG), and superoxide dismutase 3 in as

21 ases-3 and -9, and down-regulation of Bcl-2, MMP-2 and -9, NF-kappaB and IkappaBalpha.

22 downstream targets cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.

23 JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not i

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

25 ion of individual MMPs, as there are over 20 MMPs in vertebrates.

26 by the activity of matrix metalloprotease 3 (MMP-3), in contrast to NMDAR-dependent LTP regulated by

27 e cancer growth, matrix metalloproteinase-3 (MMP-3) was lower in CAFs but elevated in prostate cancer

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

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

30 esize that this antiulcer drug reduces IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with induce

31 IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.

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

33 RATIONALE: Matrix metalloproteinase-7 (MMP-7) has been implicated in interstitial lung disease

34 ream targets cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.

35 levels of matrix metalloproteinase (MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in biofluid

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

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

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

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

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

41 s including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondrocytes.

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

43 with the control group showing the abundant MMP-3 expression localized at healing junction.

44 Accordingly, MMP-targeted imaging provides important information rega

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

46 We show that active MMP-2 enhances platelet activation induced by weak stimu

47 Among these, active MMP-2 enhances platelet aggregation by favoring the acti

48 culture yielded even higher levels of active MMPs, facilitating fibronectin and laminin degradation,

49 Additionally, MMP-7 promotes VSMC apoptosis by cleavage of N-cadherin.

50 of published literature on expression of all MMP subtypes at the genetic, protein, and activity level

51 ium through inhibiting integrin alphavbeta6, MMP-2, MMP-9, and ERK phosphorylation by HT29.

52 terized as the central modulator for altered MMP-3 expression in prostate cancer cells and CAFs, but

53 More recently, significant selectivity among MMPs was achieved by blocking the enzymes' specificity p

54 drogen peroxide reduced thrombospondin 2 (an MMP-3 suppressor) expression in prostate cancer cells by

55 five mutations in its interface, that has an MMP-14 inhibition constant (Ki ) of 0.9 pm, the stronges

56 thin the proximal promoters of the MMP-1 and MMP-3 genes, which in association with AP-1 components (

57 was a positive correlation between CSF-1 and MMP-8, which both correlated negatively to IL-34, in pat

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

59 CD68, MMP-12, and MMP-13 were significantly higher in CC10-IL-13 Tg lungs.

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

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

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

63 gated gains in secreted proteases, MMP-2 and MMP-9, following radiation.

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

65 y concentrations of IL-1beta, TNF-alpha, and MMP-2/TIMP-2 complex were assessed using enzyme-linked i

66 In BAVnon-dil patients, TGF-beta1 and MMP-2 gene expression increased significantly, whereas M

67 Serum levels of calprotectin and MMP-8 are elevated in patients with AgP.

68 y/negatively correlated with TP53, EGFR, and MMP members mediated OS development, including angiogene

69 cells were infected with N. gonorrhoeae, and MMP patterns were examined.

70 ated with bronchial hyperresponsiveness, and MMP-1 activation are associated with exacerbation severi

71 ables specific detection of inflammation and MMP activity in aneurysm.

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

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

74 acrophages (GAM) were identified as TSPO and MMP sources.

75 (99m)Tc-RYM1 in vivo correlated with aortic MMP activity and CD68 expression.

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

77 0, favor neutrophil- and monocyte-associated MMP-9 release and disease relapse and opened new therape

78 Small-animal SPECT/CT-based MMP-targeted imaging of the lungs is feasible and reflec

79 alloproteinase (MT1-MMP) is a membrane-bound MMP that is highly expressed in cells with invading capa

80 by modifying the natural non-specific broad MMP inhibitor protein N-TIMP2 to interact optimally with

81 All anatomic sites potentially affected by MMP were examined apart from the esophagus (and larynx i

82 Stepwise processing of amelogenin by MMP-20 in the CS-AMEL hydrogel prevented undesirable pro

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

84 nd that amelogenin was gradually degraded by MMP-20 in the presence of chitosan.

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

86 Removal of beta-catenin causes MMPs to favor adipogenesis, resulting in osteopenia coup

87 le this compound to decipher disease causing MMP networks and to generate new treatment options throu

88 CD68, MMP-12, and MMP-13 were significantly higher in CC10-IL-

89 is of potent but nonselective zinc-chelating MMP inhibitors (e.g., 10a and 10b).

90 ermines a significant portion of circulating MMP-8 concentrations.

91 oning under the blood-brain barrier crossing MMP inhibitor doxycyline in a pre-registered, randomised

92 ted MMP-9 and an accumulation of cytoplasmic MMP-2 over time, but no significant MMP-3 or MMP-8 produ

93 We observed decreased MMP-3 activity in human glaucomatous AH compared to age-

94 ting whether alteration of miR-194-dependent MMPs and PARP-1 causes renal fibrosis in diabetes kidney

95 lation between small-animal SPECT/CT-derived MMP signal and CD68 expression in the lungs (r = 0.70, P

96 dy we evaluated in silico docking to develop MMP-subtype-selective tumor-activated prodrugs.

97 These results indicate that distinct MMPs might act as molecular switches for specific types

98 Previously, Drosophila MMPs have been categorized by their pericellular localiz

99 tears that correlated strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic sou

100 During exacerbations, MMP-1 activity increased and was associated with fall in

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

102 highlight a previously unrecognized role for MMP-28 in promoting chronic lung inflammation and tissue

103 A THPI selective for MMP-2 and MMP-9 was redesigned to incorporate non-native

104 ts into glioma-associated inflammation (GAM, MMP).

105 associated with airway smooth muscle growth, MMP-1 levels are associated with bronchial hyperresponsi

106 Infected MAV-1-resistant BALB/c mice had MMP activity levels equivalent to those in mock infectio

107 ciated in multivariable analysis with higher MMP-2 and lower superoxide dismutase 3 gene expression,

108 Recombinant human MMP-20 was added to the CS-AMEL hydrogel to cleave full-

109 a very potent and selective non-hydroxamate MMP-10/-13 inhibitor.

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

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

112 Imbalance in MMP activity can result in many diseases, such as arthri

113 induction was associated with an increase in MMP-3 expression and activity in CA1 stratum radiatum.

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

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

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

117 This coincided with increased MMP-7 activity and reduced N-cadherin protein levels in

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

119 to asthma severity by transiently increasing MMP activation, airway smooth muscle growth, and airway

120 pment of inhibitors selective for individual MMPs.

121 to understand the contribution of individual MMPs, as there are over 20 MMPs in vertebrates.

122 ound in the cell wall of fungi, both induced MMP-7.

123 he mTOR pathway via TLR9 receptor to induced MMP-7, beta-glucan-stimulated cells were mTOR-independen

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

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

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

127 tion increases enzymatic activity of two key MMPs known to be secreted and activated in neuroinflamma

128 th MMP-13 with published structures of known MMP-13.inhibitor complexes followed by molecular design

129 by an increase in matrix metalloproteinase (MMP) 13, partially because of enhanced LEF1 transcriptio

130 factor (VEGF) and matrix metalloproteinase (MMP) 13.

131 Excessive matrix metalloproteinase (MMP) activity is emerging as a key process but has not b

132 a variant within a Matrix metalloproteinase (MMP) gene member, MMP20, and 11q-deletion subtype neurob

133 f a broad-spectrum matrix metalloproteinase (MMP) inhibitor (GM6001) to block endogenous membrane typ

134 esign of selective matrix metalloproteinase (MMP) inhibitors that also possess favorable solubility p

135 elevated levels of matrix metalloproteinase (MMP)-12 in gingival tissue of patients with the chronic

136 Matrix metalloproteinase (MMP)-3 expression in CTGF-delivered tendon was organized

137 valuates levels of matrix metalloproteinase (MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in

138 egatively affected matrix metalloproteinase (MMP)-9 gene expression.

139 salivary and serum matrix metalloproteinase (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE),

140 ounded morphology, matrix metalloproteinase (MMP)-independent migration, and nuclear deformation.

141 of active enzymes (matrix metalloproteinase [MMP]-8, elastase, and sialidase) in GCF and subgingival

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

143 rotein (TSPO) and matrix metalloproteinases (MMP), may serve as specific imaging biomarkers of the gl

144 lular matrix in a matrix metalloproteinases (MMP)-dependent fashion.

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

146 Metalloproteinases (MMPs) contribute to tissue remodeling and acute inflamma

147 y regulated by different metalloproteinases (MMPs).

148 microRNAs (miRs), matrix metalloproteinases (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabe

149 nds on activating matrix metalloproteinases (MMPs) and selective chemogenetic stimulation of nNOS int

150 Matrix metalloproteinases (MMPs) are central to cancer development and metastasis.

151 Matrix metalloproteinases (MMPs) are extracellular proteases that can cleave extrac

152 gical conditions, matrix metalloproteinases (MMPs) can disrupt the BBB through their proteolytic acti

153 Matrix metalloproteinases (MMPs) contribute to conventional aqueous outflow homeost

154 Matrix metalloproteinases (MMPs) contribute to the breakdown of tissue structures s

155 field, working on matrix metalloproteinases (MMPs) has felt like riding a roller coaster, traveling t

156 ant activation of matrix metalloproteinases (MMPs) is a common feature of pathological cascades obser

157 il elastase (NE), matrix metalloproteinases (MMPs), and myeloperoxidase (MPO) in tear washes of patie

158 licated roles for matrix metalloproteinases (MMPs), particularly macrophage-derived proteinases, in C

159 Monocytes secrete matrix metalloproteinases (MMPs), which have key roles in local tissue destruction

160 and activation of matrix metalloproteinases (MMPs).

161 egulators such as matrix metalloproteinases (MMPs).

162 ity against human matrix metalloproteinases (MMPs).

163 hese design approaches led to small molecule MMP-13 inhibitors 10d and (S)-17b, which bind within the

164 role of membrane-type metalloproteinases (MT-MMPs) in excitatory synaptogenesis.

165 ivation in HT1080 fibrosarcoma cells and MT1-MMP function in MDA-MB231 breast cancer cells were not a

166 has been shown that it up-regulates both MT1-MMP gene and functions in various cell types.

167 hat cell-surface collagen degradation by MT1-MMP involves DDR2-mediated collagen signaling.

168 Cells expressing MT1-MMP-T567E phosphomimetic mutants exhibit enhanced cell m

169 A potential physiological stimulus for MT1-MMP expression is fibrillar collagen, and it has been sh

170 Furthermore, MCAs formed from MT1-MMP-T567E-expressing cells adhere avidly to both intact

171 xpression of mesenchymal genes including MT1-MMP, which was required for collagen-stimulated invasive

172 ed mesenchymal cells as collagen-induced MT1-MMP activation in HT1080 fibrosarcoma cells and MT1-MMP

173 ntegrins, inhibited the collagen-induced MT1-MMP-dependent activation of pro-MMP-2 and up-regulation

174 ed migration speed primarily by inducing MT1-MMP expression.

175 ver, the mechanisms of collagen-mediated MT1-MMP activation and its physiological relevance are not k

176 he transmembrane matrix metalloprotease, MT1-MMP to promote invasive behaviour leading to basement me

177 embrane type 1 matrix metalloproteinase (MT1-MMP) activity does not fully inhibit cell invasion.

178 embrane type 1 matrix metalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface during

179 embrane-type 1 matrix metalloproteinase (MT1-MMP) is a membrane-bound MMP that is highly expressed in

180 vation of pro-MMP-2 and up-regulation of MT1-MMP at the gene and protein levels.

181 To investigate the potential role of MT1-MMP cytoplasmic residue Thr(567) phosphorylation in regu

182 ls that express low endogenous levels of MT1-MMP were engineered to express wild-type MT1-MMP, a phos

183 tional regulation of the Thr(567) in the MT1-MMP cytoplasmic tail may function as a regulatory mechan

184 al inhibition of DDR2 also inhibited the MT1-MMP-dependent cellular degradation of collagen film, sug

185 MMP were engineered to express wild-type MT1-MMP, a phosphomimetic mutant (T567E), or a phosphodefici

186 submesothelial collagen matrix on which MT1-MMP-T567E MCAs rapidly disperse.

187 ogether, our findings support a role for MT3-MMP-dependent shedding of NgR1 in regulating excitatory

188 NCE STATEMENT In this study, we identify MT3-MMP, a membrane-bound zinc protease, to be necessary for

189 NE, MMP-8, MMP-9, and MPO levels were elevated in oGVHD tear

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

191 The high potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-1, -

192 gh potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8, -9,

193 ts, meeting the clinical criteria for ocular MMP, as having a different disease.

194 ective compound that inhibited activation of MMP-9 zymogen and subsequent generation of catalytically

195 l crystals, we hypothesized that addition of MMP-20 to CS-AMEL hydrogel could reinforce the newly gro

196 Ultrastructural analysis of MMP-3 treated matrices by transmission electron microsco

197 undamental clues into the molecular basis of MMP regulation by N-TIMP2 and identifies a promising MMP

198 an attractive system to analyze the basis of MMP specificity.

199 ependent manner, associated with blockade of MMP-2 by AEP.

200 Elevated serum and plasma concentrations of MMP-8 are associated with the risk for and outcome of ca

201 terization of sequence-level determinants of MMP-substrate specificity.

202 ve biopsies, be excluded from a diagnosis of MMP.

203 xygen species in the switching expression of MMP-3 in stromal fibroblasts and prostate cancer cells d

204 The noninvasive imaging of MMP activity in vivo could have a high impact in basic r

205 ation of TFPI-2 contributed to inhibition of MMP-2 mRNA expression, which could be reversed after the

206 elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patients with polycystic ovary s

207 ique to obtain highly specific inhibitors of MMP-14 by modifying the natural non-specific broad MMP i

208 rachial artery and higher salivary levels of MMP-2/TIMP-2 complex.

209 odulate both local and circulating levels of MMP-8 especially when associated with gingivitis.

210 In saliva, levels of MMP-8 were 5.66-fold higher in patients with AgP than in

211 Serum levels of MMP-8 were significantly elevated in patients with AgP c

212 In an in vitro and cell-based model of MMP-dependent breast cancer cellular invasiveness, this

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

214 feature-selection methods for prediction of MMP-2, -3, -7, -8, -9 and -12 substrate-cleavage sites o

215 nificant association among the production of MMP-2/TIMP-2 complex with the presence of CP (P = 0.008)

216 remodeling of the RMS through recruitment of MMP-2 by a previously unrecognized neuronal constituent.

217 mechanism underlying cytokine regulation of MMP expression via STAT-1, and increases our understandi

218 e62 in factor H) led to decreased release of MMP-8 from neutrophils compared with the major allele (V

219 athway for the transcriptional repression of MMP-3 in CAFs.

220 of an eye drop, of AAV-mediated secretion of MMP-3 into AH could have therapeutic potential for those

221 ch bind within the substrate-binding site of MMP-13 and surround the catalytically active Zn(2+) ion

222 The platelet surface target of MMP-2 and the mechanism through which it primes platelet

223 ng, and knowledge of particular functions of MMPs and their contributions to disease progression has

224 sive human glioma model, with involvement of MMPs confirmed using pharmacological inhibition.

225 1.5-fold (P < 0.05), which was dependent on MMP-1 activation.

226 JNJ0966 had no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity

227 group (ZBG), we have carried out a study on MMP-12 inhibitors with a common peptidic core but differ

228 onfirm a possible modulatory role of IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9

229 MMP-2 over time, but no significant MMP-3 or MMP-8 production was observed.

230 no effect on MMP-1, MMP-2, MMP-3, MMP-9, or MMP-14 catalytic activity and did not inhibit activation

231 nteraction between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologically or genetically is suff

232 Besides osteoblasts, MMPs also give rise to bone marrow adipocytes and stroma

233 t at least 500-fold selectivity versus other MMPs.

234 -10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8, -9, -12, and -14 enable this comp

235 inhibitor, RYM, on the basis of which a pan-MMP tracer, RYM1, was designed.

236 The macrocyclic hydroxamate-based pan-MMP inhibitor coupled with 6-hydrazinonicotinamide, RYM1

237 The newly developed pan-MMP inhibitor-based tracer (99m)Tc-RYM1 displays favorab

238 n comparison with RP805, a commonly used pan-MMP tracer in murine models of aneurysm.

239 nal Consensus on Mucous Membrane Pemphigoid (MMP) guidance, which recommends that clinically indistin

240 y typical ocular mucous membrane pemphigoid (MMP).

241 e collected to measure monomethyl phthalate (MMP), monoethyl phthalate (MEP), monobutyl phthalate (MB

242 en reduced mitochondrial membrane potential (MMP) and lowered intracellular pH, while red/NIR had the

243 Airway smooth muscle cells generated pro-MMP-1, which was proteolytically activated by mast cell

244 -induced MT1-MMP-dependent activation of pro-MMP-2 and up-regulation of MT1-MMP at the gene and prote

245 lation by N-TIMP2 and identifies a promising MMP-14 inhibitor as a starting point for the development

246 , and abrogated gains in secreted proteases, MMP-2 and MMP-9, following radiation.

247 sion of one major metalloproteinase protein (MMP-2) and unchanged expression of lysyl oxidase and a s

248 imulation of nNOS interneurons recapitulated MMP activation and t-SP induction (increase in AMPA curr

249 not inhibit activation of the highly related MMP-2 zymogen.

250 red with Hg group (P <0.05) whereas salivary MMP-8/TIMP-1 molar ratio was lower in Gh compared with H

251 However, secreted MMP-7 participated in the shedding of Syndecan-4 from th

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

253 Serum MMP-8 levels and salivary TIMP-1 levels were higher in G

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

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

256 ls, each natural log unit increment in serum MMP-7 was associated with a 3.7% absolute decrement in F

257 We measured serum MMP-7 in 1,227 participants in MESA (Multi-Ethnic Study

258 med a genome-wide association study of serum MMP-8 levels in 2 populations comprising altogether 6049

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

260 The strongest association with serum MMP-8 was found in locus 1q31.3, containing the gene for

261 oplasmic MMP-2 over time, but no significant MMP-3 or MMP-8 production was observed.

262 n was the critical distinction in this small MMP family.

263 e important distinction within this smallest MMP family.

264 ilizes the hidden shared knowledge from some MMP types to enhance predictions of other, distinct targ

265 quent ability to precisely abrogate specific MMP activity could contribute to the fight against a num

266 trials has demonstrated that broad-spectrum MMP inhibitors have limited clinical utility, which has

267 tion constant (Ki ) of 0.9 pm, the strongest MMP-14 inhibitor reported so far.

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

269 The THPI targeting MMP-8 minimized lung damage, increased production of the

270 Inspired by our recent finding that MMP-20 prevents protein occlusion inside enamel crystals

271 onsistent with other published findings that MMP-28 regulates macrophage activation.

272 We found that MMP-3 inhibition or knock-out impaired late-phase LTP in

273 We hypothesized that MMP-28 has contributory roles in emphysema via alteratio

274 RNA-seq reveals that MMPs express a number of marker genes previously assigne

275 The MMP-20 proteolysis of amelogenin was studied, and the mo

276 ced matrix degradation was suppressed by the MMP inhibitor doxycycline in vitro.

277 imal SPECT/CT and ex vivo planar images, the MMP signal was significantly higher in the lungs of CC10

278 ive within the collagenolytic members of the MMP family.

279 (SBEs) within the proximal promoters of the MMP-1 and MMP-3 genes, which in association with AP-1 co

280 a attenuated the binding of AP-2alpha to the MMP-2 promoter, therefore reducing the transcriptional a

281 with a structural pocket in proximity to the MMP-9 zymogen cleavage site near Arg-106, which is disti

282 0a, (R)-10a, and 10b were binding within the MMP-13 active site, the Zn(2+) chelating unit was replac

283 The MMPs and the sister families of "adisintegrin and metall

284 Therefore, MMPs constitute important targets for drug design, devel

285 Thus, MMPs present attractive targets for drug design and have

286 Aortic tissue MMP activity and macrophage marker CD68 expression were

287 an unprecedented pharmacological approach to MMP inhibition, providing an opportunity to improve sele

288 Total MMP activity was measured using a fluorimetric assay.

289 plasticity of dendritic spines by triggering MMP-9 activation and ECM remodelling.

290 In contrast, there are only two MMP genes in Drosophila, DmMmp1 and DmMmp2, which makes

291 ew reagents and assays, we show that the two MMPs cleave different substrates, suggesting that this i

292 -9 gene at position -1562, which upregulates MMP-9 expression, correlated with increased motivation f

293 as to investigate the feasibility of in vivo MMP-targeted molecular imaging for detection of lung inf

294 I collagen and 55% with fibronectin, whereas MMP-7 increased 57% with collagen.

295 expression increased significantly, whereas MMP-14 and ENG expression decreased versus controls.

296 To investigate whether MMP-1 could be activated by mast cells and increase asth

297 Moreover, we studied whether MMP-8-associated variants are linked to increased risk o

298 phic structure of compound 5 in complex with MMP-13 with published structures of known MMP-13.inhibit

299 r protein N-TIMP2 to interact optimally with MMP-14.

300 developed a novel hydrosoluble zwitterionic MMP inhibitor, RYM, on the basis of which a pan-MMP trac