ライフサイエンスコーパス: MMP

1 MMP-1 appears to blend selected fit with induced fit mec

2 MMP-1, -2 -7, -9, tissue inhibitor of MMP (TIMP) -1, and

3 MMP-1, MMP-3 and MMP-10 concentrations decreased with ti

4 MMP-12 activity in turn causes the destruction of alveol

5 MMP-2 and MMP-9 expression was reduced in the skin of do

6 MMP-2 significantly increased in both the HIIT group [76

7 MMP-3 and MMP-7 were also naturally upregulated during H

8 MMP-3 was specifically elevated and secreted by NICD3-ex

9 MMP-8 concentration in GCF was associated with GDM (RR:

10 MMP-9 activity was analyzed by zymography.

11 MMP-9 expression and MMP-9/TIMP-1 ratio were similar amo

12 MMP-9 has been shown to play a detrimental role in many

13 MMP-9 in the CON group was not significantly changed [11

14 MMPs function in tissue remodeling within the extracellu

15 MMPs were overexpressed in endocervical+BVAB CM and CVF

16 ression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

17 MMP-1, MMP-3 and MMP-10 concentrations decreased with time afte

18 CSF concentrations of MMP-1, MMP-3 and MMP-10 were increased in TBI patients (at base

19 nalyze expression changes in secreted MMP-1, MMP-3, and TGFbeta.

20 reaks, and increase the expression of MMP-1, MMP-3, and TGFbeta.

21 pression of the matrix metalloproteinase-12 (MMP-12).

22 t the epidermal matrix-metalloproteinase 13 (MMP-13) induces degeneration of unmyelinated axons, wher

23 ith the iNPH group (p < 0.001), while MMP-2, MMP-9 and MMP-12 did not differ between the groups.

24 of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

25 oid autoantibodies were detected in 29 of 76 MMP patients (38.2%) compared with 3 of 45 control parti

26 in coding genes, matrix metalloproteinase-8 (MMP-8) and transcription factor T-Box 3 (TBX3) by qRT-PC

27 stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that was significantly higher in the kid

28 IL]-1beta, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels) evaluations were performe

29 vities of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).

30 rget gene encoding matrix metalloprotease 9 (MMP-9).

31 the potential for matrix metalloprotease-9 (MMP-9), an endopeptidase secreted in response to neurona

32 Matrix metalloproteinase 9 (MMP-9) antisense oligonucleotides (ASO) or an MMP inhibi

33 dysregulation of matrix metalloproteinase-9 (MMP-9) has been implicated in multiple essential roles i

34 educed levels of matrix metalloproteinase-9 (MMP-9) in the plasma and brains at different time points

35 catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by

36 a(G609G/G609G)Mmp13(+/+) mice treated with a MMP inhibitor show lower SMC loss in the aortic arch tha

37 HFHF rats, the MMP inhibitor reduced active MMP-9 expression by 97%, ameliorated histologic evidence

38 MP-9) antisense oligonucleotides (ASO) or an MMP inhibitor were used to induce liver-selective MMP-9

39 hrough the epithelium, and treatment with an MMP inhibitor decreased these effects.

40 etalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

41 MP-3 similarly bridged binding of MMP-13 and MMP-14 to LRP-1.

42 Increased concentrations of MMP-2 and MMP-10 in CSF at baseline were associated with an unfavo

43 MMP-2 and MMP-9 expression was reduced in the skin of doxycycline-

44 ation accompanied by a decrease in MMP-2 and MMP-9 expression within the aortic wall in doxycycline-t

45 y, migration and invasion, reduced MMP-2 and MMP-9 expression, and reduced N-cadherin expression, but

46 migration, and invasion, increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced E-cadheri

47 matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9).

48 parallel cell-specific activity of MMP-2 and MMP-9.

49 MMP-1, MMP-3 and MMP-10 concentrations decreased with time after trauma (

50 CSF concentrations of MMP-1, MMP-3 and MMP-10 were increased in TBI patients (at baseline) comp

51 xpressing HPSE, we have identified MMP-3 and MMP-7 as important sheddases of syndecan-1 shedding in c

52 that the shedding of syndecan-1 by MMP-3 and MMP-7 supports viral egress.

53 MMP-3 and MMP-7 were also naturally upregulated during HSV-1 infec

54 PH group (p < 0.001), while MMP-2, MMP-9 and MMP-12 did not differ between the groups.

55 blasts, RHAMM promoted ERK1/2 activation and MMP-9 expression, whereas in keratinocytes, RHAMM suppre

56 ansduced D1- and D2-MSNs and astrocytes, and MMP-2,9 gelatinase activity adjacent to cell surfaces wa

57 latelet-derived growth factor subunit B) and MMP (matrix metalloprotease) 2/MMP14.

58 med to evaluate the mRNA levels of CD147 and MMP-2 in HGFs and U937 cells.

59 MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature

60 neration through suppressing hypertrophy and MMP-13 in a mouse osteoarthritis model.

61 it induced hypertrophy, mineralization, and MMP-13 in OA-MSC.

62 asis samples had higher levels of Notch3 and MMP-3 compared with patient matched visceral metastases

63 p <= 0.039) and spinal cord (substance P and MMP-1; p <= 0.041).

64 s increased expression of p16Ink4a, p21, and MMP-9.

65 interactions between a collagen peptide and MMP-1(E200A) - an active-site mutant of an archetypal ve

66 sed in the periphery (substance P, pERK, and MMP-1; p <= 0.039) and spinal cord (substance P and MMP-

67 s cued reinstatement of cocaine seeking, and MMP-induced catalysis stimulates beta3-integrins to indu

68 oxidase-derived reactive oxygen species and MMP-9.

69 NA and protein levels of IL-6, TNFalpha, and MMP-9 were elevated in diabetic rats both 2 and 3 weeks

70 Levels of VEGF and MMP-9 were consistently higher in VSP patients, with the

71 ells, we discovered endocervical+BVAB CM and MMPs significantly increased the transmigration of virus

72 cal production of inflammatory cytokines and MMPs, together with apparent mononuclear infiltrate and

73 efore, the elevated expression of S100A9 and MMPs are observed in CRS nasal tissue and S100A9 stimula

74 blast proliferation and migration as well as MMP and alpha-SMA expression.

75 with greater concentrations of BV-associated MMPs increased viral transmigration.

76 sion model estimated the association between MMPs concentration in GCF and GDM.

77 he development of selective, tightly binding MMP inhibitors.

78 monstrate that the shedding of syndecan-1 by MMP-3 and MMP-7 supports viral egress.

79 activation of non-canonical WNT/beta-catenin/MMP signaling and a YY1/lncRNA ESCCAL-1/ribosomal protei

80 y to discriminate between the most conserved MMP pair via an active site-directed mechanism of inhibi

81 disease (AD), have paved the way to consider MMP modulators as promising therapeutic strategies.

82 mice also displayed significantly decreased MMP (matrix metalloproteinases) activity in the aorta (m

83 eeking and extinguished seeking by different MMP subtypes on distinct cell populations poses MMP-2,9

84 the exact mechanism that leads to APN-driven MMP activation is unclear.

85 lized to measure the concentrations of eight MMPs in ventricular human CSF.

86 olytic cleavage of hepatic VEGF using either MMP-9 ASO or intraportal MMP inhibitor in 5-week and 10-

87 Autopsy-derived PFC samples show elevated MMP-9 levels in antidepressant-treated MDD patients comp

88 Administration of exogenous CD147 enhanced MMP-2 expression in HGFs, whereas treatment with cyclosp

89 lasts might play a role in monocyte-enhanced MMP-2 expression in HGFs.

90 Synergistically enhanced MMP-2 expression was recently observed in the coculture

91 ited CD147 expression, reduced U937-enhanced MMP-2 expression in HGFs.

92 For the entire MMP cohort, the sensitivity of all individual tests was

93 between-group differences were observed for MMP and TIMP.

94 Our findings emphasize that suspicion for MMP must remain high for patients who have Foster stage

95 ose patients received systemic treatment for MMP.

96 However, clinically tested global MMP inhibitors have low efficacy that may be due to thei

97 Herein, we harness MMPs 2, 8, 9, and 13 to validate the vicinal difluoro mo

98 ssive cicatrizing conjunctivitis likely have MMP in the absence of alternate diagnoses.

99 abdominal aortic aneurysm (AAA) and, hence, MMP-12-targeted imaging may predict AAA progression and

100 e-induced periodontitis (P > 0.05); however, MMP-9 activity was lower in the group treated with desip

101 By overexpressing HPSE, we have identified MMP-3 and MMP-7 as important sheddases of syndecan-1 she

102 This identified MMP-1 as a new LRP-1 ligand.

103 d t-test were performed to assess changes in MMP and TIMP.

104 Observed variable pattern of changes in MMP concentrations indicates that specific MMPs serve di

105 o understand the exercise-induced changes in MMP-2 and -9 in women undergoing anthracycline chemother

106 disorganization accompanied by a decrease in MMP-2 and MMP-9 expression within the aortic wall in dox

107 However, within-group decrease in MMP-9 was observed in the HIIT group [104.3(51.9) to 65.

108 n training induced long-lasting increases in MMP-2 activity adjacent to D2-MSN synapses.

109 transition (EMT)-associated genes, including MMP-9 and Snail.

110 iability, migration, and invasion, increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced

111 ing heroin-paired cues transiently increased MMP-9 activity around D1-MSN dendritic spines and synaps

112 Chronic venlafaxine increases MMP-9 levels in murine cortex, and increases both pyrami

113 ether an 8-week HIIT intervention influences MMP-9 in breast cancer patients undergoing anthracycline

114 ference datasets that do not bind or inhibit MMPs.

115 c VEGF using either MMP-9 ASO or intraportal MMP inhibitor in 5-week and 10-week HFHF rats enhanced h

116 Rescue therapy with intraportal MMP inhibitor, given after ischemia, in the 5-week HFHF

117 miscuous E3 ligases, including FBW7, a known MMP-9 and Snail regulator.

118 so been obtained in the last decades, making MMPs attractive therapeutic targets for several diseases

119 cted to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significan

120 Our study shows that MCV sT-mediated MMP-9 activation is driven through the LSD, a known E3 l

121 Matrix metalloprotease (MMP)-14-mediated Tie2 ectodomain shedding has recently b

122 onal repressor of membrane metalloproteases (MMP).

123 utically inhibiting matrix metalloproteases (MMPs) suppressed both IMPAD1- and KDELR2-mediated invasi

124 by upregulation of matrix metalloproteases (MMPs) that accompanies higher HPSE expression in infecte

125 s as an inducer of matrix metalloproteinase (MMP) expression in fibroblasts.

126 eir discovery, the matrix metalloproteinase (MMP) family proteases have been considered as therapeuti

127 Certain matrix metalloproteinase (MMP) family proteins have been associated with cell prol

128 able of exposing a matrix metalloproteinase (MMP) substrate on the surface of their filamentous assem

129 the expression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

130 crophage elastase [matrix metalloproteinase (MMP)-12] is the most upregulated MMP in abdominal aortic

131 al upregulation of matrix metalloproteinase (MMP)-2.

132 concentrations of matrix metalloproteinase (MMP)-8 and -9 in gingival crevicular fluid (GCF) during

133 ammatory mediators matrix metalloproteinase (MMP)-8 and interleukin (IL)-1beta and inversely correlat

134 oxygenase (COX)-2, matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-

135 leukin [IL]-1beta, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels) evaluations were

136 alpha [TNFalpha], matrix metalloproteinase [MMP]-9, macrophage migration inhibitory factor [MIF], MI

137 alytic activity of matrix metalloproteinases MMP-2,9.

138 ease the level of matrix metalloproteinases (MMP) -2 and -9, which increase the risk of atheroscleros

139 ing 2 (RGS2), and matrix metalloproteinases (MMPs) 1, 8, and 10 were also strongly upregulated.

140 roteases, such as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with throm

141 Matrix metalloproteinases (MMPs) and the related families of disintegrin metallopro

142 nous inhibitor of matrix metalloproteinases (MMPs) and thus associated with tumor cell invasion, clin

143 Matrix metalloproteinases (MMPs) are extracellular enzymes involved in the degradat

144 Although matrix metalloproteinases (MMPs) are implicated in the regulation of numerous physi

145 Matrix metalloproteinases (MMPs) are inducible endopeptidases that degrade extracel

146 Matrix metalloproteinases (MMPs) are involved in a spectrum of physiological proces

147 A few matrix metalloproteinases (MMPs) are known to support this key process, but its ene

148 We assessed host matrix metalloproteinases (MMPs) as the BV-associated secreted factors which disrup

149 ator (uPA) and/or matrix metalloproteinases (MMPs) as well as some of the EMT markers tested.

150 Matrix metalloproteinases (MMPs) degrade several ECM components and are crucial mod

151 e, a nonselective matrix metalloproteinases (MMPs) inhibitor, to attenuate aortic root widening and i

152 the activities of matrix metalloproteinases (MMPs), a family of zinc-dependent enzymes that promote c

153 E releases active matrix metalloproteinases (MMPs), increase expression of pro-inflammatory cytokines

154 e proteases, like matrix metalloproteinases (MMPs), that are key in extracellular matrix (ECM) degrad

155 ces expression of matrix metalloproteinases (MMPs), which are necessary for the invasive and metastat

156 the activation of matrix metalloproteinases (MMPs).

157 ugh activation of matrix metalloproteinases (MMPs).

158 plasma levels of matrix metalloproteinases ([MMP]-1, -2, -7, -8, and -9) in PTB individuals.

159 MT1-MMP is highly expressed in various types of cancer and h

160 enabling both invadopodia outgrowth and MT1-MMP exocytosis.

161 indin-1 (NUCB1) is critical for MMP2 and MT1-MMP trafficking along the Golgi apparatus.

162 extracellular vesicles (EVs) containing MT1-MMP.

163 ported in other cancers, tumor-expressed MT1-MMP is dispensable for all stages of osteosarcoma progre

164 n of RAB7, FYCO1, or Protrudin inhibited MT1-MMP-dependent extracellular matrix degradation and cance

165 ity by recycling matrix metalloprotease, MT1-MMP.

166 delivery of the matrix metalloproteinase MT1-MMP via endosomal transport by mechanisms that are not k

167 Mphis increased the expression of Mmp14 (MT1-MMP) 7 days post-MI.

168 rse remodeling post-MI and identify Mphi MT1-MMP as a key regulator of this process.

169 this study, we investigated the role of MT1-MMP during various stages of osteosarcoma development.

170 g expression of MT1-MMP, but the role of MT1-MMP in osteosarcoma progression is currently unknown.

171 We observed a strong expression of MT1-MMP in wildtype cells of both primary tumors and lung me

172 opodia formation and the polarization of MT1-MMP recycling compartments, required for invadopodia act

173 eosarcoma display a strong expression of MT1-MMP, but the role of MT1-MMP in osteosarcoma progression

174 nvasion by facilitating translocation of MT1-MMP-laden endosomes to the plasma membrane, enabling bot

175 erograde translocation and exocytosis of MT1-MMP.

176 ix degradation via selectively recycling MT1-MMP but not MT2-MMP.

177 and lung metastases, but, surprisingly, MT1-MMP deficiency did not affect primary tumor growth, bone

178 Mechanistically, we showed that MT1-MMP activates latent TGFbeta1 in Mphis, leading to parac

179 nd human osteosarcoma cells in which the MT1-MMP gene was knocked out using CRISPR/Cas9.

180 Protrudin formed contact sites with MT1-MMP-positive endosomes that contained the RAB7-binding K

181 nd retromer could directly interact with MT1-MMP.

182 MT1- and MT2-MMP showed a high degree of colocalization but were loca

183 ia selectively recycling MT1-MMP but not MT2-MMP.

184 We further found that MT2-MMP, another abundantly expressed metalloprotease, is al

185 sual acuity of patients with biopsy-negative MMP at presentation was significantly lower compared to

186 in both biopsy-positive and biopsy-negative MMP groups was significantly higher compared to patients

187 ths) and were diagnosed with biopsy-negative MMP.

188 l activity (p = 0.002) and elevated neuronal MMP-1 (p < 0.001), suggesting microscale collagen degrad

189 Non-MMP-inhibitory and oncogenic functions of TIMP-1 are med

190 By contrast, for DIF+ nonocular MMP patients, all the individual tests, apart from IgA I

191 SD-95 expression in the cortex of WT but not MMP-9-null mice.

192 nase-3 ([-1A]TIMP3) inhibits ADAMTSs but not MMPs.

193 We identified a Notch3-MMP-3 axis in human prostate cancer bone metastases that

194 GA-1, and AGA) and the methodology to obtain MMP-12 selectivity from hydroxamate-based panMMP inhibit

195 participants, whereas DIF- multisite ocular MMP differed for 1 ELISA and 3 of 7 test combinations.

196 howed limited value in DIF- multisite ocular MMP patients.

197 any site (HR = 0.17, P = .02) and of ocular MMP (HR = 0.11, P = .007) were significantly lower.

198 The rate relapse of ocular MMP was 0.020/PY (95% CI 0.009-0.038/PY), and the rate o

199 rom the C-terminal region, via the action of MMP-9 (matrix metalloproteinase 9).

200 that MCV sT contributes to the activation of MMP-9 as a result of FBW7 targeting and increases the in

201 The enzyme activities of MMP-2 released from cells were examined by zymography.

202 ated with parallel cell-specific activity of MMP-2 and MMP-9.

203 Upon addition of MMP-2, these filaments rapidly break into fragments prio

204 TIMP-3 similarly bridged binding of MMP-13 and MMP-14 to LRP-1.

205 rtance of NUCB1 as an essential component of MMP transport and its overall impact on ECM remodeling.

206 An increase in the concentration of MMP-8 and -9 in women with periodontitis stage III and I

207 CSF concentrations of MMP-1, MMP-3 and MMP-10 were increased in TBI patients (

208 Increased concentrations of MMP-2 and MMP-10 in CSF at baseline were associated with

209 CONCLUSION(S): GCF concentrations of MMP-8 and -9 at early of pregnancy are increased in wome

210 loped GDM showed increased concentrations of MMP-8 and -9 in GCF since the beginning of pregnancy (P

211 negatively correlated with concentrations of MMP-8 and IL-1beta.

212 irement for immunopathologic confirmation of MMP by autoantibody detection is inappropriate for DIF-

213 constitute a signaling pathway downstream of MMP activation that is involved in promoting the transie

214 its functional effect on the enhancement of MMP-2 expression in HGFs.

215 did not provide immunopathologic evidence of MMP in ocular-only MMP patients but showed limited value

216 d DNA breaks, and increase the expression of MMP-1, MMP-3, and TGFbeta.

217 -to-mesenchymal transition and expression of MMP-2 occurred via activation of the PI3K/AKT signaling

218 For example, the free form of MMP-1 was found to have a K(D) of 34.6 nM for LRP-1, whi

219 axons, whereas pharmacological inhibition of MMP-13 prevented axon degeneration.

220 MP-1,2, which caused transient inhibition of MMP-2 activity around D2-MSNs during cue-induced heroin

221 y NICD3-expressing tumors, and inhibition of MMP-3 rescued the NICD3-induced osteoblastic phenotypes.

222 MMP-1, -2 -7, -9, tissue inhibitor of MMP (TIMP) -1, and-2 were measured at baseline and post-

223 These failures were largely due to a lack of MMP-selective agents; accordingly, it has become importa

224 ercise has been shown to reduce the level of MMP in patients with diabetes, high intensity interval t

225 T) has not been utilized to improve level of MMP in women with breast cancer receiving anthracycline

226 n of c-Jun mediated the increasing levels of MMP-2 mRNA transcription.

227 nscriptional consequences of manipulation of MMP in HSCs within their native niche suggest a causal r

228 Using this technique, a diverse profile of MMP and serine protease activities was characterized in

229 Rates of relapse of MMP after drug-free remission are low but not zero; ther

230 0.009-0.038/PY), and the rate of relapse of MMP at any site (ocular or extraocular site) was 0.029/P

231 pared with all other treatments, the risk of MMP relapse at any site (HR = 0.17, P = .02) and of ocul

232 Significant selectivity of MMP 13 versus MMP-2 can be achieved by subtle chain cont

233 Chemical treatments of MMP-9 markedly inhibited MCV sT-induced cell migration a

234 chondrial damage, leading to upregulation of MMP-13, which in turn underlies increased epidermal extr

235 cerebrospinal fluid (CSF) concentrations of MMPs after acute TBI and in relation to clinical outcome

236 h fibroblasts to stimulate the expression of MMPs associated with periodontal extracellular matrix de

237 Increased expression of MMPs have been described in traumatic brain injury (TBI)

238 e the affinity between LRP-1 and a number of MMPs, ADAMs, ADAMTSs, TIMPs and metalloproteinase/TIMP c

239 APN and thereby induce the transcription of MMPs.

240 ernative diagnostic criteria for ocular-only MMP are required to exclude the other causes of scarring

241 unopathologic evidence of MMP in ocular-only MMP patients but showed limited value in DIF- multisite

242 ection is inappropriate for DIF- ocular-only MMP patients, resulting in missed diagnoses, delayed the

243 Ocular-only MMP serum reactivity was not significantly different for

244 n of JNK2 expression, c-Jun phosphorylation, MMP-2 transcription and, ultimately, BC invasion.

245 oups such as mobile and migrant populations (MMPs), and includes improving access to insecticide-trea

246 subtypes on distinct cell populations poses MMP-2,9 activity as an important mediator and contributo

247 show that mitochondrial membrane potential (MMP) can be used to prospectively isolate chronologicall

248 show that mitochondrial membrane potential (MMP) distinguishes quiescent from cycling-primed HSCs.

249 idative stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that was significantly higher in

250 There were 167 patients with biopsy-proven MMP who were seen at the Wilmer Eye Institute between No

251 l viability, migration and invasion, reduced MMP-2 and MMP-9 expression, and reduced N-cadherin expre

252 d epidermal growth factor receptor-regulated MMP-9 expression via ERK1/2, which resulted in cleavage

253 Recombinant human (rh) MMP-9 (10 or 20 mul; 0, 12.5, 25, 50, 100, 200, 500, and

254 al half of TIMP-1 is sufficient for TIMP-1's MMP-inhibitory activity, we propose that those C-termina

255 ed to analyze expression changes in secreted MMP-1, MMP-3, and TGFbeta.

256 Despite being mostly secreted, MMPs have been detected in the cytosol, the mitochondria

257 n the optimized novel, potent, and selective MMP-12 inhibitors with single-digit nanomolar affinity i

258 n of three novel hydroxamate-based selective MMP-12 inhibitors (CGA, CGA-1, and AGA) and the methodol

259 Liver-selective MMP-9 inhibition enhances VEGF-sdf1 signaling and recrui

260 Liver-selective MMP-9 inhibition to protect against proteolytic cleavage

261 nhibitor were used to induce liver-selective MMP-9 inhibition.

262 ques to overcome the challenges of selective MMP inhibition.

263 study introduces a novel family of selective MMP-12 inhibitors and tracers, paving the way for furthe

264 Several MMPs, ADAMTSs and TIMPs have been reported to be endocyt

265 Since MMP-13 inhibition prevents axon degeneration but does no

266 n MMP concentrations indicates that specific MMPs serve different roles in the pathophysiology follow

267 Strikingly, MMP is a stronger determinant of the quantitative and qu

268 Inhibiting TGF-betaR1 suppressed MMP-13 in OA-MSC but stimulated it in OAC.

269 ty without interfering its tumor suppressive MMP-inhibitory function.

270 nderwent a conjunctival biopsy for suspected MMP were included.

271 njunctival tissue in patients with suspected MMP.

272 n the design of therapeutic agents targeting MMPs for various purposes, leading, more recently, to en

273 We aimed to validate a tear MMP-9 in-situ immunoassay (InflammaDry) and to identify

274 Our results demonstrate that MMP is a source of heterogeneity in old HSCs, and its ph

275 Finally, we show that MMP-13 dysregulation also underlies paclitaxel-induced p

276 We previously showed that MMP activation is necessary for and potentiates cued rei

277 ormed, and GCF samples were obtained for the MMP-8 and -9 determination by Multiplex Elisa Assays.

278 combinations of feature values found in the MMP-targeting sets that are distinct from those in the r

279 9Q) of MMP1, (2) MMP9, another member of the MMP family that increases the activity of MMP1, and (3)

280 The results of the MMP-9 in-situ immunoassay varied significantly depending

281 After I/R injury in 15-week HFHF rats, the MMP inhibitor reduced active MMP-9 expression by 97%, am

282 have a K(D) of 34.6 nM for LRP-1, while the MMP-1/TIMP-3 complex had a sevenfold higher affinity (K(

283 hat is regulated by HPSE and executed by the MMPs.

284 However, attempts to target the MMPs with the hope of treating tumors have thus far fail

285 the mechanism behind the activation of these MMPs is mediated by heparanase, which is upregulated upo

286 Members of this MMP family were implicated in AD neuropathology.

287 ition to known mechanoresponsive genes (TNC, MMPs), we have identified novel candidate genes (SFRP2,

288 Specific binding of the tracer to MMP-12 was demonstrated through ex vivo competition.

289 systematic review addressed MSAs targeted to MMPs in Myanmar for malaria prevention.

290 These granules are involved in trafficking MMP-9 from the stroma to the epithelium to promote lumin

291 proteinase (MMP)-12] is the most upregulated MMP in abdominal aortic aneurysm (AAA) and, hence, MMP-1

292 To this end, we propose using MMP-targeting antibodies that can achieve high specifici

293 Significant selectivity of MMP 13 versus MMP-2 can be achieved by subtle chain contraction in a B

294 that the improved outcomes are mediated via MMP-9.

295 However, the precise functions by which MMP-13 is regulated and affects axons remained elusive.

296 pared with the iNPH group (p < 0.001), while MMP-2, MMP-9 and MMP-12 did not differ between the group

297 in those patients was shorter than the whole MMP cohort and the sample size was small.

298 Liver metastasis along with MMP-9 activation and the production of inflammatory cyto

299 studies of a potent difluorinated probe with MMP-9 are also disclosed and indicate that the structura

300 Unfortunately, clinical trials with MMP inhibitors have failed to yield any clinical benefit