ライフサイエンスコーパス: MMP-7

1 rs (pro-Crps) by matrix metalloproteinase-7 (MMP-7).

2 ro-HNP-1 and beta-defensins, are targets for MMP-7.

3 l extension, and pro-HBD-3 were resistant to MMP-7.

4 nditions associated with increased levels of MMP-7.

5 tivities consistent with MMP-12 and possibly MMP-7.

6 rp4 and pro-Crp4 molecules to degradation by MMP-7.

7 ulfide variants were degraded extensively by MMP-7.

8 on of substrate with the catalytic pocket of MMP-7.

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

10 and two of those sites were also cleaved by MMP-7.

11 ad of casein as a substrate for assaying rat MMP-7.

12 of the net charge of JR2EC upon digestion by MMP-7.

13 f matrix metalloproteinases (MMPs) MMP-3 and MMP-7.

14 ed enzymatic activities of MMP-2, MMP-3, and MMP-7.

15 e-regulate a target promoter such as that of MMP-7.

16 e peptides against proteolytic processing by MMP-7.

17 ture 36-residue form of HBD-1 was cleaved by MMP-7.

18 s used to enhance the zymographic assays for MMP-7, -1, and -13.

19 keted MMPs (e.g., MMP-1, ~850 to >50,000 nM; MMP-7, ~4000 to >25,000 nM).

20 ading MMP, such as MMP-2 (67%), MMP-3 (63%), MMP-7 (62%), and MMP-9 (60%) in hairless mouse skin.

21 matrix metalloproteinase-7 (matrilysin, EC, MMP-7(a)).

22 ation depends on matrix metalloproteinase 7 (MMP-7), a proteinase expressed in most metaplastic epith

23 rapid and sensitive detection of matrilysin (MMP-7, a biomarker involved in the degradation of variou

24 Proteolysis of pro-Crp4 with MMP-7 activated in vitro bactericidal activity to the le

25 proregion at the same residue positions that MMP-7 activates mouse pro-alpha-defensins.

26 overexpression, and the mechanism underlying MMP-7 activation in PC invasion and metastasis.

27 These findings show that MMP-7 activation of pro-Crps can occur without proteolys

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

29 Zymographic measurement of MMP-7 activity is greatly enhanced by heparin.

30 inar transdifferentiation, it was found that MMP-7 activity was sufficient to induce the process, ind

31 tuberculosis, macrophages express MMP-1 and MMP-7 adjacent to areas of tissue destruction.

32 omelysins (MMP-3 and MMP-11), or matrilysin (MMP-7) affected SF/HGF-induced responses.

33 P 9), stromelysin 1 (MMP 3), and matrilysin (MMP 7) all processed this substrate efficiently.

34 MMP 7 also processed precursor TNF alpha at the correct

35 s) are tightly bound to tissues; matrilysin (MMP-7), although the smallest of the MMPs, is one of the

36 de substrate for matrix metalloproteinase-7 (MMP-7), an enzyme that is upregulated in many cancers, t

37 Moreover, HOCl markedly activated pro-MMP-7, an MMP expressed at high levels in lipid-laden ma

38 sulted in similar proteolytic fragments with MMP-7 and -12 being the most potent proteases.

39 h and active-MMP-2, without affecting MMP-9, MMP-7 and angiostatin.

40 more than 90% recovery was accomplished for MMP-7 and C3a, showing promise for isothermal vitrificat

41 Thus, MMP-7 and FasL influence the initiation and maintenance

42 To test associations between serum MMP-7 and lung function, respiratory symptoms, interstit

43 identified here are selective for MMP-9 over MMP-7 and MMP-13.

44 at several invasion-related genes, including MMP-7 and MMP-15, are upregulated in cadherin-11-express

45 The 58-kDa bands derived from plasminogen by MMP-7 and MMP-9 both have the N-terminal sequence KVYLSE

46 MMP-7 and MMP-9 cleaved TFPI at Lys(20)-Leu(21) with add

47 In a bid to define the roles of host-derived MMP-7 and MMP-9 in the tumor-bone microenvironment, the

48 These results indicate that MMP-7 and MMP-9 may regulate new blood vessel formation

49 e tumor-bone microenvironment, the tibias of MMP-7 and MMP-9 null mice were injected with osteolytic

50 tumor-bone microenvironment, and, of these, MMP-7 and MMP-9 were found to be localized to bone-resor

51 wever, rates of cleavage were most rapid for MMP-7 and MMP-9.

52 There was no relationship between MMP-7 and MPO.

53 lar mass of fragment D-dimer, obtained after MMP-7 and MT1-MMP degradation of XL-Fb, is similar to th

54 Indeed, both MMP-7 and myeloperoxidase were colocalized to lipid-lade

55 Binding of MMP-7 and other MMPs to heparan sulfate in the extracell

56 tion induced the expression and secretion of MMP-7 and promoted the binding of T cell factor to the M

57 inase-7 (MMP-7), but the association between MMP-7 and Wnt/beta-catenin signaling in chronic kidney d

58 No binding to matrilysin (MMP-7) and collagenase 1 (MMP-1) was detected at inhibit

59 the gelatinases (MMP-2 and -9), matrilysin (MMP-7) and collagenases (MMP-1 and -13) are difficult to

60 metalloproteinase (MMP) family, matrilysin (MMP-7) and gelatinase B/type IV collagenase (MMP-9), hyd

61 tive matrix metalloproteinase 7 (matrilysin, MMP-7) and heparin-binding epidermal growth factor precu

62 rocessing enzyme matrix metalloproteinase 7 (MMP-7) and its inhibitor TIMP-1 (tissue inhibitor of mat

63 5 on human gelatinase B (MMP-9), matrilysin (MMP-7), and membrane-type 1 MMP (MT1-MMP) was further ex

64 idated using five biomarkers; LDH, CRP, PSA, MMP-7, and C3a.

65 regulatory genes such as RhoA, CDK5, TIMP-1, MMP-7, and EMMPRIN; and MIC-1.

66 or vacA, completely attenuated induction of MMP-7, and inhibition of ERK 1/2 decreased MMP-7 product

67 MMP-2, MMP-7, and MMP-9 activities increased concurrently with

68 MMP-2, MMP-7, and MMP-9 have been shown to be overexpressed in

69 he matrix metalloproteinases (MMP)-2, MMP-3, MMP-7, and MMP-9, and basic fibroblast growth factor, wh

70 3, 45, 8, and 83 nM for MMP-1, MMP-2, MMP-3, MMP-7, and MMP-9, respectively.

71 Reduced chains from MMP-3, MMP-7, and MT1-MMP digests of Fg and XL-Fb were subjecte

72 ge sites obtained by proteolysis with MMP-3, MMP-7, and MT1-MMP were found to be in very close proxim

73 A biomarker index of SP-D, MMP-7, and osteopontin enhanced diagnostic accuracy in p

74 ent of collagen XVIII was also digested with MMP-7, and the cleavage product was sequenced.

75 mutant precursors of each were digested with MMP-7, and the cleavage products were analyzed by NH(2)-

76 recursor within this complex is processed by MMP-7, and the resulting mature HB-EGF engages and activ

77 In vitro, cag(+) isolates selectively induce MMP-7, and this is dependent on activation of ERK 1/2 by

78 city, diffusing capacity of carbon monoxide, MMP-7, and treatment status.

79 t on matrilysin (matrix metalloproteinase 7 [MMP-7]) and stromelysin-2 (MMP-10), two MMPs induced by

80 compared apolipoprotein E (apoE)/MMP-3, apoE/MMP-7, apoE/MMP-9, and apoE/MMP-12 double knockouts with

81 Heparan sulfate and MMP-7 are expressed at similar stages of the rat estrous

82 The most likely docking molecules for MMP-7 are heparan sulfate proteoglycans on or around epi

83 Moreover, the matrix metalloproteinase MMP-7, associated with poor prognosis in PDA, was reduce

84 The proposed assay enabled detection of MMP-7 at clinically relevant concentrations with a limit

85 ver a novel role of the tubular beta-catenin/MMP-7 axis in controlling the fate of interstitial fibro

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

87 or the effect of matrix metalloproteinase 7 (MMP-7) blood concentration and other demographic and cli

88 The 42- and 38-kDa bands generated by MMP-7 both have the N-terminal sequence VVLLPNVETP, whic

89 deficient mice showed that MMP-9, MMP-3, and MMP-7 but not MMP-2 or MMP-12 are needed for resistance.

90 in the tumor cells of constitutively active MMP-7 but not of a catalytically inactive mutant.

91 le Fas or incubation of the tumor cells with MMP-7 but not with MMP-2 or MMP-9.

92 MMP-7 (but not MMP-1, -2, -3, and -9) cleaved corneal ep

93 onally regulates matrix metalloproteinase-7 (MMP-7), but the association between MMP-7 and Wnt/beta-c

94 Interestingly, activity of MMP-7, but none of the other MMPs, was detected in good

95 Thus, HOCl activates pro-MMP-7 by converting the thiol residue of the cysteine sw

96 bead-based multiplex assay, and S100A12 and MMP-7 by ELISA.

97 Differential induction of MMP-7 by H. pylori cag(+) isolates may explain in part t

98 he addition of heparin to the enzyme sample, MMP-7 can be detected at a level of 30 pg in transferrin

99 From the 47-residue HBD-1 precursor, MMP-7 catalyzed removal of 6 amino acids from the amino

100 und significantly elevated expression of the MMP-7, CCND1 (Cyclin D1), CX43 (Connexin 43), PPAR-delta

101 expression in tumor cells by transfection of MMP-7 cDNA in antisense orientation resulted in sensitiz

102 We also conclude that sites for MMP-7 cleavage are more common at the amino termini of a

103 equence PVVLLPNVE, 1 residue upstream of the MMP-7 cleavage site.

104 alpha-defensins resulting from mutations at MMP-7 cleavage sites exist in mouse populations.

105 Crp4 bactericidal activity was eliminated by MMP-7 cleavage.

106 MMP-7 cleaved purified recombinant 34-kDa NC1 fragment o

107 MMP-7 cleaves the collagen XVIII NC1 domain to generate

108 ne cortical slice preparations, we show that MMP-7 cleaves the NR1 subunit of the N-methyl-d-aspartat

109 embranes, a constraint that is relieved when MMP-7 cleaves the prosegment.

110 We found that MMP-7 cleaves within the pro-domain of the HNP-1 precurs

111 rast, enhanced FasL shedding, by recombinant MMP-7, completely protected neurons from Abeta neurotoxi

112 Our findings indicate cyclin D1, MMP-7, connexin 43, PPAR-delta, and ITF-2, likely play i

113 ire direct bacterial exposure, and the basal MMP-7 content of germ-free Paneth cells is sufficient to

114 In summary, levels of renal MMP-7 correlate with Wnt/beta-catenin activity, and urin

115 lammation is increased within the context of MMP-7 deficiency, which involves both Th1- and Th17-medi

116 The inability of MMP-7-deficient macrophages to infiltrate discs could no

117 formation, we showed that the combination of Mmp-7 deletion and EC4-Fc overexpression significantly i

118 In conclusion, combined Mmp-7 deletion and systemic over-expression of EC4-Fc re

119 MMP-7 deletion results in improved survival and myocardi

120 MMP-7-dependent procryptdin activation in vivo provides

121 Extensive MMP-7-dependent procryptdin processing occurs in Paneth

122 f ONO-4817 and galardin for MMP-1, MMP-2 and MMP-7 determined by the proposed colorimetric method was

123 Peptide sequencing of MMP-7 digests of purified natural procryptdins identifie

124 the initiation of procryptdin processing by MMP-7 does not require direct bacterial exposure, and th

125 ApoE/MMP-7 double knockout plaques contained significantly mo

126 MMP-7 efficiently cleaved recombinant FasL in vitro and

127 ate both in vitro and in vivo that exogenous MMP-7 enhances proNGF cleavage and provides neuroprotect

128 following seizures are stabilized by altered MMP-7 enzymatic activity, leading to increased neuronal

129 though M. tuberculosis and BCG do upregulate MMP-7 equally.

130 that molecular signals capable of initiating MMP-7 expression also have the potential to induce forma

131 We determined whether H. pylori alters MMP-7 expression and investigated the molecular pathways

132 MMP-1 but not MMP-7 expression and secretion are relatively M. tubercu

133 Suppression of MMP-7 expression by fibulin-5 was mediated by an integri

134 that selective and coordinated induction of mmp-7 expression by H. pylori cag(+) isolates may explai

135 H. pylori cag(+) strains increased MMP-7 expression in AGS cells 5-7-fold, whereas cag(-) i

136 -catenin signaling by paricalcitol inhibited MMP-7 expression in diseased kidneys and reduced the lev

137 Conversely, inhibition of MMP-7 expression in tumor cells by transfection of MMP-7

138 through ectopic expression of Wnt1 promoted MMP-7 expression in vivo, whereas delivery of the gene e

139 taset revealed patterns of Kaiso, MTG16, and MMP-7 expression supporting the hypothesis that loss of

140 cancer invasion and metastasis by activating MMP-7 expression through the ERK pathway.

141 We also observed higher levels of MMP-7 expression, which correlated with beta-catenin, in

142 stitial fibroblast survival due to decreased MMP-7 expression.

143 as sufficient to stimulate cell invasion and MMP-7 expression.

144 Matrilysin (MMP-7) expression is increased in lung injury and cleave

145 ndant in cardiomyocytes and macrophages, but MMP-7 function after MI has not been defined.

146 MMP-1 and MMP-7 gene expression and secretion are potently upregul

147 ethasone completely suppresses MMP-1 but not MMP-7 gene expression and secretion.

148 MMP-7 gene expression was significantly increased in ade

149 This SNP is located 3' of the MMP-7 gene, in an area enriched with CTCF binding sites.

150 Results from our study suggest that common MMP-7 genetic polymorphisms may contribute to breast can

151 ollagen-specific region of the N-propeptide; MMP-7 had another cleavage site close to the COOH termin

152 Mice deficient for MMP-7 had reduced endothelial area coverage and decrease

153 MMP-7 has no effect on plaque growth or stability, altho

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

155 he matrix metalloproteinases (MMP) MMP-3 and MMP-7 have been implicated in this phenomenon.

156 a cell surface complex composed of CD44HSPG, MMP 7, HB-EGF, and ErbB4 that may play an important role

157 predictive of poor transplant-free survival; MMP-7, ICAM-1, and IL-8 of overall survival; and ICAM-1

158 High concentrations of MMP-7, ICAM-1, IL-8, VCAM-1, and S100A12 predicted poor

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

160 tasis, accumulating evidence also implicates MMP-7 in cancer development.

161 esis, and H. pylori stimulates expression of MMP-7 in gastric epithelial cells in vitro.

162 Quantitative detection of MMP-7 in human plasma was further demonstrated with a LO

163 This is the first report to implicate MMP-7 in post-MI remodeling and to demonstrate that conn

164 es the in vivo requirement for intracellular MMP-7 in pro-CRS4C processing.

165 es indicate that the selective inhibition of MMP-7 in the tumor-bone microenvironment may be of benef

166 l inhibits the activity of human matrilysin (MMP-7) in vitro, suggesting that it might limit proteoly

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

168 MMP-7 increased approximately 1.5-fold in the MI only gr

169 We now report that H. pylori-mediated mmp-7 induction is transcriptionally regulated via aberr

170 The pattern and extent of MMP-7 induction were positively associated with Wnt/beta

171 n silico and in vitro substrate analyses and MMP-7 infusion induced arrhythmias in vivo.

172 In vitro, MMP-7 inhibition and EC4-Fc administration significantly

173 propose that the solubilization of RANKL by MMP-7 is a potential mechanism through which MMP-7 media

174 MMP-7 is abundant in cardiomyocytes and macrophages, but

175 Overexpression of MMP-7 is an early event in the adenoma-to-carcinoma path

176 MMP-7 is capable of processing a number of nonmatrix mol

177 (2) terminus occurs at Gly(61), not Leu(59), MMP-7 is necessary but insufficient to complete the proc

178 Matrix metalloproteinase-7 (MMP-7) is a proteolytic enzyme that can modify the intes

179 Matrix metalloproteinase-7 (MMP-7) is a small secreted proteolytic enzyme with broad

180 The matrix metalloproteinase matrilysin (MMP-7) is expressed in the tumor cells of a majority of

181 ere we show that matrix metalloproteinase-7 (MMP-7) is expressed not only in the majority of human pa

182 determined to be an excellent substrate for MMP-7 (K(M) = 43 microM, V(max) = 1.3 x 10(-)(8) M s(-1)

183 The mean (+/-SD) serum MMP-7 level was 4.3 (+/-2.5) ng/ml (range, 1.2-24.1 ng/m

184 Serum MMP-7 levels may be a quantitative biomarker of subclini

185 uterine and mammary epithelia of these mice, MMP-7 localization is altered and pro-HB-EGF processing

186 Similarly, MMP-7 (matrilysin) and MT1-MMP (membrane type 1 matrix m

187 We have shown that inactivation of MMP-7 (matrilysin) by HOCl coincides with the formation

188 MMP-7 (matrilysin) rapidly cleaved TFPI to a major 35-kD

189 rate for two MMPs, MMP-3 (stromelysin-1) and MMP-7 (matrilysin).

190 the activity of matrix metalloproteinase-7 (MMP-7, matrilysin) in vitro, suggesting that this oxidan

191 wn Kaiso target, Matrix metalloproteinase-7 (MMP-7/Matrilysin).

192 of precursors by matrix metalloproteinase-7 (MMP-7; matrilysin).

193 with Wnt/beta-catenin activity, and urinary MMP-7 may be a noninvasive biomarker of this profibrotic

194 provide evidence that one mechanism whereby MMP-7 may promote tumor survival and resistance to doxor

195 ndicate that H. pylori-mediated induction of MMP-7 may serve to protect the gastric mucosa from patho

196 iferation and apoptosis are not dependent on MMP-7-mediated bacterial eradication.

197 , studies with recombinant protein show that MMP-7-mediated cleavage of NR1 occurs at amino acid 517,

198 h membrane bilayers and to determine whether MMP-7-mediated proteolysis activates the membrane disrup

199 MMP-7 is a potential mechanism through which MMP-7 mediates mammary tumor-induced osteolysis.

200 intestine were significantly up-regulated in MMP-7(-/-) mice compared with that in control C57BL/6 mi

201 d that matrix metalloproteinase-7-deficient (MMP-7(-/-)) mice, which produce procryptdins but not mat

202 Enhanced gastritis in H. pylori-infected mmp-7-/- mice is strongly linked to accelerated epitheli

203 /-6% of control for WT and was normalized in MMP-7-/- mice.

204 imilar, but survival was greatly improved in MMP-7-/- mice.

205 ed expression of MMP-14, while MMP-2, MMP-3, MMP-7, MMP-12, and MMP-13 were not induced by this pepti

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

207 nd were analyzed for levels of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP-1 using multi

208 Proteolytic cleavage by MMP-1, MMP-7, MMP-9, and MMP-12 resulted in considerable loss o

209 The matrix metalloproteinases MMP-2, MMP-3, MMP-7, MMP-9, and MMP-13 are highly expressed in the tum

210 the in vitro IC(50) values for MMP-1, MMP-2, MMP-7, MMP-9, and MMP-14 for at least 4 h after the admi

211 itor (nM) of the activities of MMP-1, MMP-2, MMP-7, MMP-9, and MMP-14.

212 The inhibition mechanism of MMP-7, MMP-9, and MT1-MMP by Brij-35 was a mixed type as

213 rkedly increased expression of MMP-2, MMP-3, MMP-7, MMP-9, MT3-MMP, and ADAMTS5.

214 o by the secreted MMPs, MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, or MMP-13.

215 For MMP-7 movement of heparin and enzyme is almost equal; fo

216 in nephropathy), we observed upregulation of MMP-7 mRNA and protein in a time-dependent manner.

217 H. pylori increases mmp-7 mRNA levels in a cag- and p120-dependent manner an

218 As demonstrators of the assay's utility, MMP-7 mRNA was expression profiled from several colorect

219 Wild-type (WT; n=55) and MMP-7-null (MMP-7-/-; n=32) mice underwent permanent coronary artery

220 oluble RANKL were significantly lower in the MMP-7 null mice compared with wild-type (WT) controls.

221 In keeping with this observation, MMP-7 null mice had significantly fewer osteoclast numbe

222 n Lewis lung carcinoma tumor number, whereas MMP-7 null mice showed a 42% increase in tumor number, a

223 Wild-type (WT; n=55) and MMP-7-null (MMP-7-/-; n=32) mice underwent permanent cor

224 ce of processed CRS4C in protein extracts of MMP-7-null mouse ileum demonstrates the in vivo requirem

225 Consistent with a potential effect of MMP-7 on ligand binding, additional experiments demonstr

226 entical conditions, mice either deficient in MMP-7 or carrying an inactive FasL gene are severely inh

227 Depletion of MMP-7 or inhibition of p38 activity abolishes MSLN-media

228 lood vessel density, whereas deficiencies in MMP-7 or MMP-9 did not influence tumor growth or surviva

229 ontrast, hydrogen peroxide failed to oxidize MMP-7 or to inactivate the enzyme.

230 stasis assays in wild-type and either MMP-9, MMP-7, or MMP-2 null mice.

231 o mice homozygous for null alleles of MMP-2, MMP-7, or MMP-9 genes.

232 In contrast, fragments generated by MMP-2, MMP-7, or plasmin had no effect on macrophage proteinase

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

234 Thus, HOCl inactivates MMP-7, perhaps by site-specific conversion of tryptophan

235 led a prolonged PR interval in WT but not in MMP-7-/- post-MI mice.

236 Furthermore, cleavage of OPN by MMP-3 or MMP-7 potentiated the function of OPN as an adhesive and

237 calcium flux is significantly diminished by MMP-7 pretreatment of cultures.

238 ddition, the AMPA/NMDA ratio is increased by MMP-7 pretreatment.

239 f MMP-7, and inhibition of ERK 1/2 decreased MMP-7 production.

240 l of pancreatic acinar-to-ductal metaplasia, MMP-7 progressively accumulates during the metaplastic t

241 promoted the binding of T cell factor to the MMP-7 promoter in kidney epithelial cells.

242 plex occupying the Kaiso binding site on the MMP-7 promoter.

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

244 of precursors by matrix metalloproteinase-7 (MMP-7), prompting an analysis of the relative sensitivit

245 Levels of MMP-7 protein detected in the urine correlated with rena

246 . pylori cag(+) strains selectively increase MMP-7 protein levels in gastric epithelial cells in vitr

247 These findings show that MMP-7 proteolysis of pro-Crp4(20-92) at Ser(43) downward

248 S4C-1 peptide by matrix metalloproteinase-7 (MMP-7) proteolysis of the precursor proregion at the sam

249 proteolytic cleavage of the stalk region by MMP-7 reduced the bioactivity of sFasL in human cells in

250 , or deletion of matrix-metalloproteinase-7 (Mmp-7) reduced VSMC apoptosis in mouse atherosclerotic p

251 IA procollagen in situ, we demonstrated that MMP-7 removes the NH(2)-propeptide from collagen fibrils

252 ly from claudin-7 depletion, whereas that of MMP-7 resulted from inflammation.

253 hat lack disulfide bonding contain a cryptic MMP-7-sensitive site within the mature peptide moiety.

254 tion of extracellular matrix proteins in AR (MMP-7, SERPING1, and TIMP1).

255 -gene biomarker panel (COL1A2, COL3A1, UMOD, MMP-7, SERPING1, TIMP1) classified AR with high specific

256 Our data show that osteoclast-derived MMP-7 significantly contributes to tumor growth and tumo

257 o-stage study to evaluate the association of MMP-7 single nucleotide polymorphisms (SNPs) with breast

258 This study examined the effects of MMP-1 and MMP-7-sparing inhibition (sMMPi) on regional and global

259 MMP-7 specifically digests negatively charged JR2EC immo

260 as associated with autolytic cleavage of pro-MMP-7, strongly suggesting that oxygenation activates th

261 d to demonstrate that connexin-43 is a novel MMP-7 substrate.

262 Direct binding of MMP-7 to connexin-43, determined by surface plasmon reso

263 Therefore, the ability of osteoclast-derived MMP-7 to promote RANKL solubilization in the tumor-bone

264 6 appeared more stable than those cleaved by MMP-7 under the conditions tested.

265 Mature HNP-1 was resistant to processing by MMP-7 unless the peptide was reduced and alkylated, demo

266 MSLN-mediated MMP-7 upregulation in MUC16-expressing PC cells occurs v

267 MMP 7 was also elevated 5.1-fold.

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

269 Connexin-43 processing by MMP-7 was confirmed by in silico and in vitro substrate

270 MMP-7 was detected in human gastric mucosa by immunohist

271 When MMP-7 was exposed to HOCl generated by myeloperoxidase,

272 In vivo, MMP-7 was expressed in gastric epithelial cells in speci

273 MMP-7 was found to be required for Notch activation, whi

274 nfirmed that overexpression of cyclin D1 and MMP-7 was highly associated with nuclear accumulation of

275 Although active MMP-7 was only observed in good outcome recipients, leve

276 Incubation with MMP-7 was performed at various concentrations (0, 2, 4,

277 ull mice, we report that macrophage-produced MMP-7 was required for proteoglycan degradation, loss of

278 MMP-7 was required for the release of the cytokine TNF-a

279 Chondrocytic MMP-3, but not MMP-7, was required for disc resorption, as determined b

280 and activated by matrix metalloproteinase-7 (MMP-7), we determined if additional defensin molecules,

281 bserved that CSF levels of pro-MMP-2 and pro-MMP-7 were increased in association with HIVD.

282 The expression levels of fibulin-5 and MMP-7 were inversely correlated in lung tumors.

283 system by participating in the secretion of MMP-7 which in turn is important for the shedding of Syn

284 renal induction of matrix metalloproteinase (MMP-7), which induced FasL expression in interstitial fi

285 d down-regulated matrix metalloproteinase-7 (MMP-7), which promoted lung cancer cell invasion.

286 Kaiso-mediated transcriptional repression of mmp-7, which is implicated in tumorigenesis.

287 , we show that one member of the MMP family, MMP-7, which may be released from cells, including micro

288 transcription of its target genes MMP-1 and MMP-7, which regulate extracellular matrix in the prosta

289 o cleaved following treatment of slices with MMP-7, while select AMPA receptor subunits are not.

290 H. pylori cag(+) strains enhance levels of MMP-7 within inflamed mucosa.