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

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

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

5 nditions associated with increased levels of MMP-7.

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

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

8 ulfide variants were degraded extensively by MMP-7.

9 on of substrate with the catalytic pocket of 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 f matrix metalloproteinases (MMPs) MMP-3 and MMP-7.

13 sease progressors have higher uEV-associated MMP-7.

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

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

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

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

18 e peptides against proteolytic processing by MMP-7.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 MMP 7 also processed precursor TNF alpha at the correct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 5 on human gelatinase B (MMP-9), matrilysin (MMP-7), and membrane-type 1 MMP (MT1-MMP) was further ex

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

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

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

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

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

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

71 3, 45, 8, and 83 nM for MMP-1, MMP-2, MMP-3, MMP-7, and MMP-9, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 tat, an orally available potent inhibitor of MMP-7, could reduce pulmonary cavitation in M. tuberculo

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

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

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

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

122 MMP-7 deletion results in improved survival and myocardi

123 MMP-7-dependent procryptdin activation in vivo provides

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

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

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

127 ADAMTS-5 and MMP-7 displayed the highest activity toward HC2.

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

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

130 MMP-7 efficiently cleaved recombinant FasL in vitro and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 MMP-7 gene expression was significantly increased in ade

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 In particular, MMP-7 is induced by hypoxia and highly expressed around

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 /-6% of control for WT and was normalized in MMP-7-/- mice.

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

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

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

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

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

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

215 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 doglin ( p = 0.04) and IL-8 ( p < 0.001) and MMP-7 ( p < 0.001) in participants with BA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 MMP-7 specifically digests negatively charged JR2EC immo

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

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

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

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

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

271 6 appeared more stable than those cleaved by MMP-7 under the conditions tested.

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

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

274 MMP 7 was also elevated 5.1-fold.

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

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

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

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

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

280 By contrast, no significant difference in MMP-7 was found in whole urine using ELISA.

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

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

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

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

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

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

287 periostin, Mac-2-binding protein, MMP-3, and MMP-7) was examined in children with biliary atresia (BA

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

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

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

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

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

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

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

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

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

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

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

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

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