ライフサイエンスコーパス: MMP-14

1 ancer biomarker-matrix metalloproteinase-14 (MMP-14).

2 stinct MMP proteases, MMP-12 and MT1-MMP (or MMP-14).

3 P-2 and MMP-9, but not the membrane-tethered MMP-14.

4 and abolished with short hairpin RNA against MMP-14.

5 at processing triple-helical structures than MMP-14.

6 ctivities of MMP-1, MMP-2, MMP-7, MMP-9, and MMP-14.

7 to investigate its binding mode to MMP-9 and MMP-14.

8 tissue inhibitors of metalloproteinases and MMP-14.

9 ntly impaired on fibronectin, a substrate of MMP-14.

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

11 ate hydrolysis and spared ADAM10, MMP-8, and MMP-14.

12 FN-mediated inductions of MMP-9 and MT1-MMP/MMP-14.

13 as well as mRNA levels of MMP-1, MMP-2, and MMP-14.

14 Expression of MT1-MMP, MT2-MMP, and MT3-MMP (MMP 14, 15, and 16) was detected by RT-PCR and immunoblo

15 MP-3 (79-fold and 8-fold, respectively), and MMP-14 (21-fold and 1.4-fold, respectively) and reduced

16 P-2 (~2 to 50 nM), MMP-13 (~2 to 50 nM), and MMP-14 (~4 to 60 nM).

17 cy of the human matrix metalloproteinase-14 (MMP-14), a cancer biomarker.

18 ix metalloproteinase (MT1-MMP; also known as MMP-14), a key enzyme in tumor cell invasion and metasta

19 lytic domain of matrix metalloproteinase-14 (MMP-14), a promalignant protease and a drug target in ca

20 MMP-14, a membrane-anchored MMP, in particular, is close

21 MMP-14, a membrane-bound zinc endopeptidase, has been pr

22 protease classes: matrix metalloproteinases (MMP-14, a predominant target in metastasis; MMP-9, in ne

23 hibitor of gelatinases (MMP-2 and MMP-9) and MMP-14, accelerates diabetic wound healing by lowering i

24 Besides cleaving matrix proteins, MMP-14 activates proMMP-2 leading to an amplification of

25 , which disrupts the blood tumor barrier via MMP-14 activation, and TNP-Cat-B, which selectively targ

26 -degrading enzymes MMP-1, MMP-8, MMP-13, and MMP-14, although differences in the magnitude of respons

27 Gene expression of MMP-14, an MMP that degrades collagen and activates proM

28 low levels in the native tissues except for MMP-14 and -15 (MT1- and MT2-MMP, respectively).

29 variant exhibited 29 pM binding affinity to MMP-14 and 2.4 uM affinity to MMP-3, revealing 7500-fold

30 ng II-induced increase in MMP-2 activity and MMP-14 and BSG protein expression.

31 abrogated the increase in MMP-2 activity and MMP-14 and BSG proteins in ARPE-19 cells.

32 Cross-talk between MMP-14 and CD44 results in phosphorylation of EGF recept

33 ks tightly against non-conserved residues on MMP-14 and clashes with MMP-3.

34 owed protein interactions between endogenous MMP-14 and endoglin within the preeclamptic placenta.

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

36 then screened for high binding to the target MMP-14 and low binding to anti-target MMP-3.

37 MMP-14 and MMP-13 expression in rat corneas parallels th

38 performed to localize the mRNA expression of MMP-14 and MMP-13.

39 ible role of individual MMPs, membrane-bound MMP-14 and secreted MMP-9 were individually down-regulat

40 nsient injury resulted in a decrease of both MMP-14 and TIMP-2 activity and protein.

41 -2 recovered only after co-overexpression of MMP-14 and TIMP-2, but activity further decreased after

42 nt injury is caused by the downregulation of MMP-14 and TIMP-2.

43 Human MMP-14 and TIMP2 cDNA were cloned into a mammalian expre

44 MMP-14 and TIMP2 contribute to the maintenance of adequa

45 We hypothesized that combining TNP-MMP-14 and TNP-Cat-B would enhance TNP tumor accumulatio

46 roximately 900-fold improved affinity toward MMP-14 and up to 16,000-fold greater specificity toward

47 Transfection with MMP-14 and/or TIMP-2 contributed to the return of type I

48 To investigate whether overexpression of MMP-14 and/or TIMP-2 would overcome the effect of nonlet

49 Matrix metalloproteinase-14 (MMP-14) and Cathepsin-B (Cat-B) are overexpressed in gli

50 ne type-1 matrix metalloproteinase (MT1-MMP; MMP-14) and collagenase III (MMP-13) in normal and wound

51 ne type 1-matrix metalloproteinase (MT1-MMP, MMP-14) and ERK1/2 activation.

52 epsin-L (CtsL), matrix metalloproteinase-14 (MMP-14) and MMP-16.

53 g the first MT-MMP to be described, MT1-MMP (MMP-14), and mapped it to mouse chromosome 14.

54 MMP-2), and its activator protease, MT1-MMP (MMP-14), and that active gelatinase A is absolutely requ

55 ving proMMP-2, membrane type 1-MMP (MT1-MMP, MMP-14), and tissue inhibitor of metalloproteinases-2 (T

56 PE-derived matrix metalloproteinase (MMP)-2, MMP-14, and basigin (BSG) are major enzymes involved in

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

58 MMP-2, MMP-14, and cortactin colocalized at regions that appear

59 adation, and increased the levels of TIMP-2, MMP-14, and the active MMP-2 in the membrane extracts, a

60 dothelial SIRT1 depletion, downregulation of MMP-14, and the development of nephrosclerosis.

61 Immunostaining for MMP-2, MMP-14, and the typical PILS components cortactin, calde

62 ysates were collected for analysis of MMP-2, MMP-14, and TIMP-2 activity, mRNA and protein expression

63 The mRNA levels of MMP-2, MMP-14, and TIMP-2 were measured by reverse transcriptio

64 as on the protein and mRNA levels of MMP-2, MMP-14, and TIMP-2.

65 ion of a tri-molecular complex of pro-MMP-2, MMP-14, and tissue inhibitor of metalloproteinases (TIMP

66 MMP-3, MMP-13, MMP-14, and tumor necrosis factor-alpha (TNFalpha) had a

67 MMP-14 antibody disrupted ovarian tumor-stromal communic

68 intraperitoneal administration of monoclonal MMP-14 antibody.

69 The novel C-terminal peptide domains of MMP-14 are encoded by a single large exon that also enco

70 ases (MMP-2 and -9) and membrane-type 1 MMP (MMP-14) are important targets for inhibition, since thei

71 UG-KO mouse lungs express MMP-2, MMP-9, and MMP-14 as well as furin, a pro-protein convertase that a

72 s cell migration through homodimerization of MMP-14 as well as heterodimerization with the cell surfa

73 dies identified matrix metalloproteinase-14 (MMP-14) as a target of SIRT1.

74 ncer identified matrix metalloproteinase 14 (MMP-14) as the cleavage protease of endoglin.

75 d a c-Met/ETS-1/matrix metalloproteinase-14 (MMP-14) axis that controls VE-cadherin degradation, Endo

76 MMP-14, because of its unique ability to cause pericellu

77 in the P(1)' subsite was greatly favored by MMP-14 but disfavored by MMP-1.

78 -type 1 matrix metalloproteinase (MT1-MMP or MMP-14), but little is known about the mechanism by whic

79 nificant loss of inhibitory activity towards MMP-14, but not towards MMP-2 and MMP-9, resulting in in

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

81 ane type 1-matrix metalloproteinase (MT1-MMP/MMP-14) by macrophages, a membrane-tethered MMP importan

82 domain of membrane-type 1 metalloproteinase (MMP-14(cat)) with comparable K(i) values (K(i) approxima

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

84 umber of MMP and TIMP mRNAs [Str1, MT1-MMP, (MMP-14) collagenase-3 (MMP-13), gelatinase A (MMP-2), an

85 ysins), MMP-9 (considered a gelatinase), and MMP-14 (considered a member of the collagenases and of t

86 zymography of aortic extracts revealed that MMP-14 deficiency yielded decreased activation of pro-MM

87 ne type 1-matrix metalloproteinase (MT1-MMP, MMP-14)-dependent invasion through collagen-coated trans

88 model of advanced peritoneal ovarian cancer, MMP-14-dependent invasion and metastasis was effectively

89 These data point to a role of MMP-14 during transendothelial migration of monocytes an

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

91 These synthetic peptides inhibit MMP-14-enhanced cell migration in a dose-dependent manne

92 es and RGC axons during the injury response, Mmp-14 expression decreased during regeneration.

93 Taken together, these data indicate that MMP-14 expression in fibroblasts plays a crucial role in

94 Furthermore, restoration of MMP-14 expression in SIRT1-depeleted mice improved angio

95 n shedding is further amplified by increased MMP-14 expression that requires TRC105 concentration-dep

96 st SB203580, downregulated MMP-9 and MT1-MMP/MMP-14 expressions by FN-stimulated macrophages, suggest

97 s, we obtained homogeneous dual-labeled anti-MMP-14 Fabs (antigen-binding fragments) conjugated to mo

98 The knockout (KO) animals (LysM-Cre(+)MMP-14(fl/fl)) were healthy and fertile, and neither ski

99 ) values for MMP-1, MMP-2, MMP-7, MMP-9, and MMP-14 for at least 4 h after the administration of a th

100 MMP-14 from bone marrow-derived cells can influence the

101 Last, we show that MMP-14 function in mice is important for the accumulatio

102 plaque implicate SAF-1 as a key regulator of MMP-14 gene induction in macrophage cells.

103 Furthermore, induction of endogenous MMP-14 gene, MMP-14 promoter driven reporter gene expres

104 ted with the transcriptional upregulation of MMP-14 gene.

105 is facilitated by an MMP activation cascade (MMP-14 > MMP-13 > MMP-9) and a positive feedback loop of

106 blocks activity of MMP-2, MMP-9, MMP-13, and MMP-14, had reduced tumor burden.

107 Sub-nanomolar limit of detections for MMP-14 has been achieved using our hybrid bioconjugates.

108 The hemopexin (PEX) domain of MMP-14 has been proposed as the modulating region involv

109 -332 by matrix metalloproteinase (MMP)-2 and MMP-14 has been shown to yield fragments that are promig

110 In particular, MMP-2, MMP-9, and MMP-14 have been reported to be crucial for tumor angiog

111 We hypothesized that MAFB, MMP-2, and MMP-14 have integral roles in carpal/tarsal and epiphyse

112 Thus, targeting the MMP-14 hemopexin domain represents a novel approach to i

113 zation and that blade I is required for CD44 MMP-14 heterodimerization.

114 We found that blade IV is necessary for MMP-14 homodimerization and that blade I is required for

115 ploit real-time dye PL recovery triggered by MMP-14 hydrolysis of the AuNP-peptide-dye to extract qua

116 ivation energies were considerably lower for MMP-14 hydrolysis of triple-helical substrates compared

117 o analyze the function of fibroblast-derived MMP-14 in adult skin homeostasis, we generated mice with

118 of active forms of MMP-1, MMP-2, MMP-3, and MMP-14 in conditioned media, and the low-molecular-weigh

119 ia, and the low-molecular-weight fragment of MMP-14 in membrane extracts, as well as mRNA levels of M

120 sduction mechanism to detect the activity of MMP-14 in solution phase.

121 we generated mice with inducible deletion of MMP-14 in the dermal fibroblast (MMP-14(Sf-/-)).

122 Active MMP-1, active MMP-2, and MMP-14 in the ECM fraction of the left ventricle were re

123 ssion of SAF-1 and coexpression of SAF-1 and MMP-14 in the macrophages present in the atherosclerotic

124 nerated animals with conditional ablation of MMP-14 in the monocyte/macrophage lineage.

125 Specifically, Fab 3A2 bound to MMP-14 in the vicinity of the active pocket with a high

126 containing variants towards MMP-2, MMP-9 and MMP-14 in vitro revealed that most showed a significant

127 lloproteinases (MMP)-1, -2, -9, and MT1-MMP (MMP-14) in aggressive compared with poorly aggressive me

128 of MMP-2, MMP-3, MMP-9, MMP-13, and MT1-MMP (MMP-14) in hyperplastic glands and in mammary tumors of

129 brane-bound matrix metalloproteinase type 1 (MMP-14), in vivo evidence for such a function in atheros

130 reases MMP-2 activity and its key regulator, MMP-14, in RPE, inducing breakdown of the RPE basement m

131 nase as a modulator of the MMP-2 but not the MMP-14 increase.

132 Wortmannin blocked the MMP-2 but not the MMP-14 increase.

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

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

135 activity shows the potential of a selective MMP-14 inhibitor for the treatment of solid tumors.

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

137 A nanomolar MMP-2, MMP-9, and MMP-14 inhibitor was identified, compound 3, able to pot

138 hat show high selectivity to gelatinases and MMP-14 (inhibitor 3) and to only MMP-2 (inhibitors 5 and

139 used DX-2400, a highly selective fully human MMP-14 inhibitory antibody discovered using phage displa

140 e type 1-matrix metalloproteinase (MT1-MMP) (MMP-14) initiates pro-MMP-2 activation in a process that

141 MMP-14 is detected at high levels in the atherosclerotic

142 oding the catalytic domain and pro-domain of MMP-14 is distinct from previously described MMP genes,

143 RNAi studies demonstrate that MMP-14 is required to enable CLS formation and that LECs

144 These findings indicate that MMP-14 is the likely cleavage protease of endoglin in th

145 type 1 matrix metalloproteinase (MT1-MMP or MMP-14) is a collagenase that is key in leukocyte migrat

146 ne type 1-matrix metalloprotease (MT1-MMP or MMP-14) is a major activator of pro-MMP-2 and is essenti

147 brane type 1 (MT1) matrix metalloproteinase (MMP-14) is a membrane-tethered MMP considered to be a ma

148 ne type 1 matrix metalloproteinase (MT1-MMP, MMP-14) is a transmembrane collagenase highly expressed

149 type 1-matrix metalloproteinase (MT1-MMP or MMP-14) is a zinc-transmembrane metalloprotease involved

150 sociated MT1-matrix metalloproteinase (MMP) (MMP-14) is directly related to cell migration, invasion,

151 The membrane metalloproteinase, MT1-MMP (MMP-14), is required for endothelial cell (EC) tube form

152 MMP-14 may contribute to removing abnormal ECM component

153 omain represents a novel approach to inhibit MMP-14-mediated cancer dissemination.

154 le-helical peptidase activities of MMP-1 and MMP-14 (membrane-type 1 MMP; MT1-MMP).

155 ivity among MMP-1, MMP-2, MMP-8, MMP-13, and MMP-14/membrane-type 1 (MT1)-MMP.

156 Novel targets, including MMP-8, MMP-10, MMP-14, MMP-19, MMP-25 and MMP-28, are also being consid

157 e investigated the preclinical efficacy of a MMP-14 monoclonal antibody that could inhibit the migrat

158 with ovarian cancer tumors treated with anti-MMP-14 monotherapy showed a marked and sustained regress

159 ages, ox-LDLs markedly elevate the levels of MMP-14 mRNA and protein.

160 MMP-14 mRNA was expressed predominantly in the stromal k

161 Despite efficient down-regulation of MMP-14, neither intravasation nor metastasis of HT-hi/di

162 Overexpression of either MMP-14 or TIMP-2 alone before oxidant injury is not enou

163 MMP-14 or TIMP-2 overexpression alone contributed as muc

164 In some studies, overexpression with either MMP-14 or TIMP-2 was performed to revert the cells to a

165 -expressing GBM39 tumors received either TNP-MMP-14 plus TNP-Cat-B, TNP-Cat-B only, or saline.

166 Increased binding of SAF-1 to the MMP-14 promoter correlated with the transcriptional upre

167 ermore, induction of endogenous MMP-14 gene, MMP-14 promoter driven reporter gene expression and MMP-

168 resent within -213 and -1 nucleotides of the MMP-14 promoter.

169 The mouse MMP-14 protein is encoded by ten exons.

170 formed as potent and selective inhibitors of MMP-14 rather than as broad-specificity antagonists.

171 up to 16,000-fold greater specificity toward MMP-14 relative to other MMPs.

172 enzymes in these processes, but the role of MMP-14 remains largely unknown.

173 in skin proceeded in a comparable manner in MMP-14(Sf+/+) and MMP-14(Sf-/-) mice, but resolution ove

174 umulation of collagen type I was detected in MMP-14(Sf-/-) fibroblasts in culture without significant

175 In support of this, MMP-14(Sf-/-) fibroblasts lost their ability to process

176 f collagen type I accumulated in the skin of MMP-14(Sf-/-) mice without an increase in collagen fibri

177 in a comparable manner in MMP-14(Sf+/+) and MMP-14(Sf-/-) mice, but resolution over time was impaire

178 ce, but resolution over time was impaired in MMP-14(Sf-/-) mice.

179 deletion of MMP-14 in the dermal fibroblast (MMP-14(Sf-/-)).

180 r a broad-spectrum MMP inhibitor (GM6001) or MMP-14 siRNA.

181 ue transglutaminase and endoglin accompanied MMP-14 suppression.

182 s provide a preclinical proof-of-concept for MMP-14 targeting as an adjuvant treatment strategy for a

183 formation of a trimolecular complex between MMP-14, TIMP-2, and proMMP-2 at the cell surface.

184 3r alpha1, matrix metalloproteinase (MMP)-2, MMP-14, tissue inhibitor of metalloproteinase (TIMP) -1,

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

186 the membrane-bound matrix metalloproteinase MMP-14 to the plasma membrane.

187 To examine the contribution of MMP-14 to tumor growth and angiogenesis, we used DX-2400

188 In contrast, overexpression of MMP-14 together with the addition of exogenous TIMP-2 pr

189 s associated with up-regulation of MMP-1 and MMP-14, two proteases related to cell mobility.

190 To understand the induction mechanism of MMP-14 under atherogenic conditions, we examined its exp

191 ectable inhibitory activity toward MMP-3 and MMP-14 up to 10 muM.

192 wounded corneas, but not in normal controls; MMP-14 was found in both normal and wounded corneas.

193 In a cohort of 92 patients, we found that MMP-14 was increased in the serum of women with malignan

194 MMP-14 was predominately localized to the syncytiotropho

195 trix metalloproteinase-2 (MMP-2), MMP-9, and MMP-14, was significantly elevated in both integrin alph

196 ell migration and up-regulation of MMP-1 and MMP-14 were corroborated in mouse primary dermal fibrobl

197 rmost strand motifs within the PEX domain of MMP-14 were designed.

198 MafB, Mmp-2, and Mmp-14 were expressed widely, and tartrate-resistant aci

199 MMP-1, MMP-3, and MT1-MMP/MMP-14 were not inhibited effectively.

200 ctivatable theranostic nanoprobes (TNP): TNP-MMP-14, which disrupts the blood tumor barrier via MMP-1

201 AQARSAASKVKVSMKF also induced expression of MMP-14, while MMP-2, MMP-3, MMP-7, MMP-12, and MMP-13 we

202 inhibitory activity toward MMP-2, MMP-9, and MMP-14 with respect to the previously discovered compoun

203 eclampsia, we investigated the expression of MMP-14 within the placenta and the effects of its inhibi