ライフサイエンスコーパス: MMP-14

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

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

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

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

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

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

7 tissue inhibitors of metalloproteinases and MMP-14.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 -2 recovered only after co-overexpression of MMP-14 and TIMP-2, but activity further decreased after

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 MMP-14 antibody disrupted ovarian tumor-stromal communic

59 intraperitoneal administration of monoclonal MMP-14 antibody.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 -332 by matrix metalloproteinase (MMP)-2 and MMP-14 has been shown to yield fragments that are promig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 MMP-14 may contribute to removing abnormal ECM component

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 ue transglutaminase and endoglin accompanied MMP-14 suppression.

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

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

166 3r alpha1, matrix metalloproteinase (MMP)-2, MMP-14, tissue inhibitor of metalloproteinase (TIMP) -1,

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

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

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

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

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

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

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

174 MMP-14 was predominately localized to the syncytiotropho

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

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

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

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

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

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

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