ライフサイエンスコーパス: MT1-MMP

1 by membrane type 1-matrix metalloproteinase (MT1-MMP).

2 ng membrane type I matrix metalloproteinase (MT1-MMP).

3 proteolytic activity after targeting toward MT1-MMP.

4 c cytoskeletal scaffold protein palladin and MT1-MMP.

5 oiety and proteolytic activity ligand toward MT1-MMP.

6 ction or the general proteolytic activity of MT1-MMP.

7 up-regulation of vimentin, fibronectin, and MT1-MMP.

8 small molecules targeting the PEX domain of MT1-MMP.

9 traction, which appears to be independent of MT1-MMP.

10 A sites that requires the targeted action of MT1-MMP.

11 us to test whether calpain acted upstream of MT1-MMP.

12 t with TIMP-2, TIMP-1 is inefficient against MT1-MMP.

13 essential for the protumorigenic function of MT1-MMP.

14 expression of the wild-type and L50D mutant MT1-MMP.

15 s, only if combined, cause the activation of MT1-MMP.

16 M. tuberculosis-infected monocytes expressed MT1-MMP.

17 , MMP-8, MMP-13, and MMP-14/membrane-type 1 (MT1)-MMP.

18 OP, a loop region in the catalytic domain of MT1-MMP ((163)PYAYIREG(170)), as an essential region for

19 nsible of Notch1 cleavage, here we show that MT1-MMP, a membrane-tethered matrix metalloproteinase in

20 MT1-MMP were engineered to express wild-type MT1-MMP, a phosphomimetic mutant (T567E), or a phosphode

21 ns-membrane type 1 matrix metalloproteinase (MT1-MMP) accumulates.

22 However, the mechanisms of collagen-mediated MT1-MMP activation and its physiological relevance are n

23 Furthermore, DDR2-dependent MT1-MMP activation by cartilage was found to be more eff

24 formed mesenchymal cells as collagen-induced MT1-MMP activation in HT1080 fibrosarcoma cells and MT1-

25 In the course of MT1-MMP activation, the R(108)RKR(111) downward arrow Y(

26 ated by peroxynitrite and involves c-src and MT1-MMP activation.

27 Neutralization of MT1-MMP activity decreased this M. tuberculosis network-

28 Together, our findings established that MT1-MMP activity in breast tumors is essential for BVI,

29 us membrane type 1 matrix metalloproteinase (MT1-MMP) activity does not fully inhibit cell invasion.

30 s and activates several proteases, including MT1-MMP, ADAM10, and ADAM17.

31 by membrane type-1 matrix metalloproteinase (MT1-MMP), ADAMs (a disintegrin domain and metalloprotein

32 eolytic activity of multiple MMPs instead of MT1-MMP alone.

33 Up-regulated MT1-MMP also codistributed with intracellular EphA2 in i

34 of membrane type-1 matrix metalloproteinase (MT1-MMP) anchored on invasive cancer cells and its prote

35 furin expression increases the activities of MT1-MMP and ADAM10 but not that of ADAM17, as demonstrat

36 ort a co-up-regulation and colocalization of MT1-MMP and atypical protein kinase C iota (aPKCiota) in

37 3-shRNA expression depletes shed vesicles of MT1-MMP and decreases cell invasiveness when embedded in

38 a regulator of Stx4-mediated trafficking of MT1-MMP and EGFR, advancing our understanding of the rol

39 The associations between the expression of MT1-MMP and EMT-associated proteins with clinicopatholog

40 S1P and WSS synergistically activated MT1-MMP and induced cell membrane localization of MT1-MM

41 ncreased gene and protein levels of MMP2 and MT1-MMP and induced matrix contraction in FHL-124 cells.

42 ormation is based on the cytoplasmic tail of MT1-MMP and its ability to bind the subcortical actin cy

43 gulation of the plasma membrane targeting of MT1-MMP and its associated invadopodia.

44 SRC and by coordinating ECM degradation via MT1-MMP and MMP2 expression.

45 lly significant positive correlation between MT1-MMP and Snail in these tumors.

46 This ensures focal delivery of MT1-MMP and supports pericellular matrix degradation and

47 will contribute to the laboratory studies of MT1-MMP and then, ultimately, to the design of novel, mo

48 dipitously more effective against MMP-8 than MT1-MMP and was utilized successfully in a mouse model o

49 of membrane type 1 matrix metalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface dur

50 se membrane-type 1 matrix metalloproteinase (MT1-MMP) and membrane-mimicking environments interplay i

51 ne-anchored matrix metalloproteinases MMP14 (MT1-MMP) and MMP15 (MT2-MMP), which drive epithelial cel

52 es membrane-type 1 matrix metalloproteinase (MT1-MMP)- and ERK1/2-dependent scattering of pancreatic

53 In addition, we find that ARF6, MT1-MMP, and kinesin-1 are up-regulated in high-grade tr

54 gos (membrane-type 1 matrix metalloprotease [MT1-MMP] and beta3 integrin) required for invadosome for

55 This study identifies MT1-MMP as a key MMP responsible for effecting postinfar

56 Here, we identify MT1-MMP as a novel interacting partner of dual-specifici

57 e findings identify a novel role for nuclear MT1-MMP as a previously unsuspected transactivator of si

58 ed membrane type 1-matrix metalloproteinase (MT1-MMP) as the key protease for collagen breakdown.

59 e accumulation of the MMP16 substrate MMP14 (MT1-MMP) as well as L1CAM cell adhesion molecule, identi

60 ading to the decreased surface expression of MT1-MMP, as observed previously in transformed fibroblas

61 -MMP, we identify the membrane-anchored MMP, MT1-MMP, as the dominant collagenase that is operative w

62 activation of pro-MMP-2 and up-regulation of MT1-MMP at the gene and protein levels.

63 ted by phospholipase D2 drives deposition of MT1-MMP at the site of invadopodia formation and is crit

64 TIMP-2 by alpha1(IV)NC1 led to saturation of MT1-MMP binding sites, which in turn led to inhibition o

65 MT1-MMP-blocking antibodies diminished migration, prolif

66 espective inhibitory prodomains not only for MT1-MMP but also for other MMP family members.

67 not due to loss of the catalytic function of MT1-MMP but due to inefficient localization of the enzym

68 f tyrosine Y573 in the cytoplasmic domain of MT1-MMP by LIMK.

69 mbrane type-1 matrix metalloprotease (MMP14, MT1-MMP) by heterotrimeric G proteins, and in turn, the

70 Using this antibody, we have shown that the MT1-MMP-catalyzed activation of proMMP-2 is involved in

71 oxia regulates the function of DCs via KIF2A/MT1-MMP/CD44 axis, providing critical information to und

72 its L622D mutant with the single inactivated MT1-MMP cleavage site differentially regulate cell motil

73 , its Chuzhoi mutant with the two functional MT1-MMP cleavage sites, and its L622D mutant with the si

74 he membrane type-1 matrix metalloproteinase (MT1-MMP) cleavage of the PKP(621) downward arrowLI site

75 interaction in same cell-surface complexes, MT1-MMP cleaved EphA2 at its Fibronectin type-III domain

76 evidence that aPKCiota, in association with MT1-MMP-containing endosomes, phosphorylates cortactin,

77 syndrome protein and Scar homolog (WASH) on MT1-MMP-containing late endosomes in invasive breast car

78 catalytic function of the metalloproteinase MT1-MMP controls ECM structure, cell shape, and an integ

79 al. describe an unexpected function for the MT1-MMP cytoplasmic domain in imprinting spatial memory

80 To investigate the potential role of MT1-MMP cytoplasmic residue Thr(567) phosphorylation in

81 nslational regulation of the Thr(567) in the MT1-MMP cytoplasmic tail may function as a regulatory me

82 e basis of a yeast two-hybrid screen for the MT1-MMP cytoplasmic tail-binding proteins, we identify h

83 at membrane type-1 matrix metalloproteinase (MT1-MMP) deficient mice have reduced complexity of the n

84 cally to the glomerular layer was reduced in MT1-MMP-deficient mice in contrast to controls while num

85 rge parts of the RMS were fully preserved in MT1-MMP-deficient mice, but we detected an increase in c

86 MT1-MMP delivery to nascent microvesicles depends on the

87 esin motors to drive endosome tubulation and MT1-MMP delivery to the surface of cancer cells, identif

88 In contrast to MT1-MMP, DeltaPEX did not support tumor growth in vivo,

89 by membrane type-1 matrix metalloproteinase (MT1-MMP)-dependent invadopodia activity.

90 ves membrane type 1 matrix metallopatrinase (MT1-MMP)-dependent proteolysis as well as Pak, Raf, and

91 age mechanism of MT1-MMP on Notch1, and that MT1-MMP-dependent activation of Notch1 sustains melanoma

92 ng integrins, inhibited the collagen-induced MT1-MMP-dependent activation of pro-MMP-2 and up-regulat

93 ogical inhibition of DDR2 also inhibited the MT1-MMP-dependent cellular degradation of collagen film,

94 ted monocytes degraded collagen matrix in an MT1-MMP-dependent manner, and MT1-MMP neutralization dec

95 In turn, LIMK1 and LIMK2 are required for MT1-MMP-dependent matrix degradation and cell invasion i

96 In turn, MT1-MMP-dependent PI3Kdelta activation regulates the imm

97 Specific siRNA inhibition of MT1-MMP did not suppress TGFbeta2-induced matrix contrac

98 MT1-MMP downregulation in cancer cells decreased lung me

99 s have revealed a novel mechanism regulating MT1-MMP during cellular invasion and have identified the

100 ed membrane type I matrix metalloproteinase (MT1-MMP) during early steps of the metastatic cascade in

101 These data identify a critical ARF6-JIP-MT1-MMP-dynein-dynactin-kinesin-1 axis promoting an inva

102 r JIP3/JIP4 in breast tumor cells results in MT1-MMP endosome mispositioning and reduces MT1-MMP exoc

103 tivity in a tug-of-war mechanism, leading to MT1-MMP endosome tubulation and exocytosis.

104 yndrome protein and scar homologue (WASH) on MT1-MMP endosomes on which they recruit dynein-dynactin

105 r prototype that targets the cellular active MT1-MMP enzyme alone.

106 expressed, fully functional, active cellular MT1-MMP enzyme are roughly equal to 1 x 10(5) molecules/

107 mounts of the cell surface-associated active MT1-MMP enzyme in multiple cancer cell types, including

108 cell-surface levels of the active, TIMP-free MT1-MMP enzyme.

109 MT1-MMP exists in various forms: a 63-kDa proenzyme is s

110 MT1-MMP endosome mispositioning and reduces MT1-MMP exocytosis and tumor cell invasion.

111 Although Slug increased MT1-MMP expression and ERK1/2 activity, Slug-expressing

112 We find that active Notch1 and MT1-MMP expression correlate significantly in over 70% o

113 inical importance, we observed that elevated MT1-MMP expression correlated with BVI in biopsies from

114 Gene silencing of MT1-MMP expression further demonstrated its requirement

115 anoma cells affects Notch1 cleavage, whereas MT1-MMP expression in ADAM10/17 double knock-out fibrobl

116 scular endothelial cells, but did not affect MT1-MMP expression in lymphatic endothelial cells, LVI,

117 Modulation of MT1-MMP expression in melanoma cells affects Notch1 clea

118 A potential physiological stimulus for MT1-MMP expression is fibrillar collagen, and it has bee

119 in RGC axons and Muller glia, mimicking the MT1-MMP expression pattern seen in rabbits and neonatal

120 he acquisition of either wild-type or mutant MT1-MMP expression results in altered cohesion of epithe

121 reduction in RhoA and Cdc42 GTPase activity, MT1-MMP expression, and MMP-9 secretion.

122 hanced migration speed primarily by inducing MT1-MMP expression.

123 x 10(6) range in the cells with the enforced MT1-MMP expression.

124 nd membrane type 1 matrix metalloproteinase (MT1-MMP) expression.

125 st-tumor cell lines impaired the delivery of MT1-MMP from late endocytic storage compartments to the

126 dynamin-2, which control the trafficking of MT1-MMP from late endosome to the plasma membrane and pl

127 activation in HT1080 fibrosarcoma cells and MT1-MMP function in MDA-MB231 breast cancer cells were n

128 Putative MT1-MMP functions in trophoblasts were determined using

129 MT-LOOP region of MT1-MMP (LOOPAb) inhibited MT1-MMP functions, fully mimicking the phenotype of the

130 tion to cell adhesion complexes and regulate MT1-MMP functions.

131 it has been shown that it up-regulates both MT1-MMP gene and functions in various cell types.

132 CSF-2), granulocyte CSF (G-CSF, CSF-3), and MT1-MMP gene expression.

133 In order to study specificity for MT1-MMP, GNP-ActFP is treated to HT1080 and MCF7 cells,

134 MT1-MMP has a short intracellular domain (ICD) that has

135 Membrane type 1-matrix metalloproteinase (MT1-MMP) has an essential role in matrix degradation and

136 Membrane type 1-matrix metalloproteinase (MT1-MMP) has been shown by others to regulate endothelia

137 Elevated expression levels of MT1-MMP have been demonstrated to correlate with a poor

138 While changes in solvation of MT1-MMP have been recently studied, little is known abou

139 which further emphasizes the key role of the MT1-MMP ICD.

140 In human TB granulomas, MT1-MMP immunoreactivity was observed in macrophages thr

141 MP and induced cell membrane localization of MT1-MMP in a calpain-dependent manner.

142 how the requirement of the metalloproteinase MT1-MMP in endothelial cells and fibroblasts, but not ca

143 We hypothesized that reduced placental MT1-MMP in FGR impairs trophoblast functions.

144 We conclude that reduced placental MT1-MMP in FGR may contribute to the impaired trophoblas

145 MMP, we examined the expression of Snail and MT1-MMP in human PDAC tumors and found a statistically s

146 unctional importance of the interaction with MT1-MMP in pericellular matrix degradation and mesenchym

147 Here, we investigated the role of MT1-MMP in the dissemination of ESCC.

148 etect endogenous and overexpressed exogenous MT1-MMP in the Eca109 and Eca9706 cell lines, respective

149 tial expression pattern of MMP-2, -3, -9 and MT1-MMP in the healthy mouse retina.

150 and MaCSCs as well as surface expression of MT1-MMP in tumor cells harboring the P878A/P881A mutatio

151 ressed MT1-MMP upregulated the expression of MT1-MMP in vascular endothelial cells, but did not affec

152 ndependent manner, and upregulates MMP-3 and MT1-MMP, in addition to MMP-1.

153 The structure of MT1-MMP includes the hemopexin domain (PEX) that is dist

154 MT1-MMP induced EMT in ESCC both in vivo and in vitro, N

155 MT1-MMP-induced EMT led to increase migration and invasi

156 Transwell assay was used to estimate MT1-MMP-induced invasion and metastasis.

157 a membrane type 1 matrix metalloproteinase (MT1-MMP) inducer, which increased granulocyte macrophage

158 A recent study has revealed that MT1-MMP induces epithelial-to-mesenchymal transition (EM

159 e for the development of novel and selective MT1-MMP inhibitors that specifically target the PEX doma

160 l exosite target region to develop selective MT1-MMP inhibitors.

161 These data identify a critical MT1-MMP/integrin/YAP/TAZ axis operative in the stem cell

162 Importantly, we find that MT1-MMP interacts with Notch1 at the cell membrane, supp

163 vading cells, N-WASP promoted trafficking of MT1-MMP into invasive pseudopodia, primarily from late e

164 ion through pharmacological targeting of the MT1-MMP intracellular signaling.

165 ssociation of KIF5B, surface localization of MT1-MMP, invadopodia, and invasion in cancer cells.

166 ng that cell-surface collagen degradation by MT1-MMP involves DDR2-mediated collagen signaling.

167 MT1-MMP is also regulated as a membrane protein through

168 Taken together, we demonstrate that MT1-MMP is central to two key elements of TB pathogenesi

169 Understanding how MT1-MMP is delivered to the surface of tumor cells is es

170 ow that the membrane-bound metalloproteinase MT1-MMP is enriched not only at podosomes but also at di

171 The latency of MT1-MMP is maintained by its N-terminal inhibitory prodo

172 In this study, we report that MT1-MMP is mono-ubiquitinated at its unique lysine resid

173 Polarized targeting and deposition of MT1-MMP is pivotal for metastasis.

174 MT1-MMP is regulated as a proteinase by activation and c

175 MT1-MMP is stable and active over a wide range of temper

176 evidence shows that the cytoplasmic tail of MT1-MMP is subjected to phosphorylation, and this post-t

177 es the processing of Notch1, indicating that MT1-MMP is sufficient to promote Notch1 activation indep

178 Membrane-type matrix metalloproteinase 1 (MT1-MMP) is a key enzyme in these cellular processes.

179 Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a membrane-bound MMP that is highly expresse

180 Membrane type-1 matrix metalloproteinase (MT1-MMP) is a promising drug target in malignancy.

181 Membrane type 1-matrix metalloproteinase (MT1-MMP) is associated with enhanced tumorigenicity in m

182 ve membrane type-1 matrix metalloproteinase (MT1-MMP) is the primary mediator of proteolytic events o

183 Importantly, the majority of MT1-MMP islets are reused as sites of podosome reemergen

184 MT1-MMP islets become apparent upon podosome dissolution

185 MT1-MMP islets thus act as cellular memory devices that

186 lonal antibody against MT1-MMP, raised in an MT1-MMP knock-out mouse.

187 ng function by Y315F endophilin A2 mutant or MT1-MMP knockdown reduced markers for EMT and MaCSC acti

188 magnitude of LV myocardial growth, altering MT1-MMP levels caused specific matrix-dependent changes

189 MT1-MMP levels were found to be correlated with the dept

190 MT1-MMP localization was for the first time studied in a

191 pecifically recognizes the MT-LOOP region of MT1-MMP (LOOPAb) inhibited MT1-MMP functions, fully mimi

192 controls inflammatory gene responses wherein MT1-MMP(-/-) macrophages mount exaggerated chemokine and

193 This novel link between LIMK1/2 and MT1-MMP may have important consequences for therapeutic

194 certain MMP types, such as membrane type-1 (MT1) MMP, may also be involved in profibrotic cascades t

195 N-terminal sequencing of the MT1-MMP-mediated cleaved products and mutational analyse

196 entive properties of diet-derived EGCG alter MT1-MMP-mediated intracellular signaling.

197 th concentric remodeling), a 60% increase in MT1-MMP-mediated LTBP-1 hydrolysis and a 190% increase i

198 PO, significant differences in LV function, MT1-MMP-mediated LTBP-1 hydrolysis, and collagen content

199 ene expression, and this process required an MT1-MMP-mediated sequential activation of the Src and JA

200 ed membrane type 1-matrix metalloproteinase (MT1-MMP) mediates proteolysis-based invasive tumor growt

201 P combine to activate calpains, which direct MT1-MMP membrane localization to initiate endothelial sp

202 -peptide substitution (p.Thr17Arg) decreases MT1-MMP membrane localization with consequent impairment

203 Membrane type 1 matrix metalloproteinase (MT1-MMP, MMP-14) is a transmembrane collagenase highly e

204 st membrane type 1-matrix metalloproteinase (MT1-MMP, MMP-14)-dependent invasion through collagen-coa

205 antagonist SB203580, downregulated MMP-9 and MT1-MMP/MMP-14 expressions by FN-stimulated macrophages,

206 of membrane type 1-matrix metalloproteinase (MT1-MMP/MMP-14) by macrophages, a membrane-tethered MMP

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

208 n of the membrane-anchored metalloproteinase MT1-MMP (Mmp14) in mesenchymal progenitors, but not in c

209 Membrane type 1 matrix metalloproteinase (MT1-MMP/MMP14) is a zinc-dependent type I transmembrane

210 by membrane type 1-matrix metalloproteinase (MT1-MMP/MMP14), the main invadopodial matrix degradative

211 te membrane-type 1 matrix metalloproteinase (MT1-MMP; MMP14), which functions in actin-based pseudopo

212 MT1-MMP modulates inflammatory responses in a protease-i

213 MT1-MMP mRNA and active enzyme was quantified in placent

214 In FGR placentas, levels of MT1-MMP mRNA and of active MT1-MMP protein were reduced

215 In patients with TB, induced sputum MT1-MMP mRNA levels were increased 5.1-fold compared wit

216 reas overexpression of a nonphosphorylatable MT1-MMP mutant (Y573F) abrogated CSF-2 and CSF-3 transcr

217 igenic activity of wild-type MT1-MMP with an MT1-MMP mutant lacking PEX (DeltaPEX).

218 mesenchymal tumor cell invasion, whereas in MT1-MMP-negative cells, palladin overexpression was insu

219 n matrix in an MT1-MMP-dependent manner, and MT1-MMP neutralization decreased collagen degradation by

220 t the membrane-tethered matrix metalloenzyme MT1-MMP not only serves as an ECM-directed proteinase, b

221 an in vivo setting, mice heterozygous for an MT1-MMP-null allele display a distinct survival advantag

222 ing a potential direct cleavage mechanism of MT1-MMP on Notch1, and that MT1-MMP-dependent activation

223 e MT-LOOP effectively inhibited functions of MT1-MMP on the cell surface, including proMMP-2 activati

224 he membrane type 1 matrix metalloproteinase (MT1-MMP or MMP-14) is a collagenase that is key in leuko

225 Membrane type 1-matrix metalloproteinase (MT1-MMP or MMP-14) is a zinc-transmembrane metalloprotea

226 ations in membrane type-1 metalloproteinase (MT1-MMP or MMP14).

227 h for two distinct MMP proteases, MMP-12 and MT1-MMP (or MMP-14).

228 PO in MT1-MMP overexpression increased LTBP-1 hydrolysis (18%)

229 and transgenic mice with cardiac-restricted MT1-MMP overexpression or MT1-MMP reduced expression und

230 Although LV mass was similar among WT, MT1-MMP overexpression, and MT1-MMP reduced expression a

231 that the previously described Src-dependent MT1-MMP phosphorylation is a prerequisite for ubiquitina

232 The present study tested the hypothesis that MT1-MMP plays a direct role in the matrix remodeling res

233 tion of F-actin binding protein cortactin to MT1-MMP-positive endosomes and invadopodia formation and

234 , which is present in F-actin-rich puncta on MT1-MMP-positive endosomes and regulates cortactin assoc

235 hat LIMK1 regulates cortactin association to MT1-MMP-positive endosomes, while LIMK2 controls invadop

236 sm that involves tubular connections between MT1-MMP-positive late endosomes and the plasma membrane

237 In conclusion, our results suggest that MT1-MMP promotes ESCC invasion and metastasis.

238 MMP2 and MT1-MMP protein levels were analyzed by ELISA and Wester

239 MT1-MMP protein was localized in first-trimester and ter

240 centas, levels of MT1-MMP mRNA and of active MT1-MMP protein were reduced (-34.2%, P < 0.05, and -21.

241 ns of a specific monoclonal antibody against MT1-MMP, raised in an MT1-MMP knock-out mouse.

242 imilar among WT, MT1-MMP overexpression, and MT1-MMP reduced expression after PO, significant differe

243 PO in MT1-MMP reduced expression reduced left atrial dimension

244 cardiac-restricted MT1-MMP overexpression or MT1-MMP reduced expression underwent PO for 4 weeks.

245 By effecting ECM remodeling, MT1-MMP regulates stem cell shape, thereby activating a

246 Upon MT1-MMP's arrival at the plasma membrane in pseudopodia,

247 the putative membrane interaction region of MT1-MMP (Ser466Pro) resulted in lower enzyme activation

248 is essential for BVI, but not LVI, and that MT1-MMP should be further explored as a predictor and th

249 -3 in concanavalin A-activated MSCs requires MT1-MMP signaling and is inhibited by EGCG.

250 melanoma cells and identify Notch1 as a new MT1-MMP substrate that plays important biological roles

251 fection of primary human monocytes increased MT1-MMP surface expression 31.7-fold and gene expression

252 cyte networks caused a 17.5-fold increase in MT1-MMP surface expression dependent on p38 MAPK and G p

253 the submesothelial collagen matrix on which MT1-MMP-T567E MCAs rapidly disperse.

254 Cells expressing MT1-MMP-T567E phosphomimetic mutants exhibit enhanced ce

255 Furthermore, MCAs formed from MT1-MMP-T567E-expressing cells adhere avidly to both int

256 FAs and also provide molecular insights into MT1-MMP targeting and function.

257 Importantly, we have found that this MT1-MMP targeting is dependent on an association with a

258 cycle and identify a structural function of MT1-MMP that is independent of its proteolytic activity.

259 dditional post-translational modification of MT1-MMP that regulates its trafficking and cellular inva

260 nd membrane type 1 matrix metalloproteinase (MT1-MMP), the latter of which we recently identified as

261 In contrast with the wild-type MT1-MMP, the diverse proteolytic activities of the swapp

262 sed not only to visualize the trafficking of MT1-MMP through the cell compartment, but also to quanti

263 uced expression of the essential collagenase MT1-MMP, thus affecting all aspects of an invasive pheno

264 tant role for SNARE-regulated trafficking of MT1-MMP to invadopodia during cellular invasion of ECM.

265 Trafficking of MT1-MMP to invadopodia is required for the function of t

266 ediated membrane traffic in the transport of MT1-MMP to invadopodia.

267 3)PYAYIREG(170)), as an essential region for MT1-MMP to promote cellular invasion.

268 of the transmembrane matrix metalloprotease, MT1-MMP to promote invasive behaviour leading to basemen

269 te membrane type-1 matrix metalloproteinase (MT1-MMP) to podosomes or invadosomes to break extracellu

270 the membrane-type 1 matrix metalloprotease (MT1-MMP) to shedding microvesicles.

271 of membrane type I matrix metalloproteinase (MT1-MMP) to the leading edge is thought to be a crucial

272 eases, such as the transmembrane collagenase MT1-MMP, together with actin-based protrusions, to break

273 synthesizes a pool of PI(4)P that maintains MT1-MMP traffic in the degradative pathway and suppresse

274 st-translational modification is involved in MT1-MMP trafficking as well as in modulating cellular in

275 PI4KIIbeta depletion caused increased MT1-MMP trafficking to invasive structures at the plasma

276 extension of invasive pseudopods into which MT1-MMP traffics and for providing the correct cytoskele

277 and Vimentin expression was upregulated upon MT1-MMP transfection into cells.

278 NMR derived structural models indicate that MT1-MMP transiently associates with bicelles and cells t

279 However, pathways of MT1-MMP up-regulation are not clearly understood.

280 Furthermore, cancer cell-expressed MT1-MMP upregulated the expression of MT1-MMP in vascula

281 a membrane in pseudopodia, N-WASP stabilized MT1-MMP via direct tethering of its cytoplasmic tail to

282 al and fluorogenic activity of GNP-ActFP for MT1-MMP via fluorescence multi-reader.

283 pression of membrane type 1 metalloprotease (MT1-MMP) via down-regulating the kinesin-like protein KI

284 Overexpression of MT1-MMP was confirmed in Kazakh ESCC patients.

285 Expression of MT1-MMP was detected by immunohistochemistry and tissue

286 MT1-MMP was expressed predominantly in the syncytiotroph

287 Basal expression of MMP-2,-3, -9 and MT1-MMP was found in the retina of healthy, adult mice.

288 tial expression pattern of MMP-2, -3, -9 and MT1-MMP was studied in the healthy mouse retina via immu

289 In our search for noncatalytic inhibitors of MT1-MMP, we compared the protumorigenic activity of wild

290 ort for our findings that Snail can regulate MT1-MMP, we examined the expression of Snail and MT1-MMP

291 s, including MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, we identify the membrane-anchored MMP, MT1-MMP,

292 cells that express low endogenous levels of MT1-MMP were engineered to express wild-type MT1-MMP, a

293 ed membrane type-1 matrix metalloproteinase (MT1-MMP) were selectively up-regulated and coexpressed i

294 t cancer HCC1806 cells is partly mediated by MT1-MMP, which also regulates collagen-induced receptor

295 A tempting target is the membrane-associated MT1-MMP, which has well-documented importance in matrix

296 ed expression of mesenchymal genes including MT1-MMP, which was required for collagen-stimulated inva

297 ctural and energetic changes associated with MT1-MMP while interacting with substrates.

298 red the protumorigenic activity of wild-type MT1-MMP with an MT1-MMP mutant lacking PEX (DeltaPEX).

299 lso correlated the expression of cancer cell MT1-MMP with blood vessel invasion (BVI) in 102 breast c

300 was accompanied by reduced colocalization of MT1-MMP with membranes containing the endosomal markers

301 By using an MT1-MMP Y573A mutant or the Src family inhibitor PP2, we