ライフサイエンスコーパス: MMP-13

1 h no changes in matrix metalloproteinase 13 (MMP 13).

2 and (S)-17b) of matrix metalloproteinase 13 (MMP-13).

3 ctor (bFGF) and matrix metalloproteinase-13 (MMP-13).

4 etalloproteinase (MMP)-1, MMP-3, MMP-10, and MMP-13.

5 ession pattern similar to that of endogenous MMP-13.

6 of aggrecanases and collagenases, especially MMP-13.

7 sion of HDAC4 decreases the PTH induction of MMP-13.

8 inhibited the IL-1beta-induced production of MMP-13.

9 -13 promoter and subsequent transcription of MMP-13.

10 0.01), and attenuated induction of MMP-3 and MMP-13.

11 MMPs, MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, or MMP-13.

12 eading to increased production of S100A4 and MMP-13.

13 ct inhibited the IL-7-mediated production of MMP-13.

14 low to middle micromolar range for MMP-8 and MMP-13.

15 s, including Indian hedgehog, collagen X and MMP-13.

16 ar correlation with the endogenous levels of MMP-13.

17 is were prevented by inhibitors of MMP-3 and MMP-13.

18 on of the PTH-responsive minimal promoter of MMP-13.

19 omolar range, including MMP-2 (~2 to 50 nM), MMP-13 (~2 to 50 nM), and MMP-14 (~4 to 60 nM).

20 Matrix metalloproteinase-13 (MMP-13), a catabolic cartilage-degrading enzyme, is dram

21 Further, short hairpin RNA targeting MMP-13 abolishes pro-MMP-9 activation and HSC trans-diff

22 d Rac1 activity and promoted the increase in MMP-13 above that achieved by stimulation with FN fragme

23 We further demonstrate that pro-MMP-13 activation is facilitated with a membrane-associa

24 0a, (R)-10a, and 10b were binding within the MMP-13 active site, the Zn(2+) chelating unit was replac

25 t, AH23848) mimicked celecoxib by inhibiting MMP-13, ADAMST-5 expression, and proteoglycan degradatio

26 egrading enzyme production, including MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5.

27 MMP-13, ADAMTS-5, and the BMP antagonist noggin were ele

28 matrix-associated proteins (e.g., Aggrecan, MMP-13, ADAMTS-5, collagen II) in human knee joint chond

29 a key intermediate in the synthesis of dual MMP-13/aggrecanase inhibitors, is described.

30 s including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondrocytes.

31 ence of miR-146a increases the percentage of MMP-13 and ADAMTS-5 positive cells after treatment with

32 nt and in-situ levels of catabolic proteins (MMP-13 and ADAMTS-5) in the nucleus pulposus of the disc

33 rase chain reaction was performed to examine MMP-13 and DDR-2 messenger RNA (mRNA).

34 high levels of the matrix metalloproteinase MMP-13 and determined that MMP-13 directly enhances oste

35 mutation of DDR-2 reduced levels of mRNA for MMP-13 and endogenous DDR-2.

36 evels of several MMPs, including collagenase MMP-13 and gelatinase MMP-9.

37 induced the expression of MMP-2, MMP-9, and MMP-13 and hence regulated the metastasis of SKOV-3 ovar

38 not in Matrigel, IL-1 induces expression of MMP-13 and its matured form at 50 and 25 kDa, respective

39 TIMP-3 similarly bridged binding of MMP-13 and MMP-14 to LRP-1.

40 nd aggrecan expression, and decreased MMP-3, MMP-13 and RANKL expressions in cartilage, increased BMD

41 s aggrecans expression but stimulates MMP-3, MMP-13 and RANKL production by chondrocytes through ERK1

42 nds that showed a high degree of potency for MMP-13 and selectivity against other MMPs were designed

43 ch bind within the substrate-binding site of MMP-13 and surround the catalytically active Zn(2+) ion

44 y for the synergistic induction of MMP-1 and MMP-13 and the cartilage breakdown stimulated by IL-1+OS

45 oreover, the secreted collagenases MMP-1 and MMP-13 and the glycosylphosphatidylinositol-anchored mem

46 In parallel, the extent of MMP-13 and type II collagen breakdown products was eleva

47 ssion of DDR-2, matrix metalloproteinase 13 (MMP-13), and MMP-derived type II collagen fragments was

48 RNA) for matrix metalloproteinase 1 (MMP-1), MMP-13, and ADAMTS-4 also increased, while type II colla

49 Cells positive for MMP-9, MMP-13, and alpha-SMA expression were present at the are

50 Akt phosphorylation, induction of MMP-1 and MMP-13, and cartilage collagenolysis.

51 -beta 1, matrix metalloproteinase-2 (MMP-2), MMP-13, and interferon alpha-receptors 1 and 2.

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

53 trate selectivity among MMP-1, MMP-2, MMP-8, MMP-13, and MMP-14/membrane-type 1 (MT1)-MMP.

54 einases (matrix metalloproteinase 1 [MMP-1], MMP-13, and MMP-3), tissue inhibitor of metalloproteinas

55 Increased immunostaining for DDR-2, MMP-13, and MMP-derived type II collagen fragments was d

56 presented the collagen preferences of MMP-8, MMP-13, and MT1-MMP well.

57 is hydrolyzed by MMP-1, MMP-2, MMP-8, MMP-9, MMP-13, and MT1-MMP.

58 ncreased expression of alkaline phosphatase, MMP-13, and osteopontin but decreased expression of oste

59 B-1, matrix metalloproteinase 3 (MMP-3), and MMP-13, and protein expression of type X collagen were a

60 etastasis-promoting Runx2 target genes IL11, MMP-13, and PTHrP.

61 ssenger RNA for type II and type X collagen, MMP-13, and RUNX-2 was examined by real-time quantitativ

62 the matrix metalloproteinase 1 gene (MMP-1), MMP-13, and several other genes involved in the control

63 old selectivity against ADAMTS-1, ADAMTS-13, MMP-13, and TACE.

64 cies (ROS) formation as possible inducers of MMP-13, and we analyzed MMP-13-dependent damage.

65 gh potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-1, -2, -3, -7, -8, -9,

66 Elevated levels of MMP-13 are associated with alveolar bone resorption, per

67 s (MMPs), selective inhibitors of MMP-12 and MMP-13 are available and may be appropriate for developm

68 oproteinases MMP-2, MMP-3, MMP-7, MMP-9, and MMP-13 are highly expressed in the tumor-bone microenvir

69 Matrix metalloproteinases (MMPs), especially MMP-13, are key enzymes in the cleavage of type II colla

70 ory cytokine-induced production of MMP-1 and MMP-13 at the level of gene transcription and blocks col

71 on of matrix metalloproteinase 9 (MMP-9) and MMP-13, both of which have been causally linked to the i

72 ficiency yielded decreased activation of pro-MMP-13 but not of pro-MMP-2 or pro-MMP-8.

73 vitro reconstitution experiment proves that MMP-13, but not its zymogen, activates pro-MMP-9.

74 s a critical transcriptional activator of of MMP-13 by bFGF in human articular chondrocytes.

75 er with 5 HO-proline residues resulting from MMP-13-catalyzed degradation, was validated for clinical

76 Unexpectedly, MMP-1 and MMP-13 cleave the N-terminal exodomain of PAR1 at noncan

77 was not cleaved by MMP-1 (collagenase 1) or MMP-13 (collagenase 3).

78 p-regulation of matrix-metalloproteinase 13 (MMP-13, collagenase 3) in the skin.

79 elates to the unique collagen specificity of MMP-13 compared with MMP-8 and MT1-MMP, in that MMP-13 h

80 Increased expression of MMP-13 correlated with down-regulation of miR-27b.

81 possible inducers of MMP-13, and we analyzed MMP-13-dependent damage.

82 metalloproteinase MMP-13 and determined that MMP-13 directly enhances osteoclast multinucleation and

83 n pathways associated with the expression of MMP-13 down-regulated the expression of miR-27b.

84 Finally, we show that MMP-13 dysregulation also underlies paclitaxel-induced p

85 of catalytically inactive full-length human MMP-13(E223A) in complex with peptides of 14-26 aa deriv

86 MMP-13 elicited similar levels of ERK1/2 activation but

87 In addition, VEGF-induced MMP-9 and MMP-13 expression and in vitro cell invasion were signif

88 Periostin increased MMP-13 expression dose [1-10 microg/ml (EC50 0.5-1 mug/m

89 urther, in mouse xenograft models, silencing MMP-13 expression in myeloma cells inhibited the develop

90 ility of TCN to inhibit PTH- or PGE2-induced MMP-13 expression in osteoblastic cells.

91 MMP-13 expression is strongly up-regulated in arthritis,

92 1 is a direct target of NFkappaB and induces MMP-13 expression upon activation of the NFkappaB signal

93 y assay measuring repression of IL-1 induced MMP-13 expression was 3.5 nM, exhibiting 87% of the maxi

94 h or without IL-1 revealed that IL-1-induced MMP-13 expression was augmented by PGE(2) and significan

95 portance is our finding that IL-6-stimulated MMP-13 expression was independent of IL-1beta stimulatio

96 Periostin induction of MMP-13 expression was inhibited by CCT031374 hydrobromid

97 In patient cohorts, MMP-13 expression was localized to BM-associated myeloma

98 the effects on proliferation, migration, and MMP-13 expression were analyzed.

99 n (as measured by inhibition of IL-1 induced MMP-13 expression) but showing an attenuated capacity fo

100 ene deletion in vivo leads to an increase in MMP-13 expression, and overexpression of HDAC4 decreases

101 a indicate that 3 factors, DDR-2 expression, MMP-13 expression, and the degree of cartilage damage, a

102 en expression and repressing Runx2-inducible MMP-13 expression.

103 beta signals through p38 and Runx2 to induce MMP-13 expression.

104 id and dynamic repression of Runx2-inducible MMP-13 expression.

105 ed synoviocyte proliferation, migration, and MMP-13 expression.

106 However, the increased DDR2 did not induce MMP-13 expression.

107 of endogenous periostin blocked constitutive MMP-13 expression.

108 , inhibited RASF secretion of MMP-1, but not MMP-13, following induction with TNFalpha (P = 0.0007) o

109 roles have also been described for elastase, MMP-13, gelatinases, mast cell proteases and proteases d

110 We have previously shown that Mmp-13 gene expression is highly induced by PTH treatmen

111 MMP-13 gene expression was synergistically induced by NR

112 onse element of MMP-13, which contributes to MMP-13 gene expression.

113 en shown to be required for IL-1beta-induced MMP-13 gene expression.

114 Matriptase also induced MMP-1, MMP-3, and MMP-13 gene expression.

115 e observations indicate that HDAC4 represses MMP-13 gene transcription in bone.

116 2, binds the MMP-13 promoter, and suppresses MMP-13 gene transcription in the rat osteoblastic cell l

117 d S100A4 as a regulator of expression of the MMP-13 gene.

118 tated by an MMP activation cascade (MMP-14 > MMP-13 > MMP-9) and a positive feedback loop of MMP-9 >

119 Matrix metalloproteinase 13 (MMP-13) has attracted attention as a target with disease

120 Matrix metalloproteinase 13 (MMP-13) has been shown to be the main collagenase respon

121 the IL-1beta-mediated induction of MMP-1 and MMP-13 heterogeneous nuclear RNA, messenger RNA, and pro

122 -13 compared with MMP-8 and MT1-MMP, in that MMP-13 hydrolyzes type II collagen efficiently, whereas

123 ition potencies for MMP-2, MMP-8, MMP-9, and MMP-13 (IC(50) = 0.006-107 nM).

124 Compound 24f is a subnanomolar inhibitor of MMP-13 (IC(50) value 0.5 nM and K(i) of 0.19 nM) having

125 neration through suppressing hypertrophy and MMP-13 in a mouse osteoarthritis model.

126 hritic joint disease, expression of bFGF and MMP-13 in chondrocytes and their release into the synovi

127 on and the resulting increased expression of MMP-13 in chondrocytes.

128 g event in the bFGF-dependent stimulation of MMP-13 in human adult articular chondrocytes.

129 play a role in regulating the expression of MMP-13 in human chondrocytes.

130 y was to determine whether the expression of MMP-13 in human osteoarthritis (OA) chondrocytes is regu

131 and the production of IL-6, IL-8, MMP-1, and MMP-13 in human RA SFs.

132 r S100A4 was bound to the promoter region of MMP-13 in IL-1beta-treated cells.

133 ckade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in a systemi

134 -6), matrix metalloproteinase 3 (MMP-3), and MMP-13 in joint tissue as compared to ASIC-3(+/+) mice.

135 Inhibiting TGF-betaR1 suppressed MMP-13 in OA-MSC but stimulated it in OAC.

136 it induced hypertrophy, mineralization, and MMP-13 in OA-MSC.

137 y reduced PTH or PGE2 elevated expression of MMP-13 in osteoblastic cells without affecting basal lev

138 factor, and enzymes MMP-1, MMP-2, MMP-3, and MMP-13 in RA synovial membrane cell cultures.

139 rtrophic markers including Runx2, Col X, and MMP-13 in response to SDF-1 treatment.

140 munosorbent assay for secretion of MMP-1 and MMP-13 in the presence of tumor necrosis factor alpha (T

141 rostaglandin E2 (PGE2)-induced expression of MMP-13 in UMR 106-01 cells, an osteoblastic osteosarcoma

142 as able to activate latent pro-MMP-3 and pro-MMP-13 in vitro.

143 cytes with IL-1beta induces transcription of MMP-13 in vitro.

144 X collagen and matrix metalloproteinase 13 (MMP-13) in articular chondrocytes were examined by in si

145 Pharmacological inhibition of MMP-13, in contrast, largely rescued paclitaxel-induced

146 MMP-13 increased 40-fold in the MI only group (P<0.05) b

147 on of matrix metalloproteinase 1 (MMP-1) and MMP-13 induced by proinflammatory cytokines in a chondro

148 Furthermore, in a rat model of MMP-13-induced cartilage degradation, 24f significantly

149 t the epidermal matrix-metalloproteinase 13 (MMP-13) induces degeneration of unmyelinated axons, wher

150 MMP-13 induction was also reduced by loss of function of

151 Since MMP-13 inhibition prevents axon degeneration but does no

152 This highly selective MMP-13 inhibitor exhibits chondroprotective effects in m

153 The potent and selective MMP-13 inhibitor PF152 decreased human cartilage degrada

154 An effective MMP-13 inhibitor would therefore be a novel disease modi

155 the joint structural changes induced by the MMP-13 inhibitor.

156 th MMP-13 with published structures of known MMP-13.inhibitor complexes followed by molecular design

157 dentified a novel, highly selective class of MMP-13 inhibitors (compounds 1 (Q), 2 (Q1), and 3 (Q2)).

158 hese design approaches led to small molecule MMP-13 inhibitors 10d and (S)-17b, which bind within the

159 Importantly, specific MMP-13 inhibitors also decreased alkaline phosphatase-PA

160 the potential therapeutic value of selective MMP-13 inhibitors and the use of a set of appropriate bi

161 To this end, selective and potent MMP-13 inhibitors based on a N,N'-bis(benzyl)pyrimidine-

162 MMP-13 inhibitors exert chondroprotective effects and ca

163 s (MSS) was used to assess whether selective MMP-13 inhibitors have the joint toxicity associated wit

164 to evaluate the chondroprotective ability of MMP-13 inhibitors in a chronic disease model of OA.

165 was implemented for assessing the effects of MMP-13 inhibitors on cartilage degradation and joint pai

166 identify a new class of potent and selective MMP-13 inhibitors that would provide histologic and clin

167 ted in this study represent a novel class of MMP-13 inhibitors.

168 ent and selective carboxylic acid containing MMP-13 inhibitors; however, nephrotoxicity in preclinica

169 These modes of peptide-MMP-13 interactions have led us to propose how triple he

170 MMP-13 is a collagenase with a substrate preference for

171 Moreover, pro-MMP-13 is also activated by a secreted factor, which is

172 Together, these data demonstrate that MMP-13 is critical for the development of osteolytic les

173 MPs induced in HSCs by the dual stimulation, MMP-13 is most conspicuously up-regulated and meets all

174 However, the precise functions by which MMP-13 is regulated and affects axons remained elusive.

175 Matrix metallopeptidase-13 (MMP-13) is a highly active and an abundantly expressed p

176 Matrix metalloproteinase-13 (MMP-13) is a zinc-dependent protease responsible for the

177 Matrix metalloproteinase-13 (MMP-13) is an important enzyme for the modulation of bon

178 1 gene expression, which activates MMP-9 and MMP-13, leading to the invasion and scattering of SKOV-3

179 MMP-3, MMP-12, and MMP-13 levels also correlated with mean PD of affected s

180 ween MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 levels and percentage of sites with PD >4 mm.

181 in, interleukin (IL)-1beta, IL-8, MMP-8, and MMP-13 levels were measured using enzyme-linked immunoso

182 MMP-1, MMP-8, MMP-9, MMP-12, and MMP-13 levels were reduced significantly up to 6 months,

183 R-2, resulting in the elevated expression of MMP-13, may be one of the common events in OA progressio

184 llagen and aggrecan protein due to excessive MMP-13-mediated proteolysis of these key cartilage matri

185 II collagen or gelatin, levels of DDR-2 and MMP-13 messenger RNA (mRNA) in primary human articular c

186 2 regulation of matrix metalloproteinase 13 (MMP-13) messenger RNA (mRNA) and protein expression.

187 major type I collagenolytic MMPs, including MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, we identify the

188 sts harboring single deficiencies for either MMP-13, MMP-8, MMP-2, or MMP-9 to continue to degrade co

189 g (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13) and osterix (Sp7).

190 ter construct containing the 3'-UTR of human MMP-13 mRNA and inhibited the IL-1beta-induced expressio

191 ce in the 3'-untranslated region (3'-UTR) of MMP-13 mRNA complementary to the seed sequence of microR

192 n of PCAF, p300, or Runx2 by siRNA decreased Mmp-13 mRNA expression after PTH treatment in both UMR 1

193 s were stimulated with PTH or PGE2 to induce MMP-13 mRNA expression, and real-time reverse transcript

194 revealed an up-regulation of both DDR-2 and MMP-13 mRNA in human articular chondrocytes after stimul

195 preincubation with the p38 inhibitor reduced MMP-13 mRNA levels.

196 Moreover, IL-13r alpha2, MMP-13 mRNA, and MMP-13 protein were higher in KO mice t

197 achieved by the catalytic domain of MMP-1 or MMP-13, nor by full-length MMP-3.

198 results suggest that elevated expression of MMP-13 occurs through Elk-1 activation of both MAPK and

199 epithelial damage and neurotoxicity, whereas MMP-13 overexpression in zebrafish embryos rendered the

200 led to increased secretion and activation of MMP-13 (P<0.05).

201 The matrix metalloproteinase enzyme MMP-13 plays a key role in the degradation of type II co

202 The collagenase matrix metalloproteinase-13 (MMP-13) plays an important role in the destruction of ca

203 Herein we report our efforts to optimize the MMP-13 potency and pharmacokinetic properties of non-car

204 te preferences within secreted MMPs, because MMP-13 preferred the interrupted sequence, while MMP-8 s

205 axons, whereas pharmacological inhibition of MMP-13 prevented axon degeneration.

206 ic ablation or pharmacological inhibition of MMP-13 prevented isoproterenol-dependent cardiac dysfunc

207 In this study, we investigated MMP-13 production by bFGF using human articular chondroc

208 -regulated in OA cartilage and can stimulate MMP-13 production by chondrocytes, this signaling pathwa

209 artilage and the ability of Rac to stimulate MMP-13 production suggest that it could play a role in t

210 0A4 acts in an autocrine manner to stimulate MMP-13 production via RAGE.

211 age and that extracellular S100A4 stimulates MMP-13 production, a major type II collagen-degrading en

212 negative Rac, blocked FN fragment-stimulated MMP-13 production, while expression of constitutively ac

213 -induced signaling that results in increased MMP-13 production.

214 ssion of constitutively active Rac increased MMP-13 production.

215 stimulated by FN fragments, which results in MMP-13 production.

216 Again, VEGF-induced MMP-9 and MMP-13 promoter activities were down-regulated in ETS-1

217 oid hormone (PTH) regulates HDAC4 to control MMP-13 promoter activity through dissociation from Runx2

218 ls were analyzed by quantitative RT-PCR, and MMP-13 promoter activity was measured using reporter ass

219 had an additive effect on PTH stimulation of MMP-13 promoter activity, and this required their histon

220 cription, and PTH regulates HDAC4 to control MMP-13 promoter activity.

221 between p300 and PCAF to be recruited to the Mmp-13 promoter after PTH treatment.

222 nding to the reassociation of HDAC4 with the MMP-13 promoter and a decline in its transcription.

223 vents the release of HDAC4 from Runx2 on the MMP-13 promoter and also prevents the PTH stimulation of

224 n kinase-dependent release of HDAC4 from the MMP-13 promoter and subsequent transcription of MMP-13.

225 ed HDAC4 is released from Runx2 bound to the MMP-13 promoter in these cells.

226 MMP-13 promoter reporter assay was used to explore possi

227 NR4A2 directly transactivated the proximal MMP-13 promoter, and a point mutation in the DNA binding

228 se 4 (HDAC4) interacts with Runx2, binds the MMP-13 promoter, and suppresses MMP-13 gene transcriptio

229 xplore possible direct effects of TCN on the MMP-13 promoter.

230 e driven by the matrix metalloproteinase 13 (MMP-13) promoter were transfected into human chondrocyte

231 one modification in regions of the MMP-1 and MMP-13 promoters that contain binding sites for activato

232 ETS-1 bound to both MMP-9 and MMP-13 promoters.

233 eolytic lesions in MM and that targeting the MMP-13 protein - rather than its catalytic activity - co

234 inhibited the IL-1beta-induced expression of MMP-13 protein in chondrocytes.

235 Moreover, IL-13r alpha2, MMP-13 mRNA, and MMP-13 protein were higher in KO mice than that in WT mi

236 PCAF was increasingly recruited to the MMP-13 proximal promoter region after PTH treatment, and

237 , P <0.01), MMP-8 (r = 0.702, P = 0.02), and MMP-13 (r = 0.781, P = 0.01); chemerin and IL-8 (r = 0.9

238 3, P <0.01), MMP-8 (r = 0.770, P <0.01), and MMP-13 (r = 0.788, P <0.01); and progranulin and IL-8 (r

239 2, P <0.01), MMP-8 (r = 0.845, P <0.01), and MMP-13 (r = 0.813, P <0.01).

240 ase of NO and blunted induction of MMP-3 and MMP-13 release.

241 ur findings suggest that bFGF stimulation of MMP-13 required the activation of multiple MAPKs (ERK, p

242 aled two binding modes for compound 2 in the MMP-13 S1' subsite and in an S1/S2* subsite.

243 ) inhibited spontaneous MMP-1, but augmented MMP-13 secretion by OA cartilage explant cultures.

244 biological evaluation of a non-zinc binding MMP-13 selective inhibitor, 4-methyl-1-(S)-({5-[(3-oxo-3

245 BM-associated myeloma cells, while elevated MMP-13 serum levels were able to correctly predict the p

246 MMP-13 showed the opposite behavior with a decreased k(c

247 in solid-phase binding assays, we found that MMP-13 shows little affinity for Collagen Toolkit III, b

248 PKCdelta is the only isoform associated with MMP-13 stimulation among the PKC isoforms tested.

249 Moreover, we found that recombinant MMP-13 stimulation cleaved alkaline phosphatase-PAR1 in

250 inase C (PKC) delta played a key role in the MMP-13 stimulation.

251 P-9) and a positive feedback loop of MMP-9 > MMP-13, suggesting their critical roles in liver injury

252 We investigated the mechanism of MMP-13 suppression by histone deacetylase inhibitor vori

253 aluated for assessing its potential use as a MMP-13 targeting PET imaging agent.

254 of a series of carboxylic acid inhibitors of MMP-13 that do not significantly inhibit the related MMP

255 vative 4, a selective picomolar inhibitor of MMP-13, the radiolabeled counterpart [(18)F]4 was succes

256 cific recognition of immobilized peptides by MMP-13; the enzyme proved able to cleave a range of diss

257 artilage degeneration in OA by up-regulating MMP-13 through canonical Wnt signaling.

258 tion of matrix metalloproteinase (MMP)-2 and MMP-13 through its coactivation of AP-1 and PEA3.

259 and insulin-like growth factor-1 and induces MMP-13 through protein kinase Cdelta-dependent activatio

260 ytes to produce matrix metalloproteinase 13 (MMP-13) through activation of the receptor for advanced

261 uired for the adhesion of both proMMP-13 and MMP-13 to one of these, Toolkit peptide II-44, which con

262 emonstrate that beta-AR stimulation leads to MMP-13 transactivation of PAR1 in both cardiac fibroblas

263 The inhibitory effect of LG268 on MMP-1 and MMP-13 transcription appears to be mediated, at least in

264 rHDAC4 at Ser-740 is crucial for regulating MMP-13 transcription in osteoblasts.

265 uence approximately 20 kb 5' relative to the MMP-13 transcription start site (TSS).

266 ing, partial degradation, and the control of MMP-13 transcription through association with Runx2.

267 Thus, HDAC4 is a basal repressor of MMP-13 transcription, and PTH regulates HDAC4 to control

268 p300 and Runx2 to mediate PTH activation of MMP-13 transcription.

269 ator that is required for PTH stimulation of MMP-13 transcription.

270 and Runx2, is required for PTH activation of Mmp-13 transcription.

271 e due to a decrease in the rate of MMP-1 and MMP-13 transcription.

272 ter and also prevents the PTH stimulation of MMP-13 transcription.

273 al repressor of matrix metalloproteinase-13 (MMP-13) transcription and parathyroid hormone (PTH) regu

274 hat PTH induces matrix metalloproteinase-13 (MMP-13) transcription in osteoblastic cells.

275 conserved region at 20 kb upstream from the MMP-13 TSS includes a distal transcriptional response el

276 ings this region in close proximity with the MMP-13 TSS.

277 A is a potent suppressor of IL-1beta-induced MMP-13, tumor necrosis factor-alpha, and other catabolic

278 Significant selectivity of MMP 13 versus MMP-2 can be achieved by subtle chain cont

279 The effect of IL-6 on the expression of MMP-13 was determined by treating chondrocytes with reco

280 in conditioned media by immunoblotting, and MMP-13 was measured by enzyme-linked immunosorbent assay

281 bFGF stimulation of MMP-13 was mediated at the transcriptional level and, at

282 Indian hedgehog, Patched-1, collagen X, and MMP-13 was reduced and accompanied by decreases in endoc

283 Gene expression of synovial IL-6, MMP-3, and MMP-13 was significantly inhibited in MKK-6-deficient mi

284 n of binding of the free hemopexin domain of MMP-13 was similar to that of the full-length enzyme, bu

285 enases, particularly MMP-8 and MMP-13, where MMP-13 was the key collagenase.

286 MMP-13 was unable to bind to a linear peptide of the sam

287 Increased expression of type X collagen and MMP-13 were also detected in articular cartilage from tr

288 P-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-12, and MMP-13 were assessed using fluorometric kits.

289 trix metalloproteinase 8 (MMP-8), MMP-9, and MMP-13 were elevated in the cartilage of y/y mice.

290 CD68, MMP-12, and MMP-13 were significantly higher in CC10-IL-13 Tg lungs.

291 metallocollagenases, particularly MMP-8 and MMP-13, where MMP-13 was the key collagenase.

292 tant to cleavage by MMP-1, MMP-2, MMP-9, and MMP-13, whereas non-cross-linked collagen I, IV, and nat

293 these genes is matrix metalloproteinase-13 (MMP-13), which is involved in bone remodeling and early

294 by activating the zymogen forms of MMP-3 and MMP-13, which are constitutively present in articular ca

295 a distal transcriptional response element of MMP-13, which contributes to MMP-13 gene expression.

296 chondrial damage, leading to upregulation of MMP-13, which in turn underlies increased epidermal extr

297 Both sequences were selectively cleaved by MMP-13 while in linear form, but neither proved to be se

298 t genes, matrix metalloproteinases mmp-9 and mmp-13, while cortisol led to stronger upregulation of t

299 phic structure of compound 5 in complex with MMP-13 with published structures of known MMP-13.inhibit

300 new insight into the relevance of MMP-10 and MMP-13 within the MMP network and the ban of hydroxamate